创作:吴芹 审核:mildbreeze 01月08日
  • 去除菌群会导致果蝇整体和卵巢的线粒体活性和ATP水平降低,抑制卵子发生;
  • 在有菌果蝇中敲低卵泡细胞的线粒体功能,也会相似地抑制卵子发生;
  • 代谢组学分析显示,无菌果蝇的氧化磷酸化、线粒体辅酶FAD及其前体核黄素的水平均下降,而由FAD依赖性酶降解的代谢物积累;
  • 重新定植菌群或补充核黄素,可恢复无菌果蝇的线粒体功能、ATP水平和卵子发生;
  • 菌群通过提供线粒体辅酶的代谢前体,形成菌群-线粒体轴,调节宿主能量和繁殖力。
肠道菌群可促进宿主的卵子发生和繁殖力,但背后的机制仍需深入揭示。Cell Reports近期发表一项研究表明,菌群可通过产生线粒体辅酶的代谢前体(比如核黄素),来系统性地调控宿主能量水平和卵子发生。
Cell Reports [IF:8.109]

Systemic Regulation of Host Energy and Oogenesis by Microbiome-Derived Mitochondrial Coenzymes



01-05, Article

Abstract & Authors:展开

Gut microbiota have been shown to promote oogenesis and fecundity, but the mechanistic basis of remote influence on oogenesis remained unknown. Here, we report a systemic mechanism of influence mediated by bacterial-derived supply of mitochondrial coenzymes. Removal of microbiota decreased mitochondrial activity and ATP levels in the whole-body and ovary, resulting in repressed oogenesis. Similar repression was caused by RNA-based knockdown of mitochondrial function in ovarian follicle cells. Reduced mitochondrial function in germ-free (GF) females was reversed by bacterial recolonization or supplementation of riboflavin, a precursor of FAD and FMN. Metabolomics analysis of GF females revealed a decrease in oxidative phosphorylation and FAD levels and an increase in metabolites that are degraded by FAD-dependent enzymes (e.g., amino and fatty acids). Riboflavin supplementation opposed this effect, elevating mitochondrial function, ATP, and oogenesis. These findings uncover a bacterial-mitochondrial axis of influence, linking gut bacteria with systemic regulation of host energy and reproduction.

First Authors:
Yulia Gnainsky

Correspondence Authors:
Yulia Gnainsky

All Authors:
Yulia Gnainsky,Nofar Zfanya,Michael Elgart,Eman Omri,Alexander Brandis,Tevie Mehlman,Maxim Itkin,Sergey Malitsky,Jerzy Adamski,Yoav Soen