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Myung, Kyung Jae
유전체 항상성 연구단
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The HLTF–PARP1 interaction in the progression and stability of damaged replication forks caused by methyl methanesulfonate

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Title
The HLTF–PARP1 interaction in the progression and stability of damaged replication forks caused by methyl methanesulfonate
Author(s)
Shiu, Jia-Lin; Wu, Cheng-Kuei; Chang, Song-Bin; Sun, Yan-Jhih; Chen, Yen-Ju; Lai, Chien-Chen; Chiu, Wen-Tai; Chang, Wen-Tsan; Myung, Kyung Jae; Su, Wen-Pin; Liaw, Hungjiun
Publication Date
2020-12
Journal
Oncogenesis, v.9, no.12
Publisher
Nature Publishing Group
Abstract
Human HLTF participates in the lesion-bypass mechanism through the fork reversal structure, known as template switching of post-replication repair. However, the mechanism by which HLTF promotes the replication progression and fork stability of damaged forks remains unclear. Here, we identify a novel protein–protein interaction between HLTF and PARP1. The depletion of HLTF and PARP1 increases chromosome breaks, further reduces the length of replication tracks, and concomitantly increases the number of stalled forks after methyl methanesulfonate treatment according to a DNA fiber analysis. The progression of replication also depends on BARD1 in the presence of MMS treatment. By combining 5-ethynyl-2′-deoxyuridine with a proximity ligation assay, we revealed that the HLTF, PARP1, and BRCA1/BARD1/RAD51 proteins were initially recruited to damaged forks. However, prolonged stalling of damaged forks results in fork collapse. HLTF and PCNA dissociate from the collapsed forks, with increased accumulation of PARP1 and BRCA1/BARD1/RAD51 at the collapsed forks. Our results reveal that HLTF together with PARP1 and BARD1 participates in the stabilization of damaged forks, and the PARP1–BARD1 interaction is further involved in the repair of collapse forks.
URI
https://pr.ibs.re.kr/handle/8788114/9051
DOI
10.1038/s41389-020-00289-5
ISSN
2157-9024
Appears in Collections:
Center for Genomic Integrity(유전체 항상성 연구단) > 1. Journal Papers (저널논문)
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