GC content evolution of the human and mouse genomes: insights from the study of processed pseudogenes in regions of different recombination rates

Processed pseudogenes are generated by reverse transcription of a functional gene. They are generally nonfunctional after their insertion and, as a consequence, are no longer subjected to the selective constraints associated with functional genes. Because of this property they can be used as neutral...

Full description

Saved in:
Bibliographic Details
Published inJournal of molecular evolution Vol. 62; no. 6; pp. 745 - 752
Main Authors Khelifi, Adel, Meunier, Julien, Duret, Laurent, Mouchiroud, Dominique
Format Journal Article
LanguageEnglish
Published Germany Springer Nature B.V 01.06.2006
Springer Verlag
Subjects
Animals
Base Composition
Computational Biology
Databases, Genetic
Evolution
Evolution, Molecular
Genetics
Genome
Genome, Human
Humans
Life Sciences
Mice
Other
Pseudogenes
Recombination, Genetic
Time Factors
Online AccessGet full text

Cover

More Information
Summary:Processed pseudogenes are generated by reverse transcription of a functional gene. They are generally nonfunctional after their insertion and, as a consequence, are no longer subjected to the selective constraints associated with functional genes. Because of this property they can be used as neutral markers in molecular evolution. In this work, we investigated the relationship between the evolution of GC content in recently inserted processed pseudogenes and the local recombination pattern in two mammalian genomes (human and mouse). We confirmed, using original markers, that recombination drives GC content in the human genome and we demonstrated that this is also true for the mouse genome despite lower recombination rates. Finally, we discussed the consequences on isochores evolution and the contrast between the human and the mouse pattern.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0022-2844
1432-1432
DOI:10.1007/s00239-005-0186-0