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Sasi, N. K.

Publications and source records attributed to Sasi, N. K..

3 recordsLinked to original sources

Tetrameric TRF2 forms t-loop to protect telomeres from ATM signaling and cNHEJ

Telomeres often occur in the t-loop structure, formed through the base-pairing of the 3 telomeric overhang is base-paired with more internal telomeric DNA. T-loops are proposed to avert ATM kinase signaling and classical non-homologous end joining (cNHEJ) by sequestering the telomere end. The shelterin subunit TRF2 is required for t-loop formation but how it generates t-loops is not known and the t-loop model for telomere protection remains untested. We show that TRF2 binds telomeric DNA as a tetramer using two dimerization domains and that tetramerization is critical for telomere protection. Furthermore, TRF1, the TRF2 paralog that binds DNA as a dimer and does not form t-loops, gained the ability to form t-loops in vivo upon its tetramerization through the addition of a second dimerization domain. We propose that TRF2 tetramers loop telomeric DNA, resulting in torsional stress and opening of the helix, which is a requirement for t-loop formation. Importantly, t-loops formed by tetrameric TRF1 were sufficient to avert ATM signaling and blocked most cNHEJ at telomeres, demonstrating that t-loops per se protect telomeres from these threats.

cell biology↗

RTF2 controls replication repriming and ribonucleotide excision at the replisome

Genetic information is duplicated via the highly regulated process of DNA replication. The machinery coordinating this process, the replisome, encounters many challenges, including replication fork-stalling lesions that threaten the accurate and timely transmission of genetic information. Cells have multiple mechanisms to repair or bypass lesions that would otherwise compromise DNA replication1,2. We have previously shown that proteasome shuttle proteins, DNA Damage Inducible 1 and 2 (DDI1/2) function to regulate Replication Termination Factor 2 (RTF2) at the stalled replisome, allowing for replication fork stabilization and restart3. Here we show that RTF2 regulates replisome localization of RNase H2, a heterotrimeric enzyme responsible for removing RNA in the context of RNA-DNA heteroduplexes4-6. We show that during unperturbed DNA replication, RTF2, like RNase H2, is required to maintain normal replication fork speeds. However, persistent RTF2 and RNase H2 at stalled replication forks compromises the replication stress response, preventing efficient replication restart. Such restart is dependent on PRIM1, the primase component of DNA polymerase -primase. Our data show a fundamental need for regulation of replication-coupled ribonucleotide incorporation during normal replication and the replication stress response that is achieved through RTF2. We also provide evidence for PRIM1 function in direct replication restart following replication stress in mammalian cells.

molecular biology↗

DDK has a primary role in processing stalled replication forks to initiate downstream checkpoint signaling

CDC7-DBF4 kinase (DDK) is required to initiate DNA replication in eukaryotes by activating the replicative MCM helicase. DDK has also been reported to have diverse and sometimes conflicting roles in the replication checkpoint response in various organisms but the underlying mechanisms are far from settled. Here we show that human DDK promotes limited resection of newly synthesized DNA at stalled replication forks or sites of DNA damage to initiate replication checkpoint signaling. DDK is also required for efficient fork restart and G2/M cell cycle arrest. DDK exhibits genetic interactions with the ssDNA exonuclease EXO1, and we show that EXO1 is also required for nascent strand degradation following exposure to HU, raising the possibility that DDK regulates EXO1 directly. Thus, DDK has a primary and previously undescribed role in the replication checkpoint to promote ssDNA accumulation at stalled forks, which is required to initiate a robust checkpoint response and cell cycle arrest to maintain genome integrity.

cell biology↗