The role of nuclease FAN1 in DNA crosslink repair in Arabidopsis thaliana


Fanconi anemia (FA) is a severe genetic disorder in humans characterized by bone marrow failure, congenital abnormalities and cancer. This disease is caused by mutations in genes associated with DNA crosslink (CL) repair in human cells. Previous studies showed the monoubiquitination of the heterodimer FANCD2/FANCI activates CL repair pathway by recruiting the nuclease FAN1 to the CL site. Interestingly, FAN is absent in some species such as Drospphila and Saccharomyces cerevisiae. Herrmann et al. demonstrated that FAN1 homolog is present in plants and is proved to be involved in Arabidopsis thaliana CL repair. The article was published in Nucleic Acids Research.


They found FAN1 acts as a upstream factor of two CL repair-associated sub-pathways, which are defined by the Bloom syndrome homolog RECQ4A and ATPase RAD5A, respectively. The later is involved in error-free post-replicative repair. Both the virus-type replication-repair (VRR) nuclease and the ubiquitin-bingding ubiquitin-binding zinc finger (UBZ) domains are required for CL repair function. In addition, double mutations in both FAN1 and the endonuclease MUS81 led to a greater sensitivity against CLs then single mutations. The findings provide a detailed insights into FAN1 functions in the complex signaling pathways associated with plant CL repair.


Nucleic Acids Res. 2015 Mar 16. pii: gkv208.

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