PMID- 19840402
OWN - NLM
STAT- MEDLINE
DCOM- 20100112
LR  - 20211020
IS  - 1471-213X (Electronic)
IS  - 1471-213X (Linking)
VI  - 9
DP  - 2009 Oct 20
TI  - Ras promotes cell survival by antagonizing both JNK and Hid signals in the 
      Drosophila eye.
PG  - 53
LID - 10.1186/1471-213X-9-53 [doi]
AB  - BACKGROUND: Programmed cell death, or apoptosis, is a fundamental physiological 
      process during normal development or in pathological conditions. The activation 
      of apoptosis can be elicited by numerous signalling pathways. Ras is known to 
      mediate anti-apoptotic signals by inhibiting Hid activity in the Drosophila eye. 
      Here we report the isolation of a new loss-of-function ras allele, rasKP, which 
      causes excessive apoptosis in the Drosophila eye. RESULTS: This new function is 
      likely to be mediated through the JNK pathway since the inhibition of JNK 
      signalling can significantly suppress rasKP-induced apoptosis, whereas the 
      removal of hid only weakly suppresses the phenotype. Furthermore, the reduction 
      of JNK signalling together with the expression of the baculovirus caspase 
      inhibitor p35, which blocks Hid activity, strongly suppresses the rasKP cell 
      death. In addition, we find a strong correlation between rasKP-induced apoptosis 
      in the eye disc and the activation of JNK signalling. CONCLUSION: In the 
      Drosophila eye, Ras may protect cells from apoptosis by inhibiting both JNK and 
      Hid activities. Surprisingly, reducing Ras activity in the wing, however, does 
      not cause apoptosis but rather affects cell and organ size. Thus, in addition to 
      its requirement for cell viability, Ras appears to mediate different biological 
      roles depending on the developmental context and on the level of its expression.
FAU - Wu, Yue
AU  - Wu Y
AD  - Institute of Developmental Biology and Molecular Medicine and School of Life 
      Science, Fudan University, Shanghai, PR China. yue_wu@fudan.edu.cn
FAU - Zhuang, Yuan
AU  - Zhuang Y
FAU - Han, Min
AU  - Han M
FAU - Xu, Tian
AU  - Xu T
FAU - Deng, Kejing
AU  - Deng K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20091020
PL  - England
TA  - BMC Dev Biol
JT  - BMC developmental biology
JID - 100966973
RN  - 0 (Drosophila Proteins)
RN  - 0 (HID protein, Drosophila)
RN  - 0 (Neuropeptides)
RN  - 0 (Viral Proteins)
RN  - 0 (p35 protein, Baculovirus)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - EC 3.6.5.2 (ras Proteins)
SB  - IM
MH  - Animals
MH  - Apoptosis/genetics/physiology
MH  - Cell Survival/genetics/*physiology
MH  - Drosophila/cytology/embryology/metabolism
MH  - Drosophila Proteins/genetics/*metabolism/physiology
MH  - Eye/cytology/embryology/*metabolism
MH  - Fluorescent Antibody Technique
MH  - Gene Expression Regulation, Developmental
MH  - JNK Mitogen-Activated Protein Kinases/genetics/*metabolism
MH  - Neuropeptides/genetics/*metabolism
MH  - Signal Transduction/genetics/physiology
MH  - Viral Proteins/genetics/physiology
MH  - Wings, Animal/cytology/embryology/metabolism
MH  - ras Proteins/genetics/*physiology
PMC - PMC2773777
EDAT- 2009/10/21 06:00
MHDA- 2010/01/13 06:00
PMCR- 2009/10/20
CRDT- 2009/10/21 06:00
PHST- 2008/12/02 00:00 [received]
PHST- 2009/10/20 00:00 [accepted]
PHST- 2009/10/21 06:00 [entrez]
PHST- 2009/10/21 06:00 [pubmed]
PHST- 2010/01/13 06:00 [medline]
PHST- 2009/10/20 00:00 [pmc-release]
AID - 1471-213X-9-53 [pii]
AID - 10.1186/1471-213X-9-53 [doi]
PST - epublish
SO  - BMC Dev Biol. 2009 Oct 20;9:53. doi: 10.1186/1471-213X-9-53.