Decoupling developmental apoptosis and neuroblast proliferation in Drosophila.

Cell proliferation and cell death are opposing but fundamental aspects of development that must be tightly controlled to ensure proper tissue organization and organismal health. Developmental apoptosis of abdominal neuroblasts in the Drosophila ventral nerve cord is controlled by multiple upstream spatial and temporal signals, which have also been implicated in control of cell proliferation. It has therefore remained unclear whether developmental apoptosis is linked to active cell proliferation. Previous investigations into this topic have focused on the effect of cell cycle arrests on exogenous induction of apoptosis, and thus have not addressed whether potential effects of the cell cycle lie with the sensing of damage signals or the execution of apoptosis itself. In this report, we show that developmental apoptosis is not inhibited by cell cycle arrest, and that endogenous cell death occurs independently of cell cycle phase. We also find that ectopic neuroblasts rescued from cell death retain the competency to respond to quiescence cues at the end of embryogenesis. In addition, we observe multiple quiescence types in neuroblasts, and we show that cell death mutant embryos display a specific loss of presumptive G2 quiescent abdominal neuroblasts at the end of embryogenesis. This study demonstrates that upstream control of neuroblast proliferation and apoptosis represent independent mechanisms of regulating stem cell fate, and that execution of apoptosis occurs in a cell cycle-independent manner. Our findings also indicate that a subset of G2Q-fated abdominal neuroblasts are eliminated from the embryo through a non-apoptotic mechanism.

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