The 3' end of the invading strand is extended by an unknown DNA polymerase and the extended strand is then ligated back to the original homolog, generating a double Holliday junction. MSH4 and MSH5 form heterodimers which bind Holliday junctions and, in the presence of ATP, slide along the parental duplexes (Bocker et al. 1999, Snowden et al. 2004, Snowden et al. 2008). MSH4 is present at hundreds of meiotic nodules during late zygotene but only about 10% of these nodules become crossovers (Oliver-Bonet et al. 2005). Bloom Syndrome protein (BLM) and Topoisomerase IIIa (TOP3A) are also present and may promote homologous recombination repair without crossing over (Johnson et al. 2000, Wu et al. 2000).
|16123081||Temporal progression of recombination in human males||Mol Hum Reprod||2005|
|10728666||Association of the Bloom syndrome protein with topoisomerase IIIalpha in somatic and meiotic cells||Cancer Res||2000|
|15304223||hMSH4-hMSH5 recognizes Holliday Junctions and forms a meiosis-specific sliding clamp that embraces homologous chromosomes||Mol Cell||2004|
|17977839||hMSH4-hMSH5 adenosine nucleotide processing and interactions with homologous recombination machinery||J Biol Chem||2008|
|10029069||hMSH5: a human MutS homologue that forms a novel heterodimer with hMSH4 and is expressed during spermatogenesis||Cancer Res||1999|
|10734115||The Bloom's syndrome gene product interacts with topoisomerase III||J Biol Chem||2000|