Open AccessMultiple Pathways Promote Short-Sequence Recombination in Saccharomyces cerevisiae
Author(s) -
Glenn M. Manthey,
Adam M. Bailis
Publication year - 2002
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.22.15.5347-5356.2002
Subject(s) - biology , genetics , msh2 , saccharomyces cerevisiae , homologous recombination , non homologous end joining , recombination , plasmid , non allelic homologous recombination , nuclease , flp frt recombination , endonuclease , dna repair , dna , genetic recombination , gene , dna mismatch repair
In the budding yeast Saccharomyces cerevisiae, null alleles of several DNA repair and recombination genes confer defects in recombination that grow more severe with decreasing sequence length, indicating that they are required for short-sequence recombination (SSR). RAD1 and RAD10, which encode the subunits of the structure-specific endonuclease Rad1/10, are critical for SSR. MRE11, RAD50, and XRS2, which encode the subunits of M/R/X, another complex with nuclease activity, are also crucially important. Genetic evidence suggests that Rad1/10 and M/R/X act on the same class of substrates during SSR. MSH2 and MSH3, which encode subunits of Msh2/3, a complex active during mismatch repair and recombination, are also important for SSR but play a more restricted role. Additional evidence suggests that SSR is distinct from nonhomologous end joining and is superimposed upon basal homologous recombination.