High impact information on RAD57

• By several independent criteria, RAD55- and RAD57-encoded products are shown here to exist as a stable heterodimer, with a dissociation constant of <2 x 10(-10) M [1].
• Mutations in yeast Rad51 that partially bypass the requirement for Rad55 and Rad57 in DNA repair by increasing the stability of Rad51-DNA complexes [2].
• The repair of DNA double-strand breaks in Saccharomyces cerevisiae requires genes of the RAD52 epistasis group, of which RAD55 and RAD57 are members [3].
• We show that the induction by transcription does not require the products of the RAD50, RAD51, and RAD57 genes [4].
• Changing the lysine residue to arginine or alanine resulted in a mutant phenotype in DNA repair and sporulation for Rad55 but not for Rad57 [5].

Biological context of RAD57

• Mutations in the RecA-like genes RAD51 and RAD57 reduce the frequency of gene conversion/reciprocal exchange between inverted repeats 7-fold [6].
• The roles of REV3 and RAD57 in double-strand-break-repair-induced mutagenesis of Saccharomyces cerevisiae [7].
• These phenotypes were enhanced at low temperatures, similar to deletions in the S. cerevisiae RAD55 and RAD57 genes [8].
• The amino-acid sequence predicted from the nt sequence showed similarity to the RecA protein of bacteria and the RecA-like proteins from yeast: RAD51, RAD57 and DMC1 [9].
• RAD57 contains an open reading frame of 1380 bp [10].

Associations of RAD57 with chemical compounds

• RAD55 and RAD57 contain putative nucleotide binding motifs, and the importance of these motifs was determined by constructing site-directed mutations of the conserved lysine residue within the Walker A-box [5].

Other interactions of RAD57

• This suppression occurs at 23 degrees C, where these mutants are more sensitive to x-rays, as well as at 30 degrees C and 36 degrees C. In addition, a recombination defect of rad55 and rad57 mutants is similarly suppressed [3].
• Mutations in RAD51, RAD54, and RAD57 had the converse affect: they eliminated the ability of cells to generate type I survivors in a tlc1 strain [11].
• The spectrum of mutations in rad57 mutants is similar to that seen in the wild-type strain and is similarly affected by REV3 [7].
• The first, which is defined by the rad52 epistasis group, depends on the activities of the RAD50 through RAD57 genes and is responsible for repairing the larger amount of lethal damage [12].
• The results indicated that the translocation points are located close to the FUR4 locus on chromosome II and close to the RAD57 locus on chromosome IV [13].

Analytical, diagnostic and therapeutic context of RAD57

• A molecular model for "homology-dependent ligation" in rad57 cells is proposed [14].

References