Homologous recombination and its regulation

Investor logo
Investor logo

Warning

This publication doesn't include Faculty of Arts. It includes Faculty of Medicine. Official publication website can be found on muni.cz.
Authors

KREJČÍ Lumír ALTMANNOVÁ Veronika ŠPÍREK Mário ZHAO Xiaolan

Year of publication 2012
Type Article in Periodical
Magazine / Source Nucleic Acids Research
MU Faculty or unit

Faculty of Medicine

Citation
Doi http://dx.doi.org/10.1093/nar/gks270
Field Genetics and molecular biology
Keywords DOUBLE-STRAND-BREAK; REPLICATION PROTEIN-A; DNA-DAMAGE RESPONSE; RAD51 NUCLEOPROTEIN FILAMENTS; SACCHAROMYCES-CEREVISIAE SRS2; CANCER SUSCEPTIBILITY GENE; BLOOMS-SYNDROME HELICASE; JOINT MOLECULE FORMATION; ESCHERICHIA-COLI RECA; HUMAN BRCA2 PROTEIN
Description Homologous recombination (HR) is critical both for repairing DNA lesions in mitosis and for chromosomal pairing and exchange during meiosis. However, some forms of HR can also lead to undesirable DNA rearrangements. Multiple regulatory mechanisms have evolved to ensure that HR takes place at the right time, place and manner. Several of these impinge on the control of Rad51 nucleofilaments that play a central role in HR. Some factors promote the formation of these structures while others lead to their disassembly or the use of alternative repair pathways. In this article, we review these mechanisms in both mitotic and meiotic environments and in different eukaryotic taxa, with an emphasis on yeast and mammal systems. Since mutations in several proteins that regulate Rad51 nucleofilaments are associated with cancer and cancer-prone syndromes, we discuss how understanding their functions can lead to the development of better tools for cancer diagnosis and therapy.
Related projects:

You are running an old browser version. We recommend updating your browser to its latest version.