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Drosophila SETDB1 and caspase cooperatively fine-tune cell fate determination of sensory organ precursor

机译：果蝇SETDB1和caspase协同微调细胞命运确定感觉器官前体

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摘要

Drosophila produce a constant number of mechanosensory bristles called macrochaetae (MC), which develop from sensory organ precursor (SOP) cells within a proneural cluster (PNC). However, what ensures the precise determination of SOP cells remains to be elucidated. In this study, we conducted RNAi screening in PNC for genes involved in epigenetic regulation. We identified a H3K9 histone methyltransferase, SETDB1/eggless, as a regulator of SOP development. Knockdown of SETDB1 in PNC led to additional SOPs. We further tested the relationship between SETDB1 and non-apoptotic function of caspase on SOP development. Reinforcing caspase activation by heterozygous Drosophila inhibitor of apoptosis protein 1 (DIAP1) mutation rescued ectopic SOP development caused by SETDB1 knockdown. Knockdown of SETDB1, however, had little effect on caspase activity. Simultaneous loss of SETDB1 and caspase activity resulted in further increase in MC, indicating that the two components work cooperatively. Our study suggests the fine-tuning mechanisms for SOP development by epigenetic methyltransferase and non-apoptotic caspase function.
机译：果蝇产生恒定数量的机械感觉刚毛，称为巨乳（MC），其由前神经簇（PNC）内的感觉器官前体（SOP）细胞发育而来。但是，如何确定SOP细胞的精确测定仍有待阐明。在这项研究中，我们在PNC中进行了RNAi筛选，寻找与表观遗传调控有关的基因。我们确定了H3K9组蛋白甲基转移酶，SETDB1 / eggless，作为SOP发展的监管者。 PNC中SETDB1的关闭导致了其他SOP。我们进一步测试了SETDB1和胱天蛋白酶对SOP发育的非凋亡功能之间的关系。果蝇的凋亡蛋白1（DIAP1）杂合子杂合子抑制剂增强caspase活化，可以挽救SETDB1敲低引起的异位SOP的发展。但是，敲低SETDB1对caspase活性的影响很小。 SETDB1和caspase活性的同时丧失导致MC的进一步增加，表明这两个组件协同工作。我们的研究表明通过表观遗传甲基转移酶和非凋亡半胱天冬酶功能的SOP发展的微调机制。

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