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New Roads to FA/BRCA Pathway: H2AX

Alex Lyakhovich and Jordi Surralles

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We have recently described an involvement of H2AX into the Fanconi anemia (FA) BRCA pathway through recruitment of FA protein FANCD2 to the sites of stalled replication forks. We showed that BRCA1 mediates the recruitment of FANCD2 by γH2AX to damaged chromatin and cells deficient or depleted of H2AX exhibit an FA-like phenotype, including an excess of chromatid-type chromosomal aberrations and hypersensitivity to MMC. Here, we discuss a model for the FA pathway and how it could partially explain the common phenotypes of H2AX, BRCA2 and FA deficiencies.

Authors

Alex Lyakhovich

Universitat Autònoma de Barcelona, Bellaterra, Barcelona, Spain

Jordi Surralles

Universitat Autònoma de Barcelona, Bellaterra, Barcelona, Spain

This is an open-access article

 Download PDF

If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.