Abstract
Apoptosis is a fundamental remodeling process for most tissues during development. In this manuscript we examine a pro-apoptotic function for the Drosophila DNA binding protein Zfh-2 during development of the central nervous system (CNS) and appendages. In the CNS we find that a loss-of-function zfh-2 allele gives an overall reduction of apoptotic cells in the CNS, and an altered pattern of expression for the axonal markers 22C10 and FasII. This same loss-of-function zfh-2 allele causes specific cells in the NB7-3 lineage of the CNS that would normally undergo apoptosis to be inappropriately maintained, whereas a gain-of-function zfh-2 allele has the opposite effect, resulting in a loss of normal NB 7-3 progeny. We also demonstrate that Zfh-2 and Hunchback reciprocally repress each other's gene expression which limits apoptosis to later born progeny of the NB7-3 lineage. Apoptosis is also required for proper segmentation of the fly appendages. We find that Zfh-2 co-localizes with apoptotic cells in the folds of the imaginal discs and presumptive cuticular joints. A reduction of Zfh-2 levels with RNAi inhibits expression of the pro-apoptotic gene reaper, and produces abnormal joints in the leg, antenna and haltere. Apoptosis has previously been shown to be activated by Notch signaling in both the NB7-3 CNS lineage and the appendage joints. Our results indicate that Zfh-2 facilitates Notch-induced apoptosis in these structures.
