title: The Fanconi anemia pathway promotes homologous recombination repair in DT40 cell line.
abstract: Fanconi anemia (FA) is a rare hereditary disorder characterized by bone marrow failure, compromised genome stability, and increased incidence of cancer. FA is caused by abnormalities that occur in components of the FA core complex, a key factor FancD2, breast cancer susceptibility protein BRCA2/FancD1, or BRIP1/FancJ. These proteins are proposed to function in a common biochemical process (FA pathway), however, its precise role is still unclear. In this chapter, we will summarize our genetic analysis on the FA pathway using DT40 cells line. Our data revealed that (1) FA pathway promotes DNA repair mediated by homologous recombination, and likely regulates translesion synthesis, thereby protecting cells against stalled replication forks; (2) BLM helicase can be regarded as an effector molecule of the FA pathway, since its subnuclear localization is regulated by FA pathway; (3) the FA core complex has multiple roles in the activation, relocalization, and DNA repair function of FANCD2.
authors.affiliation: Department of Immunology and Molecular Genetics, Kawasaki Medical School, Kurashiki, Okayama 701-0192, Japan.
authors.forename: Minoru
authors.initials: M
authors.lastname: Takata
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Yamamoto
authors.forename: Nobuko
authors.initials: N
authors.lastname: Matsushita
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Kitao
authors.forename: Seiki
authors.initials: S
authors.lastname: Hirano
authors.forename: Masamichi
authors.initials: M
authors.lastname: Ishiai
mesh_terms: D000818:Animals; D001402:B-Lymphocytes / Q000378:metabolism; D002460:Cell Line; D002645:Chickens; D004260:DNA Repair; D005199:Fanconi Anemia / Q000235:genetics*; D011995:Recombination, Genetic