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职称:Professor of Microbiology and Immunology Telomere replication
所属学校:Cornell University
所属院系:Weill Cornell Medical College (New York City)
所属专业:Microbiology, General
联系方式: (212) 746-6506
“We recently developed a highly accurate model of ALT, a telomere recombination pathway that is utilized by a subset of cancer cells. Our model takes advantage of a non-standard fungus (Ustilago maydis) that is distantly related to budding and fission yeast, and that was originally developed by Robin Holliday to study recombinational repair. Analysis of this unusual model system uncovered BLM and MRE11 as two key factors in the ALT pathway. Current efforts are directed towards understanding this pathway in U. maydis at the molecular level and translating the findings to ALT cancer cells↪.
Chromosome ends, or telomeres, consist of repetitive DNA sequences and a plethora of protective proteins that are crucial for chromosome stability. Aberrations in either the DNA or the protein structures in this complex assembly lead to chromosome re-arrangements. The DNA repeat units are rich in G residues on the 3'-OH-bearing strand, which forms a single stranded overhang referred to as the G-tail. Shortening of telomere DNA occurs in many cells types due to incomplete end replication. This process can be counter-balanced by telomerase and DNA polymerase α, which synthesize the telomere ‘G-‘ and ‘C-strand', respectively. Abnormal telomere loss (due e.g., to telomerase deficiency) has been established as the cause of numerous diseases characterized by defective tissue renewal. Moreover, telomere dysfunction and telomerase up-regulation is known to contribute to the initiation and progression of human cancers.
