当前位置： SCI文献检索 > INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES期刊下所有文献 > DSS1 allosterically regulates the conformation of the tower domain of BRCA2 that has dsDNA binding specificity for homologous recombination.

DSS1 allosterically regulates the conformation of the tower domain of BRCA2 that has dsDNA binding specificity for homologous recombination.

Abstract：

:DSS1 is an evolutionary conserved, small intrinsically disordered protein that regulates various cellular functions. Although several studies have elucidated the role of DSS1 in stabilizing BRCA2 and its importance in homologous recombination repair (HRR), yet the structural mechanism behind the stability and HRR remains elusive. In this study, using molecular dynamics simulation we show that DSS1 stabilizes linearly arranged DNA/DSS1 binding domains of BRCA2 with many native contacts. These contacts are absent in the complexes with two missense DSS1 mutants associated with germline breast cancer and somatic mouth carcinoma. Most importantly, our protein energy-based network models show DSS1 allosterically regulates the conformation of the distant tower domain of BRCA2 that has dsDNA binding specificity for HRR. We further postulate that the unique conformation of the tower domain with kinked-helices might be responsible for DNA strand invasion and initiation of HRR. Induced conformation of the tower domain by the kinked-helices is absent in the unbound BRCA2, as well as in the two mutant DSS1-BRCA2 complexes. This suggests that DSS1 allosterically regulates the tower domain conformations of BRCA2 that affects dsDNA binding, essential for HRR. Our results add a new dimension to the function of DSS1 and its role in regulating HRR.

journal_name

Int J Biol Macromol

journal_title

International journal of biological macromolecules

authors

Alagar S,Bahadur RP

doi

10.1016/j.ijbiomac.2020.09.230

subject

Has Abstract

pub_date

2020-12-15 00:00:00

pages

918-929

issue

Pt A

eissn

0141-8130

issn

1879-0003

pii

S0141-8130(20)34593-1

journal_volume

165

pub_type

杂志文章

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