Disease relevance of PSO2

• We have used recombinant SNM1 constructs in an Escherichia coli (E. coli) expression system to demonstrate that the yeast gene encodes a 5'-exonuclease [1].

High impact information on PSO2

• The gene product bears amino acid sequence similarity to two better understood protein families, namely the PSO2 (SNM1) DNA interstrand crosslink repair proteins and the 73-kD subunit of mRNA 3' end cleavage and polyadenylation specificity factor (CPSF73) [2].
• The rejoining of single- and double-strand breaks is not only dependent on the product of the RAD51 gene (as shown by others) but also of the PSO2 gene [3].
• DNA interstrand cross-link repair in the Saccharomyces cerevisiae cell cycle: overlapping roles for PSO2 (SNM1) with MutS factors and EXO1 during S phase [4].
• In addition, the interstrand cross-link repair gene PSO2 plays a role in end joining hairpin ends that is not seen in repair of linearized plasmids and may be involved in positioning transposase cleavage at the transposon ends [5].
• We also identified and disrupted the S. pombe homologue of the Saccharomyces cerevisiae SNM1/PSO2 ICL repair gene and found that this activity is required for normal resistance to cross-linking agents, but not other forms of DNA damage [6].

Biological context of PSO2

• Here we establish a novel overlapping function for PSO2 with MutS mismatch repair factors and the 5'-3' exonuclease Exo1 in the repair of DNA ICLs, which is confined to S phase [4].
• Therefore, PSO2, EXO1, and MSH2 also appear to have overlapping roles in the processing of some forms of endogenous DNA damage that occur at an irreversibly collapsed replication fork [4].
• Mutants in RAD6 and PSO2 genes showed the same transformation efficiency with 8-MOP plus UVA treated plasmid as wild-type cells suggesting that these latter pathways involved in mutagenesis are not operating on plasmid DNA although required for the repair of 8-MOP photoadducts induced in genomic DNA [7].
• Molecular structure of the DNA cross-link repair gene SNM1 (PSO2) of the yeast Saccharomyces cerevisiae [8].
• The action of the PSO2 gene product specific for the repair of DNA crosslinks in recombination induction is discussed and compared to the actions of the excision repair genes RAD1 and RAD2 [9].

Associations of PSO2 with chemical compounds

• The role of Snm1, Rev3 and Rad51 in S-phase after cisplatin (CDDP) DNA treatment has been examined [10].

Regulatory relationships of PSO2

• Gene disruption showed that GTP1 is not an essential gene and that it has no influence on the expression of the DNA repair gene SNM1 with which it shares a 191-bp promoter region [11].

Other interactions of PSO2

• The cross-link incision kinetics of snm1 delta and rev3 delta mutants were also examined; both showed no deficiencies in incision of cross-linked DNA [10].
• Saccharomyces cerevisiae lacking Snm1, Rev3 or Rad51 have a normal S-phase but arrest permanently in G2 after cisplatin treatment [10].
• Recent progress in elucidating the molecular structure of the PSSO genes PSO2 to PSO7 is presented [12].
• The promoter of SNM1 contains a 15 bp motif, which shows homology to the DRE2 box of the RAD2 promoter [13].
• Expression of SNM1 on the smallest subclone, however, was under the control of the GAL1 promotor [14].

Analytical, diagnostic and therapeutic context of PSO2

• Molecular cloning of SNM1, a yeast gene responsible for a specific step in the repair of cross-linked DNA [14].
• Surprisingly, no inducibility of SNM1 was found after treatment with DNA-damaging agents in strains without an intact DUN1 gene, while regulation seems unchanged in sad1 mutants [13].
• In the yeast Saccharomyces cerevisiae, allelism between the pso1-1 and the rev3-1 mutants on the one hand and the pso2-1 and snm1 mutants on the other, is demonstrated by the comparison of phenotypes, complementation tests and meiotic segregation analysis [15].

References