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Mediation of organismal aging and somatic proteostasis by the germline
Experimental interventions that reduce reproduction cause an extension in lifespan. In invertebrates, such as Caenorhabditis elegans, the aging of the soma is regulated by signals from the germline. Indeed, ablation of germ cells significantly extends lifespan. Notably, germline-deficient animals ex...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4428440/ https://www.ncbi.nlm.nih.gov/pubmed/25988171 http://dx.doi.org/10.3389/fmolb.2015.00003 |
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author | Khodakarami, Amirabbas Saez, Isabel Mels, Johanna Vilchez, David |
author_facet | Khodakarami, Amirabbas Saez, Isabel Mels, Johanna Vilchez, David |
author_sort | Khodakarami, Amirabbas |
collection | PubMed |
description | Experimental interventions that reduce reproduction cause an extension in lifespan. In invertebrates, such as Caenorhabditis elegans, the aging of the soma is regulated by signals from the germline. Indeed, ablation of germ cells significantly extends lifespan. Notably, germline-deficient animals exhibit heightened resistance to proteotoxic stress. This phenotype correlates with increased potential of intracellular clearance mechanisms such as the proteasome and autophagy in somatic tissues. Here we review the molecular mechanisms by which signals from the germline regulate lifespan in C. elegans with special emphasis on clearance mechanisms. |
format | Online Article Text |
id | pubmed-4428440 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-44284402015-05-18 Mediation of organismal aging and somatic proteostasis by the germline Khodakarami, Amirabbas Saez, Isabel Mels, Johanna Vilchez, David Front Mol Biosci Molecular Biosciences Experimental interventions that reduce reproduction cause an extension in lifespan. In invertebrates, such as Caenorhabditis elegans, the aging of the soma is regulated by signals from the germline. Indeed, ablation of germ cells significantly extends lifespan. Notably, germline-deficient animals exhibit heightened resistance to proteotoxic stress. This phenotype correlates with increased potential of intracellular clearance mechanisms such as the proteasome and autophagy in somatic tissues. Here we review the molecular mechanisms by which signals from the germline regulate lifespan in C. elegans with special emphasis on clearance mechanisms. Frontiers Media S.A. 2015-01-23 /pmc/articles/PMC4428440/ /pubmed/25988171 http://dx.doi.org/10.3389/fmolb.2015.00003 Text en Copyright © 2015 Khodakarami, Saez, Mels and Vilchez. http://creativecommons.org/licenses/by/4.0/ 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 | Molecular Biosciences Khodakarami, Amirabbas Saez, Isabel Mels, Johanna Vilchez, David Mediation of organismal aging and somatic proteostasis by the germline |
title | Mediation of organismal aging and somatic proteostasis by the germline |
title_full | Mediation of organismal aging and somatic proteostasis by the germline |
title_fullStr | Mediation of organismal aging and somatic proteostasis by the germline |
title_full_unstemmed | Mediation of organismal aging and somatic proteostasis by the germline |
title_short | Mediation of organismal aging and somatic proteostasis by the germline |
title_sort | mediation of organismal aging and somatic proteostasis by the germline |
topic | Molecular Biosciences |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4428440/ https://www.ncbi.nlm.nih.gov/pubmed/25988171 http://dx.doi.org/10.3389/fmolb.2015.00003 |
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