Microbes control Drosophila germline stem cell increase and egg maturation through hormonal pathways.

Microbes control Drosophila germline stem cell increase and egg maturation through hormonal pathways.
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DOI:
10.1038/s42003-023-05660-x
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发表时间:
2023-12-20
影响因子:
5.9
通讯作者:
Kai, Toshie
Kai, Toshie
中科院分区:
生物学2区
文献类型:
--
作者:
Suyama, Ritsuko;Cetraro, Nicolas;Yew, Joanne Y.;Kai, Toshie

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生殖高度依赖于环境和生理因素,包括营养、交配刺激和微生物。在这些因素中,微生物促进宿主动物的重要功能,如营养摄入、代谢调节和在营养不良条件下提高生育能力。然而,微生物控制生殖细胞成熟并导致繁殖的详细分子机制在很大程度上仍然未知。在这项研究中,我们发现环境微生物通过加速卵巢细胞分裂和抑制凋亡,促进种系干细胞(GSC)增殖和随后的卵子成熟,从而对果蝇的卵发生产生有益的影响。此外,不需要胰岛素相关的信号;相反,蜕皮激素途径是微生物诱导的GSC增加和促进卵子成熟所必需的,而幼激素仅有助于增加GSC数量,这表明激素途径在卵子发生的不同阶段被激活。我们的研究结果表明,环境微生物可以通过调节宿主激素的释放和促进卵子生成来提高宿主的繁殖能力。环境微生物通过激素途径增加生殖系干细胞数量、抑制细胞凋亡和加速卵巢细胞分裂,从而促进果蝇的卵发生。
Reproduction is highly dependent on environmental and physiological factors including nutrition, mating stimuli and microbes. Among these factors, microbes facilitate vital functions for host animals such as nutritional intake, metabolic regulation, and enhancing fertility under poor nutrition conditions. However, detailed molecular mechanisms by which microbes control germline maturation, leading to reproduction, remain largely unknown. In this study, we show that environmental microbes exert a beneficial effect on Drosophila oogenesis by promoting germline stem cell (GSC) proliferation and subsequent egg maturation via acceleration of ovarian cell division and suppression of apoptosis. Moreover, insulin-related signaling is not required; rather, the ecdysone pathway is necessary for microbe-induced increase of GSCs and promotion of egg maturation, while juvenile hormone contributes only to increasing GSC numbers, suggesting that hormonal pathways are activated at different stages of oogenesis. Our findings reveal that environmental microbes can enhance host reproductivity by modulating host hormone release and promoting oogenesis. Environmental microbes enhance Drosophila oogenesis by increasing the number of germline stem cells, suppressing apoptosis and accelerating ovarian cell division through hormonal pathways.
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