Dataset Information

Decoupling developmental apoptosis and neuroblast proliferation in Drosophila.

ABSTRACT: 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.

SUBMITTER: Harding K

PROVIDER: S-EPMC6814563 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature

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Decoupling developmental apoptosis and neuroblast proliferation in Drosophila.

Harding Katherine K White Kristin K

Developmental biology 20190804 1

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. ...[more]

PMID: 31390535

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Project description:Optimal mitochondrial function determined by mitochondrial dynamics, morphology and activity is coupled to stem cell differentiation and organism development. However, the mechanisms of interaction of signaling pathways with mitochondrial morphology and activity are not completely understood. We assessed the role of mitochondrial fusion and fission in the differentiation of neural stem cells called neuroblasts (NB) in the Drosophila brain. Depleting mitochondrial inner membrane fusion protein Opa1 and mitochondrial outer membrane fusion protein Marf in the Drosophila type II NB lineage led to mitochondrial fragmentation and loss of activity. Opa1 and Marf depletion did not affect the numbers of type II NBs but led to a decrease in differentiated progeny. Opa1 depletion decreased the mature intermediate precursor cells (INPs), ganglion mother cells (GMCs) and neurons by the decreased proliferation of the type II NBs and mature INPs. Marf depletion led to a decrease in neurons by a depletion of proliferation of GMCs. On the contrary, loss of mitochondrial fission protein Drp1 led to mitochondrial clustering but did not show defects in differentiation. Depletion of Drp1 along with Opa1 or Marf also led to mitochondrial clustering and suppressed the loss of mitochondrial activity and defects in proliferation and differentiation in the type II NB lineage. Opa1 depletion led to decreased Notch signaling in the type II NB lineage. Further, Notch signaling depletion via the canonical pathway showed mitochondrial fragmentation and loss of differentiation similar to Opa1 depletion. An increase in Notch signaling showed mitochondrial clustering similar to Drp1 mutants. Further, Drp1 mutant overexpression combined with Notch depletion showed mitochondrial fusion and drove differentiation in the lineage, suggesting that fused mitochondria can influence differentiation in the type II NB lineage. Our results implicate crosstalk between proliferation, Notch signaling, mitochondrial activity and fusion as an essential step in differentiation in the type II NB lineage.

Dataset Information

Decoupling developmental apoptosis and neuroblast proliferation in Drosophila.

Publications

Decoupling developmental apoptosis and neuroblast proliferation in Drosophila.

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