What is it about?

The authors have demonstrated that human cells can employ mitotic DNA synthesis (MiDAS) to rescue failed replication at the fragile X syndrome locus (FRAXA) when cells are deprived of folate. They show that this rescue process occurs via a homologous recombination-dependent pathway called break-induced DNA replication (BIR) and requires the SLX1/SLX4 endonuclease complex, the RAD51 recombinase and POLD3, a subunit of polymerase delta. They also show that other loci in the human genome can under go MiDAS too under folate stress condition.

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Why is it important?

These findings provide new insight into the diverse and detrimental consequences of folate deficiency in human cells.

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This page is a summary of: Folate stress induces SLX1- and RAD51-dependent mitotic DNA synthesis at the fragile X locus in human cells, Proceedings of the National Academy of Sciences, June 2020, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.1921219117.
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