作者: Melissa M. Grabowski , Nenad Svrzikapa , Heidi A. Tissenbaum
DOI: 10.1016/J.MAD.2005.08.005
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摘要: Bloom syndrome is caused by mutation of the helicase (BLM), a member RecQ family. Loss BLM function results in genomic instability that causes high incidence cancer. It has been demonstrated important for maintaining stability playing role DNA recombination and repair; however, exact not clearly understood. To determine mechanism which controls vivo, we examined phenotypes C. elegans ortholog, HIM-6. We find loss HIM-6 leads to as evidenced an increased number insertions deletions, visible random mutant phenotypes. In addition mutator phenotype, him-6 mutants have low brood size, males, shortened life span, amount germ line apoptosis. Upon exposure temperature, are serially passed become sterile demonstrating mortal phenotype. Our data suggest model due lesions, either cannot be repaired and/or introduced fidelity events. The level him-6(ok412) having span.