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Selfish centromeres and the wastefulness of human reproduction

Many human embryos die in utero owing to an excess or deficit of chromosomes, a phenomenon known as aneuploidy; this is largely a consequence of nondisjunction during maternal meiosis I. Asymmetries of this division render it vulnerable to selfish centromeres that promote their own transmission, the...

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Autor principal: Hurst, Laurence D.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9255743/
https://www.ncbi.nlm.nih.gov/pubmed/35788750
http://dx.doi.org/10.1371/journal.pbio.3001671
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author_facet Hurst, Laurence D.
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description Many human embryos die in utero owing to an excess or deficit of chromosomes, a phenomenon known as aneuploidy; this is largely a consequence of nondisjunction during maternal meiosis I. Asymmetries of this division render it vulnerable to selfish centromeres that promote their own transmission, these being thought to somehow underpin aneuploidy. In this essay, I suggest that these vulnerabilities provide only half the solution to the enigma. In mammals, as in utero and postnatal provisioning is continuous, the costs of early death are mitigated. With such reproductive compensation, selection can favour a centromere because it induces lethal aneuploidy: if, when taken towards the polar body, it instead kills the embryo via aneuploidy, it gains. The model is consistent with the observation that reduced dosage of a murine drive suppressor induces aneuploidy and with the fact that high aneuploidy rates in vertebrates are seen exclusively in mammals. I propose further tests of this idea. The wastefulness of human reproduction may be a price we pay for nurturing our offspring.
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spelling pubmed-92557432022-07-06 Selfish centromeres and the wastefulness of human reproduction Hurst, Laurence D. PLoS Biol Essay Many human embryos die in utero owing to an excess or deficit of chromosomes, a phenomenon known as aneuploidy; this is largely a consequence of nondisjunction during maternal meiosis I. Asymmetries of this division render it vulnerable to selfish centromeres that promote their own transmission, these being thought to somehow underpin aneuploidy. In this essay, I suggest that these vulnerabilities provide only half the solution to the enigma. In mammals, as in utero and postnatal provisioning is continuous, the costs of early death are mitigated. With such reproductive compensation, selection can favour a centromere because it induces lethal aneuploidy: if, when taken towards the polar body, it instead kills the embryo via aneuploidy, it gains. The model is consistent with the observation that reduced dosage of a murine drive suppressor induces aneuploidy and with the fact that high aneuploidy rates in vertebrates are seen exclusively in mammals. I propose further tests of this idea. The wastefulness of human reproduction may be a price we pay for nurturing our offspring. Public Library of Science 2022-07-05 /pmc/articles/PMC9255743/ /pubmed/35788750 http://dx.doi.org/10.1371/journal.pbio.3001671 Text en © 2022 Laurence D Hurst https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Essay
Hurst, Laurence D.
Selfish centromeres and the wastefulness of human reproduction
title Selfish centromeres and the wastefulness of human reproduction
title_full Selfish centromeres and the wastefulness of human reproduction
title_fullStr Selfish centromeres and the wastefulness of human reproduction
title_full_unstemmed Selfish centromeres and the wastefulness of human reproduction
title_short Selfish centromeres and the wastefulness of human reproduction
title_sort selfish centromeres and the wastefulness of human reproduction
topic Essay
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9255743/
https://www.ncbi.nlm.nih.gov/pubmed/35788750
http://dx.doi.org/10.1371/journal.pbio.3001671
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