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PMID: 14739461 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S.

Extensive gene traffic on the mammalian X chromosome.

Science (New York, N.Y.) ·Vol. 303 ·No. 5657 ·2004-01-23 ·Pages 537-40

Emerson JJ, Kaessmann H, Betrán E, Long M

Abstract

Mammalian sex chromosomes have undergone profound changes since evolving from ancestral autosomes. By examining retroposed genes in the human and mouse genomes, we demonstrate that, during evolution, the mammalian X chromosome has generated and recruited a disproportionately high number of functional retroposed genes, whereas the autosomes experienced lower gene turnover. Most autosomal copies originating from X-linked genes exhibited testis-biased expression. Such export is incompatible with mutational bias and is likely driven by natural selection to attain male germline function. However, the excess recruitment is consistent with a combination of both natural selection and mutational bias.

MeSH Terms
Animals Biological Evolution Chromosomes, Human/genetics Chromosomes, Human, X/genetics Chromosomes, Mammalian/genetics Computational Biology Dosage Compensation, Genetic Female Gene Expression Profiling Genes, Duplicate Genetic Linkage Genome Genome, Human Humans Introns Male Mice Monte Carlo Method Mutation Oligonucleotide Array Sequence Analysis Ovary/metabolism Pseudogenes/genetics Recombination, Genetic Retroelements/genetics Selection, Genetic Sex Characteristics Testis/metabolism X Chromosome/genetics
Chemicals
Retroelements
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Emerson J J
Department of Ecology and Evolution, University of Chicago, Chicago, IL 60637, USA.
Kaessmann Henrik
Betrán Esther
Long Manyuan
Article Info
Journal
Science (New York, N.Y.)
Abbr.
Science
ISSN
1095-9203
DOI
10.1126/science.1090042
Published
2004-01-23
Pages
537-40
Language
English
Region
United States
NLM ID
0404511
Subset
IM
Grants
NIGMS NIH HHS · GM-065429-01A1 · United States
External Links
PubMed source DOI: 10.1126/science.1090042 View journal details
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