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The  Drosophila  gene  putzig (pzg)  encodes a nuclear protein that is an integral component of the Trf2/Dref complex involved in the transcription of proliferation-related genes. Moreover, Pzg is found in a complex together with the nucleosome remodeling factor NURF, where it promotes Notch target gene activation. Here we show that downregulation of  pzg  activity in the developing wing imaginal discs induces an apoptotic response, accompanied by the induction of the pro-apoptotic gene  reaper , repression of  Drosophila  inhibitor of apoptosis protein accumulation and the activation of the caspases Drice, Caspase3 and Dcp1. As a further consequence ‘Apoptosis induced Proliferation’ (AiP) and ‘Apoptosis induced Apoptosis’ (AiA) are triggered. As expected, the activity of the stress kinase Jun N-terminal kinase (JNK), proposed to mediate both processes, is ectopically induced in response to  pzg  loss. In addition, the expression of the mitogen  wingless  ( wg ) but not of  decapentaplegic  ( dpp ) is observed. We present evidence that downregulation of  Notch  activates Dcp1 caspase and JNK signaling, however, neither induces ectopic  wg  nor  dpp  expression. In contrast, the consequences of  Dref -RNAi were largely indistinguishable from  pzg -RNAi with regard to apoptosis induction. Moreover, overexpression of  Dref  ameliorated the downregulation of  pzg  compatible with the notion that the two are required together to maintain cell and tissue homeostasis in  Drosophila .

Loss of putzig Activity Results in Apoptosis during Wing Imaginal Development in Drosophila