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微生物通过激素途径控制果蝇生殖干细胞的增加和卵子成熟。

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

机构信息

Laboratory of Germline Biology, Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamadaoka Suita, Osaka, 565-0871, Japan.

Pacific Biosciences Research Center, University of Hawai'i at Manoa, 1993 East-West Road, Honolulu, HI, 96822, USA.

出版信息

Commun Biol. 2023 Dec 20;6(1):1287. doi: 10.1038/s42003-023-05660-x.

Abstract

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.

摘要

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,微生物促进了宿主动物的重要功能,如营养摄入、代谢调节,并在营养条件差的情况下提高生育能力。然而,微生物控制生殖细胞成熟从而导致生殖的详细分子机制在很大程度上仍然未知。在这项研究中,我们表明,环境微生物通过加速卵巢细胞分裂和抑制细胞凋亡,促进生殖细胞干细胞(GSC)增殖和随后的卵子成熟,从而对果蝇卵子发生产生有益影响。此外,不需要胰岛素相关信号;相反,蜕皮激素途径对于微生物诱导的 GSCs 增加和卵子成熟的促进是必要的,而保幼激素仅有助于增加 GSC 数量,表明激素途径在卵子发生的不同阶段被激活。我们的发现表明,环境微生物可以通过调节宿主激素释放和促进卵子发生来提高宿主的生殖力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c6e/10733356/f96b07996d44/42003_2023_5660_Fig1_HTML.jpg

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