Abstract
Fanconi anemia (FA) is a devastating hereditary disorder with impaired genome stability resulting in physical abnormalities, gradual loss of hematopoietic stem cells and development of tumours and leukaemia. It has been suggested that functions of FA genes are required to maintain genome stability by counteracting endogenous metabolites, such as aldehydes, that damage DNA and stall replication forks. Recent studies have implicated co-transcriptional R-loops, consisting of a DNA:RNA hybrid and displaced single-stranded DNA, as one of the potential endogenous sources that induce genome instability and the FA phenotype. This review focuses on recent literature, including our own, regarding the interplay between FA proteins and R-loops, and will provide readers with a concise summary of this rapidly evolving field.
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