Explaining the imperfection of the molecular clock of hominid mitochondria.

The molecular clock of mitochondrial DNA has been extensively used to date various genetic events. However, its substitution rate among humans appears to be higher than rates inferred from human-chimpanzee comparisons, limiting the potential of interspecies clock calibrations for intraspecific datin...

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Autores principales:	Eva-Liis Loogväli, Toomas Kivisild, Tõnu Margus, Richard Villems
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2009
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/05b79cced2f84cfd813304f6c784cae4
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spelling	oai:doaj.org-article:05b79cced2f84cfd813304f6c784cae42021-11-25T06:27:07ZExplaining the imperfection of the molecular clock of hominid mitochondria.1932-620310.1371/journal.pone.0008260https://doaj.org/article/05b79cced2f84cfd813304f6c784cae42009-12-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20041137/?tool=EBIhttps://doaj.org/toc/1932-6203The molecular clock of mitochondrial DNA has been extensively used to date various genetic events. However, its substitution rate among humans appears to be higher than rates inferred from human-chimpanzee comparisons, limiting the potential of interspecies clock calibrations for intraspecific dating. It is not well understood how and why the substitution rate accelerates. We have analyzed a phylogenetic tree of 3057 publicly available human mitochondrial DNA coding region sequences for changes in the ratios of mutations belonging to different functional classes. The proportion of non-synonymous and RNA genes substitutions has reduced over hundreds of thousands of years. The highest mutation ratios corresponding to fast acceleration in the apparent substitution rate of the coding sequence have occurred after the end of the Last Ice Age. We recalibrate the molecular clock of human mtDNA as 7990 years per synonymous mutation over the mitochondrial genome. However, the distribution of substitutions at synonymous sites in human data significantly departs from a model assuming a single rate parameter and implies at least 3 different subclasses of sites. Neutral model with 3 synonymous substitution rates can explain most, if not all, of the apparent molecular clock difference between the intra- and interspecies levels. Our findings imply the sluggishness of purifying selection in removing the slightly deleterious mutations from the human as well as the Neandertal and chimpanzee populations. However, for humans, the weakness of purifying selection has been further exacerbated by the population expansions associated with the out-of Africa migration and the end of the Last Ice Age.Eva-Liis LoogväliToomas KivisildTõnu MargusRichard VillemsPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 4, Iss 12, p e8260 (2009)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Eva-Liis Loogväli Toomas Kivisild Tõnu Margus Richard Villems Explaining the imperfection of the molecular clock of hominid mitochondria.
description	The molecular clock of mitochondrial DNA has been extensively used to date various genetic events. However, its substitution rate among humans appears to be higher than rates inferred from human-chimpanzee comparisons, limiting the potential of interspecies clock calibrations for intraspecific dating. It is not well understood how and why the substitution rate accelerates. We have analyzed a phylogenetic tree of 3057 publicly available human mitochondrial DNA coding region sequences for changes in the ratios of mutations belonging to different functional classes. The proportion of non-synonymous and RNA genes substitutions has reduced over hundreds of thousands of years. The highest mutation ratios corresponding to fast acceleration in the apparent substitution rate of the coding sequence have occurred after the end of the Last Ice Age. We recalibrate the molecular clock of human mtDNA as 7990 years per synonymous mutation over the mitochondrial genome. However, the distribution of substitutions at synonymous sites in human data significantly departs from a model assuming a single rate parameter and implies at least 3 different subclasses of sites. Neutral model with 3 synonymous substitution rates can explain most, if not all, of the apparent molecular clock difference between the intra- and interspecies levels. Our findings imply the sluggishness of purifying selection in removing the slightly deleterious mutations from the human as well as the Neandertal and chimpanzee populations. However, for humans, the weakness of purifying selection has been further exacerbated by the population expansions associated with the out-of Africa migration and the end of the Last Ice Age.
format	article
author	Eva-Liis Loogväli Toomas Kivisild Tõnu Margus Richard Villems
author_facet	Eva-Liis Loogväli Toomas Kivisild Tõnu Margus Richard Villems
author_sort	Eva-Liis Loogväli
title	Explaining the imperfection of the molecular clock of hominid mitochondria.
title_short	Explaining the imperfection of the molecular clock of hominid mitochondria.
title_full	Explaining the imperfection of the molecular clock of hominid mitochondria.
title_fullStr	Explaining the imperfection of the molecular clock of hominid mitochondria.
title_full_unstemmed	Explaining the imperfection of the molecular clock of hominid mitochondria.
title_sort	explaining the imperfection of the molecular clock of hominid mitochondria.
publisher	Public Library of Science (PLoS)
publishDate	2009
url	https://doaj.org/article/05b79cced2f84cfd813304f6c784cae4
work_keys_str_mv	AT evaliisloogvali explainingtheimperfectionofthemolecularclockofhominidmitochondria AT toomaskivisild explainingtheimperfectionofthemolecularclockofhominidmitochondria AT tonumargus explainingtheimperfectionofthemolecularclockofhominidmitochondria AT richardvillems explainingtheimperfectionofthemolecularclockofhominidmitochondria
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Explaining the imperfection of the molecular clock of hominid mitochondria.

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