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Delayed development induced by toxicity to the host can be inherited by a bacterial-dependent, transgenerational effect
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 st...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3933808/ https://www.ncbi.nlm.nih.gov/pubmed/24611070 http://dx.doi.org/10.3389/fgene.2014.00027 |
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author | Fridmann-Sirkis, Yael Stern, Shay Elgart, Michael Galili, Matana Zeisel, Amit Shental, Noam Soen, Yoav |
author_facet | Fridmann-Sirkis, Yael Stern, Shay Elgart, Michael Galili, Matana Zeisel, Amit Shental, Noam Soen, Yoav |
author_sort | Fridmann-Sirkis, Yael |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-3933808 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-39338082014-03-07 Delayed development induced by toxicity to the host can be inherited by a bacterial-dependent, transgenerational effect Fridmann-Sirkis, Yael Stern, Shay Elgart, Michael Galili, Matana Zeisel, Amit Shental, Noam Soen, Yoav Front Genet Genetics 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. Frontiers Media S.A. 2014-02-25 /pmc/articles/PMC3933808/ /pubmed/24611070 http://dx.doi.org/10.3389/fgene.2014.00027 Text en Copyright © 2014 Fridmann-Sirkis, Stern, Elgart, Galili, Zeisel, Shental and Soen. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Genetics Fridmann-Sirkis, Yael Stern, Shay Elgart, Michael Galili, Matana Zeisel, Amit Shental, Noam Soen, Yoav Delayed development induced by toxicity to the host can be inherited by a bacterial-dependent, transgenerational effect |
title | Delayed development induced by toxicity to the host can be inherited by a bacterial-dependent, transgenerational effect |
title_full | Delayed development induced by toxicity to the host can be inherited by a bacterial-dependent, transgenerational effect |
title_fullStr | Delayed development induced by toxicity to the host can be inherited by a bacterial-dependent, transgenerational effect |
title_full_unstemmed | Delayed development induced by toxicity to the host can be inherited by a bacterial-dependent, transgenerational effect |
title_short | Delayed development induced by toxicity to the host can be inherited by a bacterial-dependent, transgenerational effect |
title_sort | delayed development induced by toxicity to the host can be inherited by a bacterial-dependent, transgenerational effect |
topic | Genetics |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3933808/ https://www.ncbi.nlm.nih.gov/pubmed/24611070 http://dx.doi.org/10.3389/fgene.2014.00027 |
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