%0 Journal Article
%T Homologous recombination in animal mitochondria
%A James Cotton
%J Genome Biology
%D 2001
%I BioMed Central
%R 10.1186/gb-2001-2-10-reports0034
%X This is rather surprising, as this paradigm is based on indirect evidence and is challenged by a growing body of data. The original observation that paternal mitochondria do not penetrate the egg is now known to be in error, with paternal organelles persisting for several hours after fertilization. It is also known that mammalian mitochondria contain the necessary enzymatic machinery for homologous recombination, and mitochondrial fusion is well known in Drosophila. Non-homologous recombination (unequal crossing-over) has been held responsible for variation in the number of tandem repeats in a number of animal mitochondrial genomes, and has been directly observed in a nematode. Two recent population studies have also suggested that recombination has occurred in human mtDNA.With all this evidence, it would seem likely that homologous recombination does occur in animal mitochondria, but the publication of human population studies last year provoked considerable debate, emphasizing that there is much interest in whether animal mtDNA does show homologous recombination, and considerable skepticism. Many authors will no doubt remain skeptical, despite the results of this paper, in which Ladoukakis and Zouros have exploited the unusual genetic system of the mussel to uncover direct evidence for homologous recombination within animal mitochondria.The unusual biparental inheritance of mitochondria in mussels of the families Unionidea and Mytilidaehas been known for about a decade, and is an interesting exception to the otherwise universal rule of maternal inheritance for animal mtDNA. Normally, female (F) and male (M) mitochondrial sequences differ by 20% - too great an amount to expect to observe homologous recombination. Luckily, a quirk of the Mytilus system allows a unique opportunity to observe mtDNA recombination in action. Occasionally, F genomes become 'masculinized', invading the M transmission route in sperm (see Figure 1). These MF genomes can now diverge from the
%U http://genomebiology.com/2001/2/10/reports/0034