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Directional selection coupled with kin selection favors the establishment of senescence

dc.contributor.authorSzilágyi, András
dc.contributor.authorCzárán, Tamás
dc.contributor.authorSantos, Mauro
dc.contributor.authorSzathmáry, Eörs
dc.date.accessioned2023-11-15T08:58:49Z
dc.date.available2023-11-15T08:58:49Z
dc.date.issued2023-10
dc.description.abstractBackground Conventional wisdom in evolutionary theory considers aging as a non-selected byproduct of natural selection. Based on this, conviction aging was regarded as an inevitable phenomenon. It was also thought that in the wild organisms tend to die from diseases, predation and other accidents before they could reach the time when senescence takes its course. Evidence has accumulated, however, that aging is not inevitable and there are organisms that show negative aging even. Furthermore, old age does play a role in the deaths of many different organisms in the wild also. The hypothesis of programmed aging posits that a limited lifespan can evolve as an adaptation (i.e., positively selected for) in its own right, partly because it can enhance evolvability by eliminating “outdated” genotypes. A major shortcoming of this idea is that non-aging sexual individuals that fail to pay the demographic cost of aging would be able to steal good genes by recombination from aging ones. Results Here, we show by a spatially explicit, individual-based simulation model that aging can positively be selected for if a sufficient degree of kin selection complements directional selection. Under such conditions, senescence enhances evolvability because the rate of aging and the rate of recombination play complementary roles. The selected aging rate is highest at zero recombination (clonal reproduction). In our model, increasing extrinsic mortality favors evolved aging by making up free space, thereby decreasing competition and increasing drift, even when selection is stabilizing and the level of aging is set by mutation-selection balance. Importantly, higher extrinsic mortality is not a substitute for evolved aging under directional selection either. Reduction of relatedness decreases the evolved level of aging; chance relatedness favors non-aging genotypes. The applicability of our results depends on empirical values of directional and kin selection in the wild. Conclusions We found that aging can positively be selected for in a spatially explicit population model when sufficiently strong directional and kin selection prevail, even if reproduction is sexual. The view that there is a conceptual link between giving up clonal reproduction and evolving an aging genotype is supported by computational results.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.doi10.1186/s12915-023-01716-wpt_PT
dc.identifier.urihttp://hdl.handle.net/10451/60548
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherBMCpt_PT
dc.relationOpen access funding provided by ELKH Centre for Ecological Research. National Research, Development and Innovation Office (Hungary) K140164pt_PT
dc.relationolyai János Research Fellowship of the Hungarian Academy of Sciencespt_PT
dc.relationinisterio de Ciencia e Innovación (Spain) PID2021-127107NB-I00pt_PT
dc.relationGeneralitat de Catalunya 2021 SGR 00526pt_PT
dc.relationDistinguished Guest Scientists Fellowship Programme of the Hungarian Academy of Sciencespt_PT
dc.relationVolkswagen Foundation (initiative “Leben? –Ein neuer Blick der Naturwissenschaften auf die grundlegenden Prinzipien des Lebens,” project “A unified model of recombination in life”)pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.titleDirectional selection coupled with kin selection favors the establishment of senescencept_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.issue1pt_PT
oaire.citation.titleBMC Biologypt_PT
oaire.citation.volume21pt_PT
person.familyNameSantos
person.givenNameMauro
person.identifier.ciencia-id6A12-5321-627A
person.identifier.orcid0000-0002-6478-6570
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublication215be051-54a0-45ec-b3d0-f76c7d3519fc
relation.isAuthorOfPublication.latestForDiscovery215be051-54a0-45ec-b3d0-f76c7d3519fc

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