8th Sino –Singapore Conference in Biotechnology

dactylonomyskittlesBiotechnology

Feb 12, 2013 (4 years and 10 months ago)

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-

1

-

9
th

Sino


Singapore
Symposium
on

Biology

第九届中国
-
新加坡生物学

学术研讨会



11
-
13 November 2008

Yunnan University, Kunming, China














A Conference jointly organized by National University of Singapore,

Tsinghua University, Xiamen University and Yunnan Unive
rsity


2

Scientific program: The 9
th

Sino
-
Singapore
Symposium

on Biology

11
-
13 November 2008

Yunnan University, Kunming, China


Time

Activity

11 Nov, Tues

Opening Ceremony

9:00


9.2
0 am

Welcome Address by Prof. Zhang Keqin, vice
-
President,
Yunnan Univer
sity

Opening Address by

Prof. Lai Choy Heng
,
Vice Provost,
National University of Singapore

9:2
0


10.00 am

Plenary Lecture



Chaired by Li Peng
(Tsinghua University)


Paul Matsudaira

(National University of Singapore)


The Mechanics of Cell Migration on
2D and in 3D Matrices

10:00


10:30 am

Group Photo
-
taking and Coffee break

Session I

Adipose regulation & diabetic mechanism

Chair: Ding Ming
-
Xiao
(Peking University)

10:30


10:50 am

Li Peng

(Tsinghua University)


Regulation of Adipose Tissue Identity

by CIDE Proteins

10:50


11:10 am

Zheng Ling

(Wuhan University)

Alteration of Transcriptional Machinery in the Retinas of Diabetic
Rat

11:10


11:30 am

Zhai Yonggong

(Beijing Normal University)

SAW inhibits adipocyte differentiation and adipogenesis me
diated
by LXR and PPARγ pathway

11:30


11:50 pm

Wang Hongyan
(Fudan University)

Whole genome microarray evaluation of genomic imbalance in
Chinese patients with metal retardation

12:00 pm
-
2:00 pm

Lunch


3

Session II

Structure Biology & Chemical Biology

Chair: Hew Choy Leong
(National University of Singapore)

2:00


2:20 pm

Davis T.W. Ng
(Temasek Life sciences Laboratory and National
University of Singapore)

Intrinsic structural sensors report glycoprotein folding failures by
displaying bipartite degrad
ation signals

2:20


2:40 pm

Liu Xinqi

(Nankai university)


The mechanism of antigen activated T cell apoptosis

2:40


3:00 pm

Song
Jianxing
(National University of Singapore)

Molecular Mechanism and Drug Design to Enhance
Regeneration of the Injured CNS

Axons by Targeting Nogo
-
NgR
and Eph
-
eprin Signalling Interfaces

3:00


3:20 pm

Zhu

Zuoyan

(Peking University)

A Glance at Science and the Journals in China

3:20


3:50 pm

Coffee break

Session III

Cell & Developmental Biology

Chair: Lin Shengcai
(Xiame
n University)

3:50


4:10 pm

Wei Wensheng

(Peking University)

Effect of Wnt
-
signaling components in anthrax toxicity

4:10


4:30 pm

Hwang Gwo
-
jiunn

(Nanchang University)

Investigation on the effects of mutations in the yeast ribosomal
protein L36 on th
e functioning of assembled ribosomes and on
the expression of its target genes

4:30


4:50 pm

Cynthia He
(National University of Singapore)

A tale of two centrins

4
:
5
0


5
:
1
0 pm

Liu
Dong
(Peking University)

Foxi1 and Sox9 Act in a Molecular Switch that
Regulates
Transition of Preplacodal Ectoderm into Otic Placode


End of Day 1


Conference Banquet hosted by Yunnan University


4

12


Nov Wed

Day 2

Session IV

Biodiversity and Ecology

Chair: Ye Hui (Yunnan University)

9:00


9:20 am

Li Wenjun

(Yunnan Unive
rsity)

Studies on Biodiversity and Systematics of Actinobacterial
Resources under Extreme Environments in the West of China

9:20


9:40 am

Richard T. Corlett

(National University of Singapore)

Climate change and plant migration potential on the edge of th
e
tropics

9:40


10:00 am

Xu Ping

(Shanghai Jiaotong University)

Recent Developments in Microbial Degradation of Sulfur,
Nitrogen and Oxygen Heterocycl

10:00


10:20 am

Coffee break

10:20


10:40 am

Shen Yuemao
(Xiamen University)


A metagenomic approac
h to the biosynthetic origin of plant
maytansinoids

10:40


11:00 am

Huang Xiaowei
(Yunnan University)

Virulence of
Bacillus nematocida

to

Caenorhabditis elegans
: A
novel bacterial pathogenesis


End of Day
2

11:00am
-

6:00 pm

Lunch and sightseeing at Sto
ne forest National Park

7:00 pm

Conference Banquet hosted by National University of
Singapore






5


13 Nov
,

Thurs

Day 3

Session V

Genetic & Genomics

Chair : Niu Liwen
(University of Science and Technology of
China)

9:00


㤺㈰ 慭

Wang Qiang

(
Nanjing Un
iversity
)

Insertion/deletion: the inner cause of genomic mutation


9:20


㤺㐰 慭

Yu Haijing

(Yunnan University)

The Human
-
Specific Gene c1orf37
-
dup Encodes a
Transmembrane Protein

9:40


㄰:0
0 慭

Wang Xuelu
(Fudan University)

Regulatory mechanisms of br
assinosteroid signaling in plants

10:00
-
10:30 am

Coffee Break

10:30


㄰:R
0 慭

H
ao
Yu
(National University of Singapore)


A Genetic Framework for Flower Initiation

10:50


ㄱ:㄰



Tao
Yi
(Xiamen University)

The power of genetics in dissecting plant sha
de avoidance
signaling pathway

11:10


ㄱ:P
0 慭

He
Xionglei
(Sun Yat
-
sen University)

A network view on the action of plant hormones

11:30
-
11:5
0 am



12:00


2:00 pm

LUNCH










6

Session VI

Cellular Biology and Signal Transduction

Chairs: S
h
u H
ongb
in
(Wuhan University)

2:00


2:20 pm

Wu

Geng
(Shanghai Jiao Tong University)

Studies on the regulations of beta
-
catenin phosphorylation and
ubiquitination

2:
2
0


2
:
4
0 pm

Li

Wenhua
(Wuhan University)


IGF
-
1 promote BPH
-
1 cell proliferation primarily via
activating
mTOR
-
dependent translational increases in cyclin D proteins

2
:
4
0


3:
0
0 pm

Lin Shengcai

(Xiamen University)

To die or not to die

3:0
0


3:
2
0 pm


3:20 pm

Closing Remarks

4:00 pm

Depart for Lijiang




7

The Mechanics of Cell Migration on 2D a
nd in 3D Matrices


Paul Matsudaira


Member, Whitehead Institute for Biomedical Research

Professor, Departments of Biology and Biological Engineering, MIT

matsudaira@wi.mit.edu

from January 1, 2009,
dbsmpt@nus.edu.sg


Cell migration is fundamental to the development of the embryo and in the maintenance of the
adult. The organization of embryonic tissues results from various types of cell movements. Some
cells migrate ind
ividually to distant sites where they establish new compartments in the body
plan. In other cases, confluent masses of cells stream to cover new surfaces. In the adult,
migratory macrophages and neutrophils survey tissues as part of the immune system. Epit
helial
cells migrate along the length of the intestinal villus but in colon cancer, they lose their
organization and migrate as mesenchymal cells that negotiate their way through the surrounding
connective tissue to establish metastatic tumors at distant s
ites. These examples of cell movement
are more complex and not easily understood from the current models of individual cells that
migrate over a flat surface. From first principles, we can identify three distinct types of cell
movements: movements of indiv
idual cells through a 3D matrix, migration of cell sheets on a 2D
basement membrane, and amoeboid motility. What are the distinctive features of these three types
of movements and how can we study their properties from experimental and computational
perspe
ctives?



8

Regulation of Adipose Tissue Identity by CIDE Proteins


Peng Li


Department of Biological Sciences and Biotechnology

Tsinghua University, Beijing, China


Adipose tissues can be divided into brown adipose tissue (BAT) and white adipose tissue (WAT
).
Both BAT and WAT contain abundant amount of lipid and can serve as energy storage organs.
BAT plays a unique role in energy expenditure by uncoupling oxidative phosphorylation and
dissipating

energy
as

heat to maintain core body temperature in animals
when expose to cold.
The
primary role of WAT is to store energy in the form of triglycerides (TAG) in lipid droplets and
immobilize the energy in time of needs such as starvation. Adipose tissue can also s
erve as an
endocrine organ to secret crucial hormones such as Leptin and Adiponectin for the control of
whole
-
body energy homeostasis. Cide proteins, including Cidea and Fsp27 (Cidec in human),
were originally identified by their sequence homology to the N
-
terminal region of DNA
fragmentation factor DFF40/45. While Cidea is expressed at higher levels in BAT, Fsp27
mRNAs and proteins were detected in WAT and BAT
. To understand the physiological role of
Cide proteins, we generated
Cidea

and
Fsp27
-
nu
ll mice by homologous recombination.
Interestingly

we observed that mice deficient in
Cidea

or
Fsp27

exhibited higher energy
expenditure and were resistant to high
-
fat
-
diet induced obesity and diabetes. Here, we will
compare the detail phenotype of
Cidea
a
nd
Fsp27
-
null mice and analyze the underlying
mechanism of Cide proteins in the regulation of adipose tissue identity.


9

Alteration of
T
ranscriptional
M
achinery in the
R
etina
s

of
D
iabetic
R
ats


Z
HENG Ling
1, 2

*
, L
IU
Shuqing

3, 4
, S
UN
Ming
-
Z
hong

3, 4
, C
HANG

Jinsook
3
,
M
ISHRA
Rangnath
1
, C
HANCE
Mark
3
, K
ERN
Timothy
1, 5, 6


1

Department of Medicine, Case Western Reserve University, Cleveland, Ohio, 44106

2

Present address: College of life science
,
Wuhan

University,
Wuhan
, China,
430072

3

Center for
P
roteomics
, Case Western Reserve University, Cleveland, Ohio, 44106

4
Present address:
Department of Biochemistry and Molecular Biology, Dalian Medical
University, Dalian, China, 116027

5
Department of Ophthalmology, Case Western Reserve University, Cleveland, Ohio,

44106

6
Louis Stokes Cleveland Department of Veterans Affairs Medical Center, Cleveland, Ohio,
44106


Author for correspondence:
ZHENG Ling
.

Tel
/Fax
: +86
027 68755559



E
-
M
ail:
lzheng
@
whu
.edu.cn
;

lzheng217
@
hotmail.
com


Numerous metabolic abnormalities have been championed as contributing to diabetic retinopathy,
yet therapies against these pathways generally have not inhibited the retinopathy in patients. Thus,
we have
used a proteomic approach to study diabetes
-
induced changes in cell regulation of retinal
metabolism. Two
-
dimensional differential in gel electrophoresis (2D DIGE) was used to profile
global protein expression changes in retinas from diabetic rats for 3 mo
nths. Of about 2400 spots
detected in 2D DIGE,
80 spots showed differences in intensity between retinas of diabetic and
nondiabetic rats. Among these spots, several histone proteins were identified

by MS/MS. Western
blots of total histones (such as histone

H2A, H2B, H3) and acetylated histones (such as
acetylated
-
histone H2A, H2B, H3 and H4) were performed, and the results demonstrated
statistically significant increases in levels of acetylated, but not total histones, in retinas of
diabetic rats compared t
o nondiabetic rats. Since acetylated histones are associated with
activation of gene transcription, we further investigated the transcription factor levels by
transcription factor array. DNA binding affinities of several transcription factors were increase
d
in the retina of diabetic rats compared to nondiabetic rats, and expression levels of some of these
transcription factors were verified by Western blots. Levels of several inflammatory gene
products, which are regulated by these transcription factors, we
re also increased in retinas of
diabetic rats. The present study indicates that diabetes activates numerous aspects of
transcriptional machinery in retina, including acetylation of histones, activation of certain
transcription factors, and upregulation of
inflammatory genes transcription.


10

SAW inhibits adipocyte differentiation and adipogenesis

mediated by LXR and
PPAR
γ

pathway


XIAO Lei, ZHANG Jun, XIE Xinni, ZHAI Yonggong


The Key Laboratory for
Cell P
roliferation

and Regulation
of the Ministry of Education, P. R.
China, and
Key
Laboratory
of Beijing
,

Beijing Normal University
,
Beijing 100875

P. R.
China


Author for

correspondence:
ZHAI Yonggong
.

Tel
/Fax
: +86
10 58806656
; E
-
Mail:
ygzhai@bnu.edu.cn



SAW
, a
kind of herb plant,
has been used
as
a Traditional Chinese Medicine (TCM) to eliminate
stomach heat, help in the digestio
n
body fat
and
regulate fatty acid metabolism.

Here, we report
that SAW inhibits adipocyte differentiation
of
3T3
-
L1 preadipocytes and suppresses the mitotic
clonal expansion

(MCE)

of 3T3
-
L1 preadipocytes

in a time
-

and

dose
-
dependent manner
.
Gene
expressi
on analysis

show

that
SAW reduced

expression of lipogenic genes such as
LXR and its
target gene
ADD1/SREBP1c
,

FAS
, and LPL,
and substantially decreased the expression of the
adipocyte
-
specific genes encoding PPAR
γ
(peroxisome proliferator
-
activated recept
or
γ
) and aP2.

B
ased on cell cycle analysis, SAW initiates MCE, during which preadipocytes synchronously
reenter the cell cycle. MCE is a prerequisite for terminal differentiation. Taken together, our
results indicate that
SAW

inhibits preadipocyte differe
ntiation and adipogenesis in cultured cells.

These studies
also
suggest that

SAW
works on multiple molecular targets as an inhibitor of
PPAR
γ
. SAW

has the

potential
function to regulate lipid metabolism and be developed
as
a
candidate
drug

for regulation
o
f
lipid metabolism
.


11

Intrinsic
S
tructural
S
ensors
R
eport
G
lycoprotein
F
olding
F
ailures

by
D
isplaying
B
ipartite
D
egradation
S
ignals


Wei Xie
1,2
, Kazue Kanehara
1
, and Davis T.W. Ng
1,2


1
Temasek Life Sciences Laboratory and
2
Department of Biological Sciences,

National University
of Singapore, Singapore 117604


Author for correspondence: Davis Ng.
Tel: 65 6872 7822;
E
-
Mail:
davis@tll.org.sg


Endoplasmic reticulum (ER) quality control mechanisms monitor the folding of nascent
polypeptides of the secretory pathwa
y. These are dynamic processes that retain folding proteins,
promote the transport of conformationally mature proteins, and target misfolded proteins to ER
-
associated degradation (ERAD) pathways. Aided by the identification of numerous ERAD factors,
late f
unctions that include substrate extraction, ubiquitination, and degradation are fairly well
described. By contrast, the mechanism of substrate recognition and the molecular logic used to
differentiate folding, folded, and misfolded proteins remain mysterio
us.

For some substrates, a
specific N
-
linked glycan forms part of the recognition code but how it is read is unclear. In this
study, systematic analysis of model substrates revealed such glycans mark structural determinants
that are sensitive to the overal
l folding state of the molecule. Normally, these segments fold into
the mature structure to pass the ERAD checkpoint. However, should a molecule fail to fold
completely, they form a bipartite signal that comprises the unfolded local structure and
enzymatic
ally modified glycan. Only when both elements are present will ERAD recognize and
target the molecule for degradation.





12

The mechanism of antigen activated T cell apoptosis


Xinqi Liu
1
, Yanan Zhu
2
, Shaodong Dai
2
, Janice White
2
, Philippa Marrack
2

and John

W.
Kappler
2


1
College of Life Sciences, Nankai University
,
94 Weijin Road, Tianjin, 300071, China

2
Howard Hughes Medical Institute
,
National Jewish Medical and Research Center
,
1400
Jackson Street
,
Denver, CO
,

80206, USA.


The appearance of antigen in an
imals makes antigen specific T cells divide and then die.
It is now well known that the death of these cells is to a large extent governed by
members of the Bcl
-
2 family of proteins. Over expression of anti
-
apoptotic members,
such as Bcl
-
2 and Bcl
-
xl, the
P
rotectors, inhibit activated T cell death as do double
deficiencies in members of the family, Bak and Bax, the so
-
called Executioners, which
are supposed to actually kill the T cells. A third group of proteins in this family, the so
-
called Messengers, als
o affect T cell death and deficiencies and one of these proteins,
Bim, also protects T cells against death.


The fact that members of three different groups of Bcl
-
2 related proteins affect activated
T cell death causes difficulties in figuring out the exa
ct course of events which kills or
protects the cells. It is agreed that the Protectors somehow prevent death and the
Messengers and Executioners drive death. What is not clear, however, is which protein
must interact with which in order to control these e
vents. Two models have been
suggested. In the first model, in healthy T cells, the Protectors are supposed to be bound
to the Messengers and the Executioners are in some innocuous form. After activation, as
the T cells approach death, it is suggested that
some of the Messengers are released from
the Protectors and these now freed proteins directly or indirectly activate the killing
properties of the Executioners. In an alternate model, the Protectors are normally bound
to the Executioners, and, perhaps, th
e Messengers. When the activated T cells approach
death the ratio of these proteins changes such that the Executioners are released from the
protective custody of the Protectors and, are thus able to kill the cell.


The experiments described here test th
e second of these possibilities, by examining
whether the Protectors must bind the Executioners in order to kill the cell. Here we show
that we cannot co
-
immunoprecipitate Executioners with Protectors, so we cannot detect
any direct binding of the
two
. In
a more stringent test of the same idea, a Bcl
-
xl variant,
lacking its flexible loop (Bcl
-
xl
Δ
L) which even at high concentrations in over expression
experiments shows no evidence of binding the Executioner, Bax, protects activated T
cells very well from dea
th. Bcl
-
xl
Δ
L continues to bind the Messenger, Bim, however.
Thus, these experiments suggest that, in activated T cells, the Protectors act by binding to
Messengers and not by engaging the Executioners directly.


A
ccompanying
these experiments is a high re
solution structure, by X
-
ray crystallography,
of the structure of Bcl
-
xl bound to a peptide from Bim. This structure reveals the
structure of a few more of the residues of the flexible loop (amino acids 22
-
82) of Bcl
-
xl.
Engagement of Bcl
-
xl by Bim renders

a site in the loop sensitive to proteolytic cleavage,

13

and changes the conformation of the loop amino acids which can be resolved. Moreover,
Bcl
-
xl
Δ
L binds Bim less well than wild type Bcl
-
xl does. Thus the loop domain of Bcl
-
xl may play a role in some currently unknown function of Bcl
-
xl.


In spite of many years of work, we still don’t know exactly how the Executioners, Bak
and Bax, are triggered to

kill activated cells. The work described here suggests that
triggering does not occur because of release of Bak and Bax from the embrace of
Protectors such as Bcl
-
2 and Bcl
-
xl.
As to the activation of
the Executioners
, p
erhaps
Bim acts, as has been sugges
ted in the past, via “hit and run” in which a very quick, low
level interaction between Bim and the Executioners catalyzes a catastrophic change in the
conformation of a lot of the Executioner proteins.


14

Molecular Mechanism and Drug Design to Enhance Regen
eration of the Injured
CNS Axons by Targeting Nogo
-
NgR and Eph
-
eprin Signalling Interfaces


Jianxing Song
1,2


1
Department of Biological Sciences, Faculty of Science,
2
Department of Biochemistry, Yong Loo
Lin School of Medicine and National University of Si
ngapore; Singapore 119260


Author for correspondence: SONG Jianxing. Tel: 65 65161013; Email: bchsj@nus.edu.sg


Patients with central nervous system (CNS) injuries such as spinal cord injury, traumatic brain
injury, stroke and neurodegenerative diseases of
ten result in permanent disability due to the
inability of CNS neurons to regenerate axons after injury. Recent discoveries indicate that the
failure of CNS regeneration largely results from the presence of inhibitory molecules of axon
outgrowth in adult C
NS myelin. So far, two classes of inhibitory proteins have been identified:
one initiating their action via Nogo
-
66 receptor (NgR) such as Nogo, myelin
-
associated
glycoprotein (MAG) and oligodendrocyte myelin glycoprotein (OMgp); and another including
tran
smembrane Eph receptor tyrosine kinases and their ligands ephrin. As a consequence, the
interfaces between Nogo
-
NgR and Eph
-
ephrin represent promising targets for designing drugs to
treat CNS axonal injury.

In my laboratory, we have extensively utilized m
olecular biology, activity assay and various
biophysical methods including NMR spectroscopy and crystallography to delineate molecular
mechanisms and further to design molecules to block Nogo
-
NgR and Eph
-
ephrin interactions,
with an ultimate goal to develo
p drugs to enhance the CNS regeneration. 1) We have
systematically studied three Nogo proteins, thus providing the first structural picture of Nogo
proteins (1
-
2). 2) We have determined the first three
-
dimensional structure of Nogo
-
66, and based
on this,
a structured and soluble Nogo
-
66 mimic and an antagonist were designed (3
-
6). 3) We
have determined the first structure of the ephrinB2 cytoplasmic domain and further revealed how
tyrosine
-
phosphorylation disrupted its structure for the reverse signaling i
nitiation (7). 4) We
have determined structures of the adaptor protein Nck2 and revealed how it transmitted the signal
from ephrinB to downstream effectors critical for cytoskeletal remodeling (8
-
9). 5) We also
determined the extracellular domain structure
s of Eph and ephrin and more importantly showed
that this interface could be targeted by small molecule antagonists (10
-
12). Our studies offer
important information in understanding the signal transductions mediated by Nogo
-
NgR and Eph
-
ephrin. Strikingly,

we demonstrated that molecules can be designed or discovered to antagonize
these signaling processes, which may have extensive therapeutic applications.


1.
Li M and
Song J*

(2007)
Proteins
. 68, 100
-
108

2.

Li M and
Song J*

(2007)
BBRC

360, 128
-
34.

3.

Li
M, Liu J and
Song J*

(2006)
Protein Sci.

15, 1835
-
41

4.

Li M, et. al., and
Song J*

(2006)
Biophys.
J.

91:4201
-
4209

5.

Li M, Shi J, Wei Z, Teng F, Tang B,
Song J*

(2004)
Eur J Biochem

271, 3512
-
22

6.

Li M, Li Y, Liao X, Liu J, Qin H, Xiao Z and
Song J
* (20
08)
BBRC
373, 498
-
503.

7. Song J*

(2003)
J Biol Chem.

278, 24714
-
20

8.

Ran X &
Song J*

(2005)
J. Biol. Chem.

280(19):19205
-
12.

9.

Liu J, Li M, Ran X, Fan J and
Song J*

(2006)
Biochemistry

45, 7171
-
84

10.

Liu J, Li M, Ran X, Fan J and
Song J*

(2006)
J Biom
ol NMR.
38, 171.

11.

Ran X, Qin H, Liu J, Fan JS, Shi J and
Song J
* (2008)
Proteins
. 72, 1019

1029.

12.

Qin H, Shi J, Noberini R, Pasquale E. B, and

Song J*
(2008)

J. Biol. Chem.

In press


15


Effect of Wnt
-
signaling
C
omponents in
A
nthrax
T
oxicity


Wensheng W
ei


College of Life Sciences, Peking University, Beijing 100871


Although the conventional countermeasures against infectious diseases by directly targeting on
pathogens have been largely successful, drug
-
resistance strains emerged, esp. after the increasi
ng
antibiotic use. Since microbial infection requires host genes and pathways to exert its pathogenic
effect, much
attention is now shifting to host
-
oriented countermeasures
. In the study of a model
system for toxin
-
secreting bacterial infection, we have f
irst identified that some components of
Wnt
-
signalling pathway are involved in the anthrax toxin internalization and killing mechanism.
Anthrax is caused by a gram
-
positive, spore
-
forming bacterium,
Bacillus anthracis
, which exerts
its toxigenic effect by
secreting three poly
-
peptides, PA (protective antigen), LF (lethal factor),
and EF (edema factor). Genetic screening approach identified LRP6, a cell surface receptor
protein involved in Wnt
-
signaling pathway, as the co
-
receptor for anthrax toxin lethality
.
However, both supporting and controversial results have been reported by other groups, arguing
against the universal role of LRP6 in anthrax toxicity. Our recent results reveal that another Wnt
component, besides LRP6, also contributed to the toxin endoc
ytosis pathway. Down
-
regulation of
this gene leads to elevated level of cellular resistance to toxin. In addition, three out of seven of
the monoclonal antibodies against this protein are able to protect RAW264.7 cells from anthrax
toxin killing. These fin
dings suggest that some components of Wnt signaling pathway are
involved in bacterial toxin entry mechanism, although their specific role in certain toxin
internalization pathway is arguably replaceable by certain other host factors. Detailed results will
be presented.




16

Investigation on the
E
ffects of
M
utations in the
Y
east
R
ibosomal
P
rotein L36 on the
F
unctioning of
A
ssembled
R
ibosomes and on the
E
xpression of its
T
arget
G
enes


P
eng xiaogang
,

Ma chengying
,

Yi cong
,

Zhang yahui
,

H
w
ang
gw
o
-
j
i
u
n
n
*


Life Sci
ence Institute, Nanchang University, #999 XueFu Ave, Hong Gu Tan District, Nanchang,
Jiangxi 330031, China


Ribosomal proteins are generally considered as components of assembled ribosomes and their
physiological roles are mainly in the process of mRNA tra
nslation. However, recent studies have
clearly indicated that improper (reduced) expression of some ribosomal protein genes is closely
linked to the development of carcinomas or certain genetic diseases in animals. This study
focuses on the functional ch
aracterization of the eukaryote
-
specific ribosomal protein, RPL36, for
its role in the assembled ribosomes. We first deleted the two RPL36 paralogues in the yeast
Saccharomyces cerevisiae

genome. At the same time, a plasmid containing a wild type copy of

yeast RPL36B gene was transformed into this RPL36 deleted strain to maintain survival of the
strain. Point mutations were then introduced to a cloned RPL36B gene harbored in a different
yeast plasmid. By performing plasmid shuffling to replace the wild
type RPL36B gene originally
present in the deleted strain, we were able to screen for the mutations which could give rise to
distinct mutant phenotypes but are still viable when the mutant Rpl36bp becomes the only source
of Rpl36 protein in the transformed

cells. Some mutations result in severe slow
-
growth
phenotype and cause reduced expression of other ribosomal protein genes consistent with the
concerted expression of ribosomal protein genes in relation to cell growth. In addition, some
other mutant phe
notypes include appearance of half
-
mer pattern in the polysomal profile,
significant reduction in the level of mature 25S rRNA, and accumulation of small RNAs. In the
following experiments, we plan to further characterize the effects of mutations on the p
rocessing
and maturation of rRNA, on the assembly of the ribosomal subunits, and on the translational
efficiency of different types of mRNAs. Besides, we also intend to isolate the polysomal and
non
-
polysomal RNAs from the wild type and mutant strains to
be used for microarray analysis in
order to identify the structural features embedded in the kinds of mRNAs of which the
translational efficiency is sensitive to the mutations. With all of these information available, we
will try to model the physical pos
ition of Rpl36 protein in the assembled ribosome in yeast to
better understand the roles of this protein in the functioning of assembled ribosomes. From this
study, we expect we can not only learn more about the structural orientation and the functional
m
echanism concerning the ribosomal protein L36 in the assembled eukaryotic ribosomes, but
start probing the regulated network connecting ribosome biogenesis and cell growth.


17

A T
ale of
T
wo
C
entrins


Jie Shi
1
, Joseph Franklin
2
, Jordan Yelinek
2
, Ingo Ebersber
ger
3
, Graham Warren
3

and Cynthia He
1


1
Department of Biological Sciences, National University of Singapore, Singapore

2
Department of Cell Biology, Yale University, New Haven, CT, USA

3
Max F. Perutz Laboratories, Vienna, Austria


Centrins are small calcium
binding proteins conserved in all eukaryotes and have been found to
be important for a variety of cellular functions including cell signaling, centrosomal duplication,
DNA repair and mRNA export. Using
Trypanosoma brucei
, a protozoan parasite responsible f
or
African sleeping sickness, as a model organism, we study the function of centrins in organelle
duplication and cell division.


In
T. brucei
, 5 putative centrins were identified in the complete genome, and 3 of them were
found essential to parasite growt
h. While Centrin 1 locates on the basal bodies which seed the
flagellum, Centrin2 and Centrin4 are additionally present on a bi
-
lobed structure closely
associated with the single Golgi apparatus in this parasite cell. Depletion of Centrin2 and
Centrin4 fro
m the bi
-
lobed structure by inducible RNA interference appeared to exhibit opposite
phenotypes on organelle duplication, karyogenesis and cytokinesis, suggesting different functions
and yet interesting interplay of Centrin isoforms in regulating cell cycle

progress in
T. brucei
.



18

Studies on Biodiversity and Systematics of
Actinobacteria
l Resources under
Extreme Environments in the West of
China


LI
Wen
j
un
*,

T
ANG
Shu
k
un,

ZHI Xiaoyang,
X
U

Li
h
ua
, JIANG Chengling


The Key Laboratory for Microbial Resources of

the Ministry of Education, P. R. China, and

Laboratory for Conservation and Utilization of Bio
-
Resources,

Y
unnan Institute of Microbiology,
Yunnan University, Kunming 650091,Yunnan,
P. R.
China


Author for correspondence:
LI Wenjun
.

Tel
/Fax
: +86 871 503
33
35
;

E
-
Mail:
wjli
@ynu.edu.cn

l
iact@
hotmail.
com


Actinobacteria play a quite important role in natural ecological system and they are also prolific
producers of antibiotics, an
titumor agents, enzymes, enzyme inhibitors and immunomodifiers,
which have been widely applied in industry, agriculture, forestry and pharmaceutical industry. In
the past, the research work on actinobacteria was mainly concentrated on that of common habita
ts.
Actinobacterial resources under extreme environments
(including extreme high and low
temperature, extreme high or low pH, high salt concentration etc)
have received comparatively
little attention from microbiologists. Actinobacteria

are regarded as one

kind of sideline
microorganisms and
those

under

extreme environments are better materials for biological
evolution and phylogenetic development

in

research.
There are
many

more unknown species and
much more worth researching

for actinobacteria under

extre
me environments.

There are many extreme environmental resources in
the
west

of

China. For example,
wide range

snow
-
mountains, basified soil and lakes, widely distributed acid and
alkaline

hot
-
springs in
Yunnan provinces; more than 73.3 million hectares ba
sified soil and salt lakes in Xinjiang
Province and many unusual environments in Qinghai Province and other western Provinces. They
were mostly precious natural resources and were destroyed relatively fewer
, which
can provided
us with unique conditions for

study on

biodiversity and system
a
tics of

actinobacterial

resource
s
under

extreme environments.


In recent years, our main work was focus
ed

on
the stud
y

of

extremophilic
actinobacterial

resources

in the west of China, including isolation methods, fast iden
tification and syste
matics.
Our results combining Culture
-
Dependent and
-
Independent Methodologies

showed that large
amount of unknown actinobacterial resources existed in natural extreme environments.
Additionally,
g
enus
-
specific PCR primers of the genera

Streptomonospora
,
Actinopolyspora
,

Nesterenkonia

and
Prauserella

were deigned and verified

for rapid identification of moderate
halophilic actinobacteria
.

Furthermore,

many new taxa
were isolated and characterized
using a
polyphasic approach, including 2
suborder, 6 new families, 17 new genera and more than 100
new species.



19

Climate
C
hange and
P
lant
M
igration
p
otential on the
e
dge of the
T
ropics


Richard T. Corlett


Department of Biological Sciences, National University of Singapore, Singapore


Many organ
isms have responded to global warming over recent decades by migration towards the
poles or to higher altitudes, but the climate changes predicted for the next 100 years will be so
rapid that some species may be unable to keep up. A ‘migration lag’ is part
icularly likely for
poorly dispersed species, such as many plants, and where habitats are highly fragmented, as in
southern China and much of Southeast Asia. This may lead to the loss of biodiversity and the
release of additional carbon dioxide. Vegetatio
n models for the tropics and subtropics necessarily
aggregate plant species into a smaller number of plant functional types (PFTs). PFTs based only
on physiological tolerances have been used to predict vegetation changes over the next century,
but these mo
dels do not take into account the ability of the plant species involved to migrate over
the distances required in the time available, or the impact of habitat fragmentation and the loss of
dispersal agents on this ability. Plant migration potential depends

on many factors, including
successional status and plant demographic variables, but the major limiting factor is likely to be
the ability of each plant species to disperse across the large (1
-
100 km) gaps between surviving
habitat patches. Existing data c
an be used to make general predictions about which dispersal
types will be most vulnerable and to identify knowledge gaps that must be filled by new research.



20

Recent Developments in M
icrobial
D
egradation of
S
ulfur,
N
itrogen and
O
xygen
H
eterocycles


Pin
g Xu



Key
Laboratory

of Microbial Metabolism, Ministry of Education, College of Life Science &
Biotechnology, Shanghai Jiao Tong University, Shanghai 200240,

People’s
Republic

of China


Sulfur (S), nitrogen (N) and oxygen (O) heterocycles are among the mo
st potent environmental
pollutants. Microbial degradation of these pollutants is attracting more and more attention
because such bioprocesses are environmentally friendly.

The biotechnological potential of these
processes is being investigated, for examp
le, to achieve better sulfur removal by immobilized
biocatalysts with magnetite nanoparticles or by solvent
-
tolerant bacteria, and to obtain valuable
intermediates from these heterocycles.

Other recent advances have demonstrated the mechanisms
of angular
dioxygenation of nitrogen heterocycles by microbes.

However, these technologies are
not yet available for large
-
scale applications so future research must investigate proper
modifications for industrial applications of these processes.

This
presentation

focuses on recent
progress in understanding how microbes degrade S, N and O heterocycles.







Mailing address:
School

of Life Science
s

and

Biotechnology, Shanghai Jiao Tong University, Shanghai
200240, P. R. China.

E
-
mail
:
pingxu@sjtu.edu.cn

(P. Xu).
Tel: +86
-
21
-
34206647; Fax: +86
-
21
-
34206723.


21

A M
etagenomic
A
pproach to the
B
iosynthetic
O
rigin of
P
lant
M
aytansinoids


Yuemao Shen


School of Life Sciences, Xiamen University


Maytansinoids are a family of 19
-
membered macrocyclic lactams having extraordinary cytotoxic
and antineoplastic activities. They have been found in a microorganism (
Actinosynnema
pretiosum
), mosses and three closely related plant families, Celastraceae, Rhamnaceae and
Euphorbiaceae. To te
st the hypothesis that maytansinoids isolated from higher plants are
produced by endophytes, we used the metagenomic approach to isolate the gene cluster
responsible for maytansinoids biosynthesis in
Trewia nudiflora
. The studies include enrichment
of endo
phytes, isolation of metagenomic DNA, construction, evaluation and screening of
metagenomic library.


AHBA synthase is a key enzyme for the biosynthesis of AHBA starter unit of maytansinoids. A
DIG labeled AHBA gene fragment was used to screen the biosynth
etic gene cluster of
maytansinoids in the metagenomic library. One positive fosmid clone was recovered from 75,000
clones and was subjected to DNA sequencing. The results showed that this fosmid contains not
only all the genes required for the biosynthesis

of AHBA but also type I PKS genes, and an amide
synthase gene for the formation of macrolactam. Particularly, a unique
intramolecular
C
-
C
coupling gene,
Tnm8
, showed highest sequence similarity to the berberine bridge enzyme
-
encoding gene cloned from

Esch
scholtzia californica
, implying that this gene may be involved in
the formation of treflorine from trewiasine. Therefore, this fosmid could host part of the
maytansinoid biosynthetic genes.



22

Virulence of
Bacillus nematocida

to

Caenorhabditis elegans
: A
N
o
vel
B
acterial
P
athogenesis


Huang Xiaowei, Niu Qiuhong, Zhang Lin, Wei Kangbi, Yang Dongmei, Zhang Keqin*


Laboratory for Conservation and Utilization of Bio
-
Re
sources, and Key Laboratory for Microbial
Resources of the Ministry of Education, Yunnan Univers
ity, Kunming, Yunnan, 650091, China


The mechanisms by which p
athogenic
microorganisms

cause disease can provide

crucial
information for understanding the patterns and evolution of host
-
pathogen

interactions
and
for
designing effective strategies for contr
olling either
the

pathogens or the hosts.

The nematode
Caenorhabditis elegans

is a simple model host for a number of bacterial pathogens. In this study
a novel

host

pathogen interaction
was established
between
C
.

elegans

and the gram
-
positive
bacterium

Bac
illus nematocida
, and we report an integral pathogenesis including recognition,
invasion and degradation from the pathogenic bacterium.

Biological assay suggested this
bacterial
pathogen with relatively limited mobility
has glamour strateg
y

to capture its
host

effectively
, and
SPME/GC
-
MS
a
nalysis

confirmed a variety of potent volatile organic compounds that overall are
much more attractive than those from dietary bacteria.

Then
the bacteria
are swallowed to
colonize in the intestine of
C. elegans
, and two p
rotease
s secrete
d
digest intestinal tissues

and

cause nematode

death
s
.

G
ene
-
knock
experiment confirmed that two important virulence proteases
,
an alkaline serine protease Bace16 and a neutral protease Bae16, kill
ed

the nematodes
with severe
des
tructions ob
served in

the nematode
alimentary tract, especially the structure
intestinal
microvillus.
Furthermore, the fluorescent localization

demonstrated for the first time that the
alimentary tract in nematodes is the primary target of proteases but not the cuticl
e as previously
suggested.

To reason the death of nematodes, we compared the nematode
mortalities

of different
treatment including
microinjection of proteases into gut, solo activity on cuticle and both
, and
our
data
concluded

that intestinal damage by pro
teases Bace16 and Bae16 were the main cause of
nematode death by
B. nematocida
.

Meanwhile, the
proteomic analyses

identified

that both
proteases
have broad

substrate ranges, including

twelve

preferentially targeted proteins that are
likely involved in the
maintenance of enteric Brush
-
Border structure, local innate immune
response, and proper intestinal function of the epithelia.
Together, our data represent a new
insight into elucidating host
-
pathogen interactions.


23

Whole
G
enome
M
icroarray
E
valuation of
G
en
omic
I
mbalance in Chinese
P
atients
with
M
etal
R
etardation


Hongyan Wang
1
*, Yuwu Jiang
2
*, Xiaoli Chen
3
*, Yiping Shen
4
*, Shilin Li
1
, Hong Fang
4
,
Xiaohong Gong
1
, Xiaoming Shen
4
, Hong Shao
4
, Li Jin
1#
, Xiru Wu
2#
, Ting Zhang
3#
, Bai
-
Lin
Wu
1,4#


1
Institutes of Bio
medical Science and School of Life Science, Fudan University, Shanghai, China;
2
Department of Pediatrics, Peking University First Hospital, Peking University, Beijing, China;
3
Capital Institute of Pediatrics, Capital Medical University, Beijing, China;
4
Ch
ildren’s Hospital
Boston and Harvard Medical School, Harvard University, Boston MA, USA

*Equally contributed. #Senior author of each institute in the collaboration


Genomic imbalances/rearrangements are a common cause of developmental delay, mental
retar
dation and autism spectrum disorders, which have been demonstrated by studies with cohorts
of the western countries. One type of such genomic imbalance appears recurrently with reciprocal
microdeletion and duplication in different individuals involving the

same genomic region and of
the similar size, these events occur due to segmental duplication mediated non
-
allelic
homologous recombination; another type of imbalance appears randomly and presumably occurs
due to non
-
homologous end
-
joint recombination. The

overlapping nature of regions involved in
imbalance from individuals with similar clinical phenotype may eventually help to pinpoint
critical regions/key genes responsible for such clinical phenotype. In order to detect the genomic
imbalances in Chinese p
atients with primary diagnosis of mental retardation, we employed two
most current high
-
resolution whole genome microarrays (Agilent 244K CGH array and
Affymetrix SNP 6.0 array) to evaluate/compare the deletions and duplications in a pilot cohort
consistin
g of 150 patients. During the process, we also cross
-
validated the findings between the
two DNA chip platforms and the results showed very high concordance rate. We identified both
types of genomic imbalances in the Chinese cohort: 16p11.2 deletion, 16p13.
3 duplication and
17q12 duplication are the examples of imbalance events that belong to the first category
(recurrent reciprocal imbalance), all of these microdeletion/duplication are recently recognized
genomic disorders/syndromes; two unrelated cases wit
h overlapping duplication involving 2p12
exemplify the second type of imbalance (randomly or de novo imbalance); the remaining findings
belong to the second category and include 13q13.1q14.1 and 7q31.1 deletion. The high
-
resolution
whole genome array also
detects multiple imbalance events in each patient sample but many
events are benign copy number variants (CNV). Based on current database and literature, we
identified clinically relevant genomic imbalances in about 10% of total cases. Our data
demonstrate
d the utility of whole genome array for detecting genomic imbalance. The detection
of recurrent genomic imbalance events among Chinese patient further confirmed shared
etiologies among patients of different ethnicities. Since mental retardation is a broad
clinical
diagnosis of heterogeneous genetic etiologies, extensive clinical phenotype evaluation and further
dissection of genomic rearrangement are of great importance towards better understanding of the
disorder and for eventual better patient care.




24

T
he Human
-
Specific Gene c1orf37
-
dup Encodes a Transmembrane Protein


Haijing Yu, Jiping Lou, Weihong Hu, Shengjie Nie, Chunjie Xiao


Key Laboratory of Bioresources Conservation and Utilization and Human Genetics Center of
Yunnan University, Kunming 650091,
PR China


Gene origination is a basic biological phenomenon and studies on new gene

origination, evolution
and function contribute to the knowledge on organism evolution and speciation. We identified a
human
-
specific new gene, c1orf37
-
dup, via genomic anal
yses. Through analyzing the variation
pattern of the new gene and its neighboring DNA regions, we found that c1orf37
-
dup had been
fixed in human populations in a short period of time and evolved under strong Darwinian positive
selection. Protein structure
prediction and chimeric green fluorescent protein localization
suggested that it encodes a cell membrane protein. The c1orf37
-
dup gene expresses specifically in
brain, heart, placenta, lung and liver, in which its expression in brain may have important
imp
lications relevant to human evolution.




25

Study on thermotolerance of
Agaricus bisporus


Siyang Song


School of Life Sciences, Xiamen University


Agaricus bisporus

is a
n

edible mushroom which has high

economic value and important ecology
significance.

Prev
iously, we obtained two strains of this species

the strain 02 is thermotolerant
but poor in quality, the strain 8213 is
thermolabile

but has high quality. In this study, we focus on
the difference between the thermotolerance of these two strains by means o
f differential
expression analysis at both transcription and translation levels. We applied Suppression
Subtractive Hybridization (SSH) and real
-
time PCR to investigate the transcriptional differences,
and
two

D
imensional
E
lectrophoresis

(2
-
DE)
with

Mass
S
pectrometry

(MALDI
-
TOF/MS)

for
translational differences. We obtained two SSH libraries containing large numbers of
differentially expressed thermo
-
related genes

and

many differential thermo
-
related proteins. The
differential

genes and proteins can be clas
sified into
the
following categories: heat
-
shock proteins
and molecular chaperons , members of cell wall and membrane, metabolisms and energy
transportation, signal transduction members, injury recovery proteins. Some of the results from
transcription are
in accordance with translation analysis,
such
as
peptidyl prolyl
cis
-
trans

isomerase
. This work indicates that the thermotolerant mechanism of
A. bisporus

is a complicated
process which involves multiple genes, proteins and signaling pathways. Environment
temperature is the main restriction factor in the development of mushrooms, which greatly limits
their cultivation season.
Therefore,
understanding the
thermotolerant

mechanism of

A. bisporus

has important theor
etical

and

practic
al

significance.



26

A Geneti
c Framework for Flower Initiation


Hao Yu


Department of Biological Sciences and Temasek Life Sciences Laboratory

National University of Singapore, Singapore


Author for correspondence: Hao Yu. Tel: 65
-
65163048; Email: dbsyuhao@nus.edu.sg


The transition f
rom vegetative to reproductive growth is the most dramatic phase change in the
life of flowering plants. This developmental switch responds to various environmental and
endogenous signals and results in the generation of flowers, which bear reproductive or
gans for
seed production. In the last two decades, intensive investigations have progressively unraveled
the underlying mechanisms of flower initiation in the model plant Arabidopsis. Our recent studies
suggest that several MADS
-
box transcription factors p
lay key roles in mediating the successive
changes of flower initiation, including flowering time control, floral meristem specification and
floral organ patterning. This talk will discuss the molecular functions and genetic interactions of
these regulators

in flower initiation.




27

The
P
ower of
G
enetics in
D
issecting
P
lant
S
hade
A
voidance
S
ignaling
P
athway


Yi Tao


School of Life Sciences, Xiamen University


Plants grown at high densities perceive
light with decreased red to far
-
red (R:FR)

ratio, resulting
f
rom absorption of red light by leaves from neighboring plants. Th
is

change in light quality
trigger
s

a series of responses known collectively as the shade avoidance syndrome

(SAS)
.
A
predominant response of the SAS is elongation growth of
stems
and petiole
s,

allowing the plant
to outgrow its competitors. Such elongation growth requires re
-
allocation of energy resources and
occurs
at the expense of leaf and storage organ expansion
.

Thus
, the
SAS
, a strategy of major
adaptive significance to plants growing in

natural communities, significantly impacts yield in
high
-
density plantings typical of modern agriculture
.
Changes in light quality are perceived by the
phytochromes, a family of red and far
-
red light photoreceptors.

However,
little is known about
the unde
rlying mechanisms linking photoperception to changes in physiology and development.
Here, we describe a
forward
genetic screen in
Arabidopsis
for mutants unable to elongate in
simulated shade light.

W
e identified several loci in
Arabidopsis,
mutations in w
hich lead to plants
defective in multiple shade avoidance outputs.
One of the genes encodes TAA1 (
T
ryptophan
A
minotransferase of
A
rabidopsis
)/SAV3 (
S
hade
Av
oidance mutant 3).

We

show
ed

that SAV3
catalyzes the formation of indole
-
3
-
pyruvic acid (IPA) from
L
-
t
ryptophan

(L
-
Trp)
, the first step
in a previously proposed, but uncharacterized, auxin biosynthetic pathway

in plants
. This
pathway can be rapidly deployed to biosynthesize auxin at the high levels required to initiate the
multiple changes in body plan
associated with shade avoidance.

28

A

N
etwork
V
iew on the
A
ction of
P
lant
H
ormones


Yuanyan Xiong & Xionglei He


State Key Laboratory of Bio
-
control, College of Life Sciences, Sun Yat
-
sen University,
Guangzhou 510275, China.


Correspondence to: Xionglei He; C
ollege of Life Sciences, Sun Yat
-
Sen University, 135 Xingang
West, Guangzhou, 510275, China

Phone: (86) 20
-
39332844, Fax: (86) 20
-
34022356

Em
ail:
hexiongl@mail.sysu.edu.cn


Auxin, CK, GA, ABA, Ethylene, BR
and JA are the 7 major plant hormones actively involved in
almost every aspect of plant growth and development. It is well known that at the physiological
level different hormones cross
-
talk, the underlying molecular basis, however, remains to be one
of t
he major challenges of plant biologists, athough several bridging genes have been identified
using traditional genetics approaches.
H
ere
,

w
e adopt a systems
-
biology approach
to
attempt to
discover new genes that mediate the interaction of hormones.
W
e co
nstructed a genome
-
wide
protein
-
protein interaction (PPI) network of
Arabidopsis thaliana
, and investigated the locations
of thousands of hormone
-
responsive (HR) genes in the PPI network.
W
e found that the
distribution of HR genes in the network is highly

heter
o
geneous, with significant enrichment in
certain network modules.
O
f the most interest is one module in which both ABA and CK related
HR genes are >10 fold enriched, indicating cross
-
talk of these two hormones via this module.
Gene Ontology analysis

revealed that >80% of genes within this module are involved in
translation; strikingly, ABA related HR genes within this module are almost exclusively down
-
regulated while CK related HR genes are always up
-
regulated. This finding is consistent with the
r
ole of ABA on maintaining seed dormancy, and the role of CK on stimulating cell growth. A
motif, GAAGAAGA, was discovered in the promoter regions using MEME for >90% of both
ABA and CK related HR genes of this module.
I
nterestingly, this motif is shared
by a group of
secretion
-
related genes which are under the control of NPR1, and important in plant systemic
acquired resistance (SAR). This may explain a recent observation that ABA can reduce the level
of SAR




29


Regulatory
M
echanisms of
B
rassinosteroid
S
ignaling in
P
lants


Niyan Wang, Haijiao Wang, Ying Wei, and Xuelu Wang


State Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University,
Shanghai, 200433, China



Brassinosteroids (BRs) play essential roles in regulating

a large arra
y of
physiological and
developmental processes in plants. BRs are perceived at
cell surface

by a leucine
-
rich repeat
(LRR) receptor serine/threonine kinase, BRI1.
A newly
identified

protein, BKI1

specifically

interacts with

BRI1
.
The phenotypes of Arabidop
sis plants that over
-

or under
-
express BKI1 and
the phosphorylation status of BES1, suggest it is a negative regulator of BR signaling, acting in
the BR

signaling
pathway. BRs regulate the subcellular localization of a BKI1
-
YFP fusion
protein, causing its

rapid dissociation from the plasma membrane in an active BRI1 kinase
-
dependent manner. BKI1 serves as a substrate of BRI1 kinase.

Using genetic, biochemical, and
proteomic approaches, we are investigating the underlying mechanisms by which BKI1 is
regula
ted. We have dissected the functional domains of BKI1 to understand how BRI1 regulates
the movement of BKI1
in the

cell. These researches provide novel insights into the regulatory
mechanism
s of the brassinosteroid signaling in plants.





30

Studies on the
R
egulations of
B
eta
-
catenin
P
hosphorylation and
U
biquitination


G
eng Wu, Guozhou Xu, Brenda Schulmann, Philip Jeffrey, Nikola Pavletich, Xi He


School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, China,
200240


Author for cor
respondence:
Geng Wu
; Tel
: 13601767804

E
mail:
geng.wu@sjtu.edu.cn


B
eta
-
catenin is a central component in the Wnt signaling pathway which plays essential roles in
cell proliferation and differentiation. In the ab
sence of Wnt, beta
-
catenin is phosphorylated at its
N
-
terminal Ser/Thr residues by a multi
-
protein complex including GSK3, Axin, CK1, and APC.
Phosphorylated beta
-
catenin is then ubiquitinated by the E3 ubiquitin ligase SCF
betaTRCP
, and
degraded through th
e 26S proteosome pathway. Deregulations of beta
-
catenin phosphorylation,
ubiquitination, and degradation are associated with many kinds of human cancers.

First
ly
, I am
going to talk about my earlier
structural

biological work on how beta
-
catenin is recogn
ized by
beta
-
TRCP, the F
-
box subunit of SCF
beta
-
TRCP
. Base
d

on our structure, we presented a mechanistic
model of how beta
-
catenin is ubiquitinated by SCF
beta
-
TRCP
, and we performed biochemical
experiments to confirm the prediction based on our model.

Sec
ond
ly
, I am going to talk about the
role which Thr41 of beta
-
catenin plays in its N
-
terminal phosphorylation. Using a biochemical
approach, we showed that Thr41 acts as a phosphorylation relay residue, and the SXXXS motif is
obligatory for beta
-
catenin pho
sphorylation. We have also shown that beta
-
catenin
phosphorylation/degradation and its regulation can occur normally in the absence of Thr41 as
long as the SXXXS motif is
preserved
. Our results suggested that Thr41 of beta
-
catenin functions
to bridge seque
ntial phosphorylation of beta
-
catenin N
-
terminal Ser/Thr residues.

Finally, I will
talk about how beta
-
catenin phosphorylation is regulated by the Wnt co
-
receptor LRP6. On
activation by Wnt, LRP6 is phosphorylated at multiple
conserved

intracellular PPPSP
XS motifs
by GSK3 and CK1, resulting in recruitment of Axin to LRP6. As a result, beta
-
catenin
phosphorylation is inhibited. We
reconstituted

Axin
-
dependent beta
-
catenin phosphorylation by
GSK3 and CK1 in vitro using purified recombinant proteins, and foun
d that the phosphorylated
PPPSPXS motifs directly inhibited beta
-
catenin phosphorylation by GSK3 in a sequence and
phosphorylation
-
dependent manner. Based on our results, we proposed a model that Axin
recruitment to the phosphorylated LRP6 places GSK3 in t
he vicinity of multiple phosphorylated
PPPSPXS motifs, which directly inhibit GSK3 phosphorylation of beta
-
catenin.


31


Foxi1 and Sox9 Act in a Molecular Switch that Regulates Transition of Preplacodal
Ectoderm into Otic Placode


Dong Liu
1,2

and Monte W
esterfield
1


1
Institute of Neuroscience, University of Oregon, Eugene, Oregon, USA 97403
-
1254

2
Center of Developmental Biology and Genetics, College of Life Sciences, Peking University,
Beijing 100871 P. R. CHINA


The vertebrate inner ear and cranial gang
lia arise from ectodermal thickenings, termed placodes,
that are derived from a specialized preplacodal ectoderm (PPE) at the border between the neural
plate and non
-
neural ectoderm. Signaling systems, including Bmps and Fgfs, and a variety of
transcriptio
n factors are implicated in PPE formation, although the mechanisms by which the PPE
and individual placodes are specified are unknown. We have identified a key molecular switch
that regulates the transition of the caudal PPE into otic placode. The Foxi1 tr
anscription factor
maintains Bmp signaling and suppresses responsiveness to Fgf in ventral cells as they converge
toward the neural plate to form the PPE. Maintained Bmp signaling and increased exposure to Fgf
as the cells approach the neural plate lead to

expression of Sox9 that subsequently suppresses
Foxi1, thus permitting increased Fgf sensitivity and otic specification.



32

IGF
-
1
P
romote
BPH
-
1
C
ell
P
roliferation
P
rimarily
via
A
ctivating mTOR
-
D
ependent
T
ranslational
I
ncreases in
C
yclin D
P
roteins


Chaoyan
g Liu, Ke Gong and Wenhua Li*


Department of Cell Biology,
College of Life Sciences, Wuhan University,

Wuhan 430072, PR China.

*
Author for correspondence:

Email:
whli@whu.wdu.cn
;
Tel: 86
-
27
-
68756711


I
nsulin
-
like g
rowth factor
-
1

(IGF
-
1
)

and its

binding protein (IGFBP
-
3
) play a
crucial
role in the
initiation and progression
of
prostate and benign prostatic hyperplasia (BPH)
.
We have
previously
report
ed

that
stromally
expressed c
-
Jun protein modulate
s

epithelial
proli
feration via

regulat
ing

production and paracrine signals of IGF
-
1
, which

promote the BPH
-
1 cells
proliferation
through

upregulation of cyclin D protein levels.

I
n this study, the exact molecular
mechanisms of these regulations were
investigate
d. We found t
hat
IGF
-
1 increas
es

cyclin D
proteins

and promotes cell cycle
transition

from G0 to S phase, bringing in cell proliferation.
IGF
-
1 has a minimal effect on

cyclin D mRNA levels and it
primarily stimulates
post
-
transcriptional

increases in cyclin D proteins.

IGF
-
1 stimulation increases cyclin D protein in
translation levels via activation
of
mammalian target of rapamycin

(mTOR) pathway in BPH
-
1
cells. Two vital factors

downstream of
mTOR
,
the eukaryotic translation initiation factor
-
4E
binding protein
-
1

(
4EBP
1
)

and
70
-
kD ribosomal protein

S6 kinase

(p70
S6K
), were
activated

after
IGF
-
1 treatment.
B
locking mTOR will decrease cyclin D levels and offset IGF
-
1 stimulation.
Moreover, we found that, i
n
BPH
-
1cells, activated
mTOR by

IGF
-
1
increases cyclin D protein
ex
pression is mediated through activation

of the PI3K/Akt pathways cells
, but not MAP kinase
pathway. Also, our data indicate that IGF
-
1 probably
influence
s the combination of cyclin D and
ubiquitin, and then stabilize
s

the cyclin D protein.
These results e
lucidate

the molecular
transduction pathways

of IGF
-
1 promote BPH
-
1 cell proliferation, which will help to
improve our
understanding
of BPH and develop new clinical therapy for

it.




33

To
D
ie or
N
ot to
D
ie


Sheng
-
Cai Lin


School of Life Sciences, Xiamen Uni
versity


Many factors exert roles in cellular commitment to undergo cell arrest or apoptosis following
genotoxic stresses; how they are orchestrated to selectively reach respective thresholds remains
unclear. We have found that Axin scaffolds with HIPK2, p
53 and Pirh2, forming distinct
complexes in cellular commitment to cell
-
cycle arrest or apoptosis. Pirh2 strongly abrogates
Axin
-
based genotoxic induction of p53 Ser
-
46 phosphorylation by HIPK2. Unexpectedly, Prih2
does not ubiquitinate p53 despite its E3
activity; rather, it excludes HIPK2 from association with
the Axin/p53 complex, rendering the Axin
-
bound p53 unphosphorylated at Ser
-
46. Further, Pirh2
occupation with Axin is preferentially formed in cells arrested upon sublethal UV or Doxorubicin
treatme
nt, and that Pirh2
-
Axin interaction is disrupted by binding of Axin to other factors in
apoptotic cells upon lethal treatment. Thus, we have identified distinct complexes that control the
levels of p53 activation to trigger cell
-
cycle arrest or apoptosis u
pon different severity of
genotoxic stress. Mutation in
Axin
Fu

mice promotes tumorigenesis following DMBA treatment,
further emphasizing the importance of Axin in tumor suppression. I will also discuss about the
implications of the above recent findings in

stress biology as a whole.



34

Phylogeny and biogeography of the family Salamandridae (Amphibia: Caudata)

inferred from complete mitochondrial genomes


Peng Zhang
a,b
, Theodore J. Papenfuss
a
, Marvalee H. Wake
a
, Lianghu Qu
b
, David B. Wake
a


a

Department
of Integrative Biology, Museum of Vertebrate Zoology, 3101 Valley Life Sciences
Building, University of California, Berkeley, CA 94720
-
3160, USA

b

Key Laboratory of Gene Engineering of the Ministry of Education, Zhongshan University,
Guangzhou 510275, Peop
le’s Republic of China



Phylogenetic relationships of members of the salamander family Salamandridae were examined
using

complete mitochondrial genomes collected from 42 species representing all 20 salamandrid
genera

and five outgroup taxa. Weighted maxim
um parsimony, partitioned maximum likelihood,
and partitioned

Bayesian approaches all produce an identical, well
-
resolved phylogeny; most
branches are

strongly supported with greater than 90% bootstrap values and 1.0 Bayesian
posterior probabilities.

Our r
esults support recent taxonomic changes in finding the traditional
genera Mertensiella, Euproctus,

and Triturus to be non
-
monophyletic species assemblages. We
successfully resolved the current polytomy

at the base of the salamandrid tree: the Italian newt
genus Salamandrina is sister to all remaining salamandrids.

Beyond Salamandrina, a clade
comprising all remaining newts is separated from a clade containing

the true salamanders. Among
these newts, the branching orders of well
-
supported clades are:

primiti
ve newts (
Echinotriton
,
Pleurodeles
, and
Tylototriton
), New World newts (
Notophthalmus
-
Taricha
),

Corsica
-
Sardinia
newts (
Euproctus
), and modern European newts (
Calotriton
,
Lissotriton
,
Mesotriton
,
Neurergus
,

Ommatotriton
, and
Triturus
) plus modern Asian ne
wts (
Cynops
,
Pachytriton
, and
Paramesotriton
).

Two alternative sets of calibration points and two Bayesian dating methods
(BEAST and

MultiDivTime) were used to estimate timescales for salamandrid evolution. The
estimation difference

by dating methods is sl
ight and we propose two sets of timescales based on
different calibration choices.

The two timescales suggest that the initial diversification of extant
salamandrids took place in Europe

about 97 or 69 Ma. North American salamandrids were
derived from thei
r European ancestors by dispersal

through North Atlantic Land Bridges in the
Late Cretaceous (
~
69 Ma) or Middle Eocene

(
~
43 Ma). Ancestors of Asian salamandrids most
probably dispersed to the eastern Asia from Europe,

after withdrawal of the Turgai Sea (
~
2
9 Ma).




35

Involvement of
OsSPX1

in phosphate homeostasis in ric
e


Chuang Wang
1
, Shan Ying
1
, Hongjie Huang, Kuan Li, Ping Wu, Huixia Shou
*


State Key Laboratory of Plant Physiology and Biochemistry, College of Life Science
s
, Zhejiang
University, Hangzhou,
3100
58
, P. R. China
.


1

Th
e

authors contribute
d

equally.

*Author for correspondence, Fax
:

0086
-
0571
-
88206133; e
-
mail:
huixia@zju.edu.cn


Arabidopsis thaliana

SPX
(
S
YG/
P
HO81/
X
PR1)
-
domain genes
have

recently
been
s
hown to be
involved in
the phosphate (
Pi
)

signal
ing

pathway. W
e
showed here that a rice (
Oryza sativa
)
SPX

gene,
OsSPX1
, is specifically induced by Pi starvation in roots. Suppression of
OsSPX1

by RNA
interference resulted in severe
signs of
toxic
ity cause
d by

the
overaccumulation
of
Pi, similar to
that found in

pho2

(
Pho
sphate responsive mutant 2
)

mutants and
OsPHR2

(
P
hosphate
S
tarvation
R
esponse transcription factor 2
)
overexpressors.
Quantitative r
everse transcription PCR showed
that the expression of
Os
SPX1

was strongly induced in

OsPHR2

overexpression and
pho2
mutant
plants,
indicating

that
OsSPX1

is downstream of

OsPHR2

and
PHO2
.
The expression of ten
genes associated with the phosphate starvation signal pathways was analyzed.

T
he expression of
OsPT2

(
P
hosphate
T
ransporter 2
)
and

OsPT8
were i
n
duced significantly in
OsSPX1
-
RNAi
(
OsSPX1
-
Ri) plants, suggesting that the overaccumulation of Pi in the
OsSPX1
-
Ri plants
results
from

an increase in
Pi transport.
In contrast
,

overexpression of
OsSPX1

suppresse
d

t
he induction
of
the expression of all ten

PSI genes

tested
, including

IPS1

(
I
nduced by
P
hosphate
S
tarvation 1)
,
IPS2, OsPAP10
(
P
urple
A
cid
P
hosphatase

10)
,

OsSQD2

(
S
ulfo
q
uinovosyl
d
iacylglycerol 2),
miR399 (
Mi
cro
R
NA
399
), OsPT2, OsPT3, OsPT6,
and
OsPT8
,

by P
i starvation.
This suggests
that
OsSPX1
acts via a negative feedback loop to optimi
z
e growth under phosphate limited
conditions.


36

A unique display of Toll
-
like receptor 4 Asp299Gly and Thr399Ile polymorphisms
in non
-
Han Chinese Hani population

Bingrong Zhe
ng
1
, Chuanyu Wei
1
,
Tao Shou
2
, Qin Li
2
, Minghui Yang
3
Li Yi
1
, Ruoyu Zhou
1
,
Jingru Shao
1

and Chunjie Xiao
1



1
Key Laboratory of Bioresources Conservation and Utilization and Human Genetics Center of
Yunnan University, Yunnan Kunming 650091, PR China

2

Kunhua Affiliated Hospital
o
f Kunming Medical College
, Kunming, Yunnan
650032, P.R.
China


3

The Second People’s Hospital of
Honghe Hani and Yi Autonomous Prefecture, Jianshui,
Yunnan 654300, P.R. China


Abstract

By using PCR
-
RFLP and DNA sequencing, 938 s
ubjects from 2 populations of non
-
Han Chinese
the Hani minority, (residing in Honghe and Lvchun counties inYunnan Province of China) were
sampled to investigate the polymorphisms of TLR4 Asp299Gly (TLR4/A896G) and Thr399Ile
(TLR4/ C1196T). 6 heterozygotes
for both Asp299Gly and Thr399Ile were detected and these
two

TLR4 polymorphisms are all in cosegregation to form the

Asp299Gly/ Thr399Ile haplotype.
The highest polymorphism frequencies for both Asp299Gly and Thr399Ile (0.98%) existed in the
Honghe populat
ion, the next (0.47%) from Lvchun. As a control, the incidence of these two
polymorphisms were also studied in a Han sample of 980 individuals residing in Kunming,
Yunnan . Although this is a relatively larger sample when compared with other previous studi
es
on Chinese Han populations, the findings from the present study are consistent with the earlier
results from other authors: It failed to detect any of these two genetic variations in Han group.
This study also suggests a possibility that both TLR4/A896G

and C1196T polymorphisms may
be rarely present in Chinese Han populations. But the results from non
-
Han Chinese Hani, for the
first time, actually detect the TLR4 Asp299Gly and Thr399Ile single nucleotide polymorphisms
(SNPs) in Oriental, suggest that the
re is something special for these two polymorphisms in non
-
Han Chinese Hani compared with the Han Chinese and some other Oriental populations.


37

Insertion/deletion: the inner cause of genomic mutation


Tian D
,
Wang Q
,
Zhang P
,
Araki H
,
Yang S
,
Kreitman M
,
Nagylaki T
,
Hudson R
,
Bergelson J
,
Chen JQ
.


State Key Laboratory of Pharmaceutical Biotechnology, Department of Biology, Nanjing
University, Nanjing 210093, China.


Mutation hotspots are commonl
y observed in genomic sequences and

certain human disease loci,
but general mechanisms for their formation

remain elusive. Here we investigate the distribution
of

single
-
nucleotide changes around insertion/deletions (indels) in six

independent genome
compa
risons, including primates, rodents, fruitfly,

rice, and yeast. In each of these genomic
comparisons, nucleotide

divergence (D) is substantially elevated surrounding indels and

decreases monotonically to near
-
background levels over several hundred

bases. D

is significantly
correlated with both size and abundance of

nearby indels. In comparison of closely related
species, derived

nucleotide substitutions surrounding indels occur in significantly

greater
numbers on the lineage containing the indel than on the

one

containing the ancestral (non
-
indel)
allele; the same holds within

species for single
-
nucleotide mutations surrounding polymorphic

indels. We propose that heterozygosity for an indel is mutagenic to

surrounding sequences, and
use yeast genome
-
wide pol
ymorphism data to

estimate the increase in mutation rate. The
consistency of these

patterns within and between species suggests that indel
-
associated

substitution is a general mutational mechanism.


38


Participant’s Contact

Name

Position

E
-
mail

Address

Choy
-
Leong Hew

Professor

dbshewcl@nus.edu.sg

Department of Biological
Sciences, National University of
Singapore, 14 Science Dr 4

Singapore 117453

Cynthia He

Assistant
Professor

dbshyc@nus.edu.sg

Department of Biological
Sciences, National University of
Singapore, 14 Science Dr 4

Singapore 117453

Cynthia Lee

Manager

dbsleesc@nus.edu.sg

Department of Biological
Sciences, National Unive
rsity of
Singapore, 14 Science Dr 4

Singapore 117453

Ding Ming
-
Xiao

Professor,
former Dean

dingmx01@pku.edu.cn


College of Life Sciences

Peking University

Beijing China 100871

Hao Yu

Associate
Professor

dbsy
uhao@nus.edu.sg

Department of Biological
Sciences, National University of
Singapore, 14 Science Dr 4

Singapore 117453


He Xionglei


Professor


hexiongl@mail.sysu.edu.cn


College of Life Sciences

Sun Yat
-
S
en University,

135 Xingang West

Guangzhou,
510275, China

Phone: (86) 20
-
39332844
Fax:
(86) 20
-
34022356

Hong Yi
-
Jiang



yjhong2008@163.com

Nanchang University

Tel: 13970965768

Hong Yunhan

Assoc

Professor

dbshyh
@nus.edu.sg

Department of Biological
Sciences, National University of
Singapore, 14 Science Dr 4

Singapore 117453

Huang Xiao
-
Wei

Associate
Professor

xiaoweihuang2001@hotmail.com

School of Life Science,
Yunnan
University, Kunming, 650091

Hwang Gwo
-
Jiunn

Professor

gjhuang58@163.com

Life Science Institute of
Nanchang University

Tel: 13687005285

Lai Choy Heng

Professor and
Vice Provost

pvoap@nus.edu.sg

Office of th
e Provost

U Hall, Level 5

National Univ of Singapore

Singapore 119260

Li Peng

Professor

li
-
peng@mail.tsinghua.edu.cn

Department of Biological
Sciences and Biotechnology,
Tsinghua University, Haidian
di
strict, Beijing,100084, China


39

Tel:+86
-
10
-
62785474 Fax

+86
-
10
-
62788604

Li Wen
-
Hua

Associate
Professor

whli@whu.edu.cn

School of Life Science, Wuhan
University,

Li Wen
-
Jun

Professor

wjli@ynu.edu.cn

School of Life Science, Yunna
n
University, Kunming, 650091


Lin Shengcai


Dean/ Professor



linsc@xmu.edu.cn

School of Life Science, Xiamen
University,
Tel: 86
-
592
-
2182993


Liou Yih
-
Cherng


Assistant

Professor


dbslyc@nus.edu.sg

Department of Biological
Sciences, National Univers
ity of
Singapore, 14 Science Dr 4

Singapore 117453


Liu Dong


Professor


dliu@uoneuro.uoregon.edu

College of Life Sciences

Peking University

Beijing, China 100871

Liu Xin
-
Qi

Professor

liu2008@nankai.edu.cn

School of Life Sciences, NanKai
University.

Tel: 022
-
23505130


Ng, Davis Tai Wai


Associate

Professor


dbsdntw
@nus.edu.sg

Department of Biological
Sciences, National
University of
Singapore, 14 Science Dr 4

Singapore 117453


Paul Matsudaira


Professor

matsudaira@wi.mit.edu

from January 1, 2009,
dbsmpt@nus.edu.sg

Member, Whitehead I
nstitute for
Biomedical Research

Professor, Departments of
Biology and Biological
Engineering, MIT


Richard Corlett


Professor


Corlett@nus.edu.sg

Department of Biological
Sciences, National University of
Singapore, 14 Science Dr 4

Singapore 117453


Shen

Yue
-
Mao


Professor


yshen@mail.kib.ac.cn

School of Life Science, Xiamen
University.
Tel: 86
-
592
-
2184180

Shu Hong
-
Bin

Dean/ Professor

shuh@whu.edu.cn

School of Life Scien
ce, Wuhan
University.


Song Jianxing


Associate

Professor


bchsj@nus.edu.sg

Department of Biological
Sciences, National University of
Singapore, 14 Science Dr 4

Singapore 117453


Song Siyang


Professor


yitao@xmu.e
du.cn

422 South Siming Road,
Xiamen, Fujian 361005, School
of Life Sciences, Xiamen

40

University.

Tel: 86
-
592
-
2184180


Sui Sen
-
Fang


Professor


suisf@mail.tsinghua.edu.cn

Department of Biological
Sciences
and Biotechnology,
Tsinghua University, Haidian
district, Beijing,100084, China

Tel: 010
-
62784768


Tao Yi


Professor


yitao@xmu.edu.cn

422 South Siming Road,
Xiamen, Fujian 361005, School
of Life Sciences, Xiamen
University.

Tel: 86
-
592
-
2182992


Wang
Hong
-
Yan


Professor


wanghy@fudan.edu.cn

State Key Laboratory of Genetic
Engineering, School of Life
Sciences, Fudan University,
Shanghai, 200433
.

Tel: 13918799082


Wang Q
iang


Associate
Professor


wangqiang1997@gmail.com


State Key Laboratory of
Pharmaceutical Biotechnology,
Department of Biology, Nanj
ing
University, Nanjing 210093,
China.


Wang Xue
-
Lu


Professor


Xueluw@gmail.com

State Key Laboratory of Genetic
Engineering, School of Life
Sciences, Fudan University,
Shanghai, 200433, China

021
-
65102247, 1
3023146652

Wang Yu
-
Jiong

Professor

wyj@nxu.edu.cn


School of Life Science, Ningxia
University, Yinchuan, Ningxia,
750021 PR China

Wang Yan
-
Yi

Assistant
Professor

yywang@whu.ed
u.cn

School of Life Science, Wuhan
University.


Wei Wensheng


Professor


wswei@pku.edu.cn

College of Life Sciences


Peking University


Beijing China 100871

Tel: +86 10
-
6275 7227


Wu Geng


Professor


geng.wu@sjtu.edu.cn

College of Life Science &
Biotechnology, Shanghai
Jiaotong University,1954
Huashan Rd, Shanghai 200030,
China
.
Tel:13601767804

Xiao ChunJie

Vice Dean/

Professor

cjxiao@public.km.yn.cn


School of Life Science, Yunnan
University, Kunming, 650091

Xiao Heng

Professor

xiaoheng@ynu.edu.cn


School of Life Science, Yunnan
University, Kunming, 650091

Xu

P
ing

Professor

pingxu@sjtu.edu.cn

College of Life Science &
Biotechnology, Shanghai Jiao
Tong University, Shanghai
200240


41

Ye Hui

Dean/

Professor

yehui@ynu.edu.cn


School of Life Science, Yun
nan
University, Kunming, 650091

Yu Haijing

Associate
Professor

yuhj@mail.kiz.ac.cn

School of Life Science, Yunnan
University, Kunming, 650091

Zhang Ke
-
Qin

Vice President/

Professor

kqzhang1@yahoo.com.cn

School of Life Science, Yunnan
University, Kunming, 650091


Zhang Peng


Professor


alarzhang@gma
il.com


Key Laboratory of Gene
Engineering of the Ministry of
Education, Zhongshan
University, Guangzhou 510275

Zheng Bingrong

Associate
Professor

Bingrong_zheng@163.com


School of Life Science, Yunnan
Unive
rsity, Kunming, 650091

Zheng Ling

Professor

lzheng@whu.edu.cn

School of Life Science, Wuhan
University.
Tel: 027

68753795

Zhai Yong
-
Gong

Vice Dean/
Professor

ygzhai@bnu.e
du.cn

College of Life sciences, Beijing
Normal University

Tel: 010
-
58806656

Zhou Hai
-
Meng

Vice Dean/
Professor

zhm
-
dbs@mail.tsinghua.edu.cn

Department of Biological
Sciences and Biotechnology,
Tsinghua University, Haidian
district, Beijing,100084, China


Zhu You
-
Lin


Vice President/

Professor



bio_study@yahoo.com.cn

Laboratory of Molecular
Biology and Gene
Engineering, College of Life
Science, Nanchang University,
Nanchang 330047, China