NYMC Faculty Publications

Fanconi Anemia and mTOR Pathways Functionally Interact During Stalled Replication Fork Recovery

Author Type(s)

Faculty

Journal Title

FEBS Letters

First Page

595

Last Page

603

Document Type

Article

Publication Date

3-2021

Department

Cell Biology and Anatomy

Abstract

We have previously demonstrated that Fanconi anemia (FA) proteins work in concert with other FA and non-FA proteins to mediate stalled replication fork restart. Previous studies suggest a connection between the FA protein FANCD2 and the non-FA protein mechanistic target of rapamycin (mTOR). A recent study showed that mTOR is involved in actin-dependent DNA replication fork restart, suggesting possible roles in the FA DNA repair pathway. In this study, we demonstrate that during replication stress mTOR interacts and cooperates with FANCD2 to provide cellular stability, mediate stalled replication fork restart, and prevent nucleolytic degradation of the nascent DNA strands. Taken together, this study unravels a novel functional cross-talk between two important mechanisms: mTOR and FA DNA repair pathways that ensure genomic stability.

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