Male-Killing Spiroplasma Alters Behavior of the Dosage Compensation Complex during Drosophila melanogaster Embryogenesis.
Male-Killing Spiroplasma Alters Behavior of the Dosage Compensation Complex during Drosophila melanogaster Embryogenesis.
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DOI：
10.1016/j.cub.2016.03.050
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发表时间：
2016-05-23
期刊：
影响因子：
--
通讯作者：
Ferree PM
中科院分区：
文献类型：
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作者：
Cheng B;Kuppanda N;Aldrich JC;Akbari OS;Ferree PM
许多节肢动物体内含有母体传播的细菌，这种细菌会导致雄性优先死亡。这种针对性别的致命性有利于细菌，因为男性是细菌传播的“死胡同”，他们的缺席可能会导致他们的存活雌性兄弟姐妹获得额外的资源，从而可以更成功地传播细菌。虽然这些共生菌扰乱了一系列的发育过程，但潜在的细胞机制在很大程度上是未知的。以前的研究表明，果蝇剂量补偿途径基因的突变可以抑制由螺旋体细菌引起的雄性死亡。这一结果表明，剂量补偿是螺旋体的一个靶点。然而，目前还不清楚这一途径是如何受到影响的，以及潜在的相互作用是否需要男性特有的细胞环境。在这里，我们研究了螺旋体诱导的雄性黑腹水母胚胎致死的细胞学基础。我们发现，在杀死阶段之前，用于乙酰化男性X染色质的剂量补偿复合体(DCC)错误定位于细胞核的异位区域。伴随这种效应的是不适当的组蛋白乙酰化和全基因组基因表达的错误调节。通过转基因表达DCC特异性基因msl-2，在感染的雌性体内人工诱导DCC的形成，导致该复合体错误定位于非X区，并导致螺旋体早期死亡，反映了男性的杀伤效果。这些发现有力地表明，螺旋体通过直接靶向剂量补偿机制并独立于男性特有的其他细胞特征来启动男性杀戮。
Numerous arthropods harbor maternally transmitted bacteria that induce the preferential death of males. This sex-specific lethality benefits the bacteria because males are ‘dead ends’ regarding bacterial transmission and their absence may result in additional resources for their viable female siblings who can thereby more successfully transmit the bacteria. Although these symbionts disrupt a range of developmental processes, the underlying cellular mechanisms are largely unknown. It was previously shown that mutations in genes of the dosage compensation pathway of Drosophila melanogaster suppressed male killing caused by the bacterium, Spiroplasma. This result suggested that dosage compensation is a target of Spiroplasma. However, it remains unclear how this pathway is affected, and whether the underlying interactions require the male-specific cellular environment. Here we investigated the cellular basis of male embryonic lethality in D. melanogaster induced by Spiroplasma. We found that the dosage compensation complex (DCC), which acetylates X chromatin in males, becomes mis-localized to ectopic regions of the nucleus immediately prior to the killing phase. This effect was accompanied by inappropriate histone acetylation and genome-wide mis-regulation of gene expression. Artificially induced formation of the DCC in infected females, through transgenic expression of the DCC-specific gene msl-2, resulted in mis-localization of this complex to non-X regions and early Spiroplasma-induced death, mirroring the killing effects in males. These findings strongly suggest that Spiroplasma initiates male killing by targeting the dosage compensation machinery directly and independently of other cellular features characteristic of the male sex.