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Pathogen‐induced maternal effects result in enhanced immune responsiveness across generations
Parental investment theory postulates that adults can accurately perceive cues from their surroundings, anticipate the needs of future offspring based on those cues, and selectively allocate nongenetic resources to their progeny. Such context‐dependent parental contributions can result in phenotypic...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5415515/ https://www.ncbi.nlm.nih.gov/pubmed/28479992 http://dx.doi.org/10.1002/ece3.2887 |
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author | Rosengaus, Rebeca B. Hays, Nicole Biro, Colette Kemos, James Zaman, Muizz Murray, Joseph Gezahegn, Bruck Smith, Wendy |
author_facet | Rosengaus, Rebeca B. Hays, Nicole Biro, Colette Kemos, James Zaman, Muizz Murray, Joseph Gezahegn, Bruck Smith, Wendy |
author_sort | Rosengaus, Rebeca B. |
collection | PubMed |
description | Parental investment theory postulates that adults can accurately perceive cues from their surroundings, anticipate the needs of future offspring based on those cues, and selectively allocate nongenetic resources to their progeny. Such context‐dependent parental contributions can result in phenotypically variable offspring. Consistent with these predictions, we show that bacterially exposed Manduca sexta mothers oviposited significantly more variable embryos (as measured by mass, volume, hatching time, and hatching success) relative to naïve and control mothers. By using an in vivo “clearance of infection” assay, we also show that challenged larvae born to heat‐killed‐ or live‐Serratia‐injected mothers, supported lower microbial loads and cleared the infection faster than progeny of control mothers. Our data support the notion that mothers can anticipate the future pathogenic risks and immunological needs of their unborn offspring, providing progeny with enhanced immune protection likely through transgenerational immune priming. Although the inclusion of live Serratia into oocytes does not appear to be the mechanism by which mothers confer protection to their young, other mechanisms, including epigenetic modifications in the progeny due to maternal pathogenic stress, may be at play. The adaptive nature of maternal effects in the face of pathogenic stress provides insights into parental investment, resource allocation, and life‐history theories and highlights the significant role that pathogen‐induced maternal effects play as generators and modulators of evolutionary change. |
format | Online Article Text |
id | pubmed-5415515 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-54155152017-05-05 Pathogen‐induced maternal effects result in enhanced immune responsiveness across generations Rosengaus, Rebeca B. Hays, Nicole Biro, Colette Kemos, James Zaman, Muizz Murray, Joseph Gezahegn, Bruck Smith, Wendy Ecol Evol Original Research Parental investment theory postulates that adults can accurately perceive cues from their surroundings, anticipate the needs of future offspring based on those cues, and selectively allocate nongenetic resources to their progeny. Such context‐dependent parental contributions can result in phenotypically variable offspring. Consistent with these predictions, we show that bacterially exposed Manduca sexta mothers oviposited significantly more variable embryos (as measured by mass, volume, hatching time, and hatching success) relative to naïve and control mothers. By using an in vivo “clearance of infection” assay, we also show that challenged larvae born to heat‐killed‐ or live‐Serratia‐injected mothers, supported lower microbial loads and cleared the infection faster than progeny of control mothers. Our data support the notion that mothers can anticipate the future pathogenic risks and immunological needs of their unborn offspring, providing progeny with enhanced immune protection likely through transgenerational immune priming. Although the inclusion of live Serratia into oocytes does not appear to be the mechanism by which mothers confer protection to their young, other mechanisms, including epigenetic modifications in the progeny due to maternal pathogenic stress, may be at play. The adaptive nature of maternal effects in the face of pathogenic stress provides insights into parental investment, resource allocation, and life‐history theories and highlights the significant role that pathogen‐induced maternal effects play as generators and modulators of evolutionary change. John Wiley and Sons Inc. 2017-03-22 /pmc/articles/PMC5415515/ /pubmed/28479992 http://dx.doi.org/10.1002/ece3.2887 Text en © 2017 The Authors. Ecology and Evolution published by John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Research Rosengaus, Rebeca B. Hays, Nicole Biro, Colette Kemos, James Zaman, Muizz Murray, Joseph Gezahegn, Bruck Smith, Wendy Pathogen‐induced maternal effects result in enhanced immune responsiveness across generations |
title | Pathogen‐induced maternal effects result in enhanced immune responsiveness across generations |
title_full | Pathogen‐induced maternal effects result in enhanced immune responsiveness across generations |
title_fullStr | Pathogen‐induced maternal effects result in enhanced immune responsiveness across generations |
title_full_unstemmed | Pathogen‐induced maternal effects result in enhanced immune responsiveness across generations |
title_short | Pathogen‐induced maternal effects result in enhanced immune responsiveness across generations |
title_sort | pathogen‐induced maternal effects result in enhanced immune responsiveness across generations |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5415515/ https://www.ncbi.nlm.nih.gov/pubmed/28479992 http://dx.doi.org/10.1002/ece3.2887 |
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