Delayed development induced by toxicity to the host can be inherited by a bacterial-dependent, transgenerational effect.
Delayed development induced by toxicity to the host can be inherited by a bacterial-dependent, transgenerational effect.
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DOI：
10.3389/fgene.2014.00027
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发表时间：
2014
影响因子：
3.7
通讯作者：
Soen Y
中科院分区：
文献类型：
--
作者：
Fridmann-Sirkis Y;Stern S;Elgart M;Galili M;Zeisel A;Shental N;Soen Y
包括苍蝇在内的许多物种的共生肠道细菌是其宿主的组成部分，并且已知影响其发育和世代内的稳态。在这里，我们报告了一个意想不到的影响宿主微生物的相互作用，介导多代，非孟德尔遗传的压力诱导的表型。我们先前已经表明，暴露于G418抗生素的蝇幼虫诱导转代遗传表型，包括幼虫发育延迟，肠道中的基因诱导和形态学变化。我们现在表明，G418选择性地消耗葡萄糖醋酸杆菌物种，这种消耗解释了遗传延迟，但不是其他表型的遗传。值得注意的是，延迟的遗传是由令人惊讶的跨代效应介导的。具体而言，从F1胚胎中去除细菌并没有引起F1幼虫的显著延迟，但仍然导致F2的相当大的延迟。这种效应维持了由细菌非依赖性G418对宿主的毒性诱导的延迟。与这些发现一致，重新引入分离的醋酸杆菌属物种防止了延迟的遗传。我们进一步表明，这种预防部分是由这些细菌产生的维生素B2（核黄素）介导的;外源性核黄素导致部分预防，核黄素合成的抑制损害了细菌防止遗传的能力。这些结果确定宿主-微生物相互作用作为迄今未被认识的能够介导非孟德尔遗传的应激诱导表型的因子。
Commensal gut bacteria in many species including flies are integral part of their host, and are known to influence its development and homeostasis within generation. Here we report an unexpected impact of host–microbe interactions, which mediates multi-generational, non-Mendelian inheritance of a stress-induced phenotype. We have previously shown that exposure of fly larvae to G418 antibiotic induces transgenerationally heritable phenotypes, including a delay in larval development, gene induction in the gut and morphological changes. We now show that G418 selectively depletes commensal Acetobacter species and that this depletion explains the heritable delay, but not the inheritance of the other phenotypes. Notably, the inheritance of the delay was mediated by a surprising trans-generational effect. Specifically, bacterial removal from F1 embryos did not induce significant delay in F1 larvae, but nonetheless led to a considerable delay in F2. This effect maintains a delay induced by bacterial-independent G418 toxicity to the host. In line with these findings, reintroduction of isolated Acetobacter species prevented the inheritance of the delay. We further show that this prevention is partly mediated by vitamin B2 (Riboflavin) produced by these bacteria; exogenous Riboflavin led to partial prevention and inhibition of Riboflavin synthesis compromised the ability of the bacteria to prevent the inheritance. These results identify host–microbe interactions as a hitherto unrecognized factor capable of mediating non-Mendelian inheritance of a stress-induced phenotype.
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影响因子：
64.5
作者：
Ashe A;Sapetschnig A;Weick EM;Mitchell J;Bagijn MP;Cording AC;Doebley AL;Goldstein LD;Lehrbach NJ;Le Pen J;Pintacuda G;Sakaguchi A;Sarkies P;Ahmed S;Miska EA
通讯作者：
Miska EA
影响因子：
64.5
作者：
Carone BR;Fauquier L;Habib N;Shea JM;Hart CE;Li R;Bock C;Li C;Gu H;Zamore PD;Meissner A;Weng Z;Hofmann HA;Friedman N;Rando OJ
通讯作者：
Rando OJ
影响因子：
4.1
作者：
Lee ER;Blount KF;Breaker RR
通讯作者：
Breaker RR
影响因子：
3.4
作者：
BAKULA, M
通讯作者：
BAKULA, M
影响因子：
11.4
作者：
Lim, Jana P.;Brunet, Anne
通讯作者：
Brunet, Anne