High impact information on ELG1

• We propose that Elg1-RFC functions both in normal DNA replication and in the DNA damage response [1].
• We find that elg1 mutants display DNA replication defects and genome instability, including increased recombination and mutation frequencies, and minichromosome maintenance defects [1].
• As expected from its genetic interactions, elg1 mutants are sensitive to DNA damage [1].
• Mutants in elg1 show genetic interactions with pathways required for processing of stalled replication forks, and are defective in recovery from DNA damage during S phase [1].
• ELG1, a regulator of genome stability, has a role in telomere length regulation and in silencing [2].

Biological context of ELG1

• We discuss alternative models to explain how Elg1p affects telomere length [2].
• Strains lacking Elg1p exhibit elevated levels of recombination between homologous and nonhomologous chromosomes, as well as between sister chromatids and direct repeats [3].
• Three ORFs (O3513, O3521, O3548) present significant similarities to proteins of unknown function and three ORFs (O3510, O3536, O3545) lack homology to sequences within the databases screened [4].

Associations of ELG1 with chemical compounds

• Deletion of ELG1 resulted in less efficient repair of phleomycin-induced DSBs in G2/M phase-arrested cells [5].

Other interactions of ELG1

• ELG1, a yeast gene required for genome stability, forms a complex related to replication factor C [3].
• Genetic data indicate that the Elg1, Ctf18, and Rad24 RFC-like complexes work in three separate pathways important for maintaining the integrity of the genome and for coping with various genomic stresses [3].
• Genetic and biochemical data indicate that the Elg1, Ctf18 and Rad24 RLCs work in three separate pathways important for maintaining the integrity of the genome and for coping with various genomic stresses [6].

Analytical, diagnostic and therapeutic context of ELG1

• Importantly, we found that two of the later steps in HR-mediated repair of an HO endonuclease-induced DSB, primer extension after strand invasion and ligation, were less efficient in elg1 mutants [5].

References