- sws-1 [Browse genome (BioProject PRJNA13758)] [Search on AGR]
Caenorhabditis elegans Predicted to enable zinc ion binding activity. Predicted to be involved in double-strand break repair via homologous recombination. Predicted to be part of Shu complex. Human ortholog(s) of this gene implicated in ovarian dysgenesis 10 and spermatogenic failure 71. Is an ortholog of human ZSWIM7 (zinc finger SWIM-type containing 7).
- SHU2 [Search on AGR]
Saccharomyces cerevisiae Component of Shu complex (aka PCSS complex); Shu complex also includes Psy3, Csm2, Shu1, and promotes error-free DNA repair, Shu complex mediates inhibition of Srs2p function; promotes formation of Rad51p filaments; important for both mitotic and meiotic homologous recombination, and contains a conserved SWIM domain that is necessary for both
- CSM2 [Search on AGR]
Saccharomyces cerevisiae Subunit of the Shu complex (aka PCSS complex); Shu complex also includes Psy3, Shu1, Shu2, and promotes error-free DNA repair; Shu complex mediates inhibition of Srs2p anti-recombinase function; promotes formation of Rad51p filaments; Psy3p and Csm2p contain similar DNA-binding regions which work together to form a single DNA binding site; required for accurate chromosome segregation during meiosis
- set-1 [Browse genome (BioProject PRJNA13758)] [Search on AGR]
Caenorhabditis elegans Enables histone H4K20 monomethyltransferase activity. Involved in embryo development. Located in nucleus. Expressed in several structures, including P3.p hermaphrodite; P4.p hermaphrodite; P5.p hermaphrodite; P7.p hermaphrodite; and P8.p hermaphrodite. Is an ortholog of human KMT5A (lysine methyltransferase 5A).
- PSY3 [Search on AGR]
Saccharomyces cerevisiae Component of Shu complex (aka PCSS complex); Shu complex also includes Shu1, Csm2, Shu2, and promotes error-free DNA repair; promotes Rad51p filament assembly; Shu complex mediates inhibition of Srs2p function; Psy3p and Csm2p contain similar DNA-binding regions which work together to form a single DNA binding site; deletion of PSY3 results in a mutator phenotype; deletion increases sensitivity to anticancer drugs oxaliplatin and cisplatin but not mitomycin C