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首页> 外文期刊>The Journal of Comparative Neurology >Drosophila caspases involved in developmentally regulated programmed cell death of peptidergic neurons during early metamorphosis.
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Drosophila caspases involved in developmentally regulated programmed cell death of peptidergic neurons during early metamorphosis.

机译：果蝇胱天蛋白酶参与早期变态期间肽能神经元的发育调控程序性细胞死亡。

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摘要

A great number of obsolete larval neurons in the Drosophila central nervous system are eliminated by developmentally programmed cell death (PCD) during early metamorphosis. To elucidate the mechanisms of neuronal PCD occurring during this period, we undertook genetic dissection of seven currently known Drosophila caspases in the PCD of a group of interneurons (vCrz) that produce corazonin (Crz) neuropeptide in the ventral nerve cord. The molecular death program in the vCrz neurons initiates within 1 hour after pupariation, as demonstrated by the cytological signs of cell death and caspase activation. PCD was significantly suppressed in dronc-null mutants, but not in null mutants of either dredd or strica. A double mutation lacking both dronc and strica impaired PCD phenotype more severely than did a dronc mutation alone, but comparably to a triple dredd/strica/dronc mutation, indicating that dronc is a main initiator caspase, while strica plays a minor role that overlaps with dronc's. As for effector caspases, vCrz PCD requires both ice and dcp-1 functions, as they work cooperatively for a timely removal of the vCrz neurons. Interestingly, the activation of the Ice and Dcp-1 is not solely dependent on Dronc and Strica, implying an alternative pathway to activate the effectors. Two remaining effector caspase genes, decay and damm, found no apparent functions in the neuronal PCD, at least during early metamorphosis. Overall, our work revealed that vCrz PCD utilizes dronc, strica, dcp-1, and ice wherein the activation of Ice and Dcp-1 requires a novel pathway in addition to the initiator caspases.
机译：果蝇中枢神经系统中的大量陈旧幼虫神经元被早期变态过程中发育性程序性细胞死亡（PCD）所消除。为了阐明在此期间发生神经元PCD的机制，我们对PCD中一组七个中间神经元（vCrz）中目前已知的果蝇半胱天冬酶进行了遗传解剖，这些中间神经元在腹神经索中产生了Corazonin（Crz）神经肽。 vCrz神经元中的分子死亡程序在产后1小时内启动，这由细胞死亡和caspase激活的细胞学迹象证明。在dronc-null突变体中PCD被显着抑制，而drdd或strica的null突变体中PCD却没有被抑制。缺少dronc和strica的双重突变比单独的dronc突变更严重地损害PCD表型，但与三倍drdd / strica / dronc突变相比，表明dronc是主要的起始胱天蛋白酶，而strica的作用较小，与dronc的。对于效应半胱天冬酶，vCrz PCD同时需要ice和dcp-1功能，因为它们协同工作以及时去除vCrz神经元。有趣的是，Ice和Dcp-1的激活并不仅仅依赖于Dronc和Strica，这意味着激活效应子的另一种途径。剩下的两个效应半胱天冬酶基因，衰减和达姆，至少在早期变态期间，在神经元PCD中没有发现明显的功能。总的来说，我们的工作表明vCrz PCD利用dronc，strica，dcp-1和ice，其中Ice和Dcp-1的激活除了启动子半胱天冬酶还需要一条新途径。

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