Research article

Ras promotes cell survival by antagonizing both JNK and Hid signals in the Drosophila eye

Yue Wu¹ , Yuan Zhuang^1,2 , Min Han^1,3 , Tian Xu^1,4 and Kejing Deng¹

¹Institute of Developmental Biology and Molecular Medicine and School of Life Science, Fudan University, Shanghai 200433, PR China

²Department of Immunology, Duke University Medical Center, Durham, NC 27708, USA

³Howard Hughes Medical Institute and Department of MCDB, University of Colorado, Boulder, CO 80309-0347, USA

⁴Howard Hughes Medical Institute and Department of Genetics, Yale University School of Medicine, New Haven, Connecticut, CT 06536, USA

author email corresponding author email

BMC Developmental Biology 2009, 9:53doi:10.1186/1471-213X-9-53

Published:	20 October 2009

Abstract

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, ras^KP, 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 ras^KP-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 ras^KP cell death. In addition, we find a strong correlation between ras^KP-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.