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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.

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