Abstract:
:The HIV auxiliary protein Vpr potently blocks the cell cycle at the G2/M transition. Here, we show that G2/M arrest results from untimely activation of the structure-specific endonuclease (SSE) regulator SLX4 complex (SLX4com) by Vpr, a process that requires VPRBP-DDB1-CUL4 E3-ligase complex. Direct interaction of Vpr with SLX4 induced the recruitment of VPRBP and kinase-active PLK1, enhancing the cleavage of DNA by SLX4-associated MUS81-EME1 endonucleases. G2/M arrest-deficient Vpr alleles failed to interact with SLX4 or to induce recruitment of MUS81 and PLK1. Furthermore, knockdown of SLX4, MUS81, or EME1 inhibited Vpr-induced G2/M arrest. In addition, we show that the SLX4com is involved in suppressing spontaneous and HIV-1-mediated induction of type 1 interferon and establishment of antiviral responses. Thus, our work not only reveals the identity of the cellular factors required for Vpr-mediated G2/M arrest but also identifies the SLX4com as a regulator of innate immunity.
journal_name
Celljournal_title
Cellauthors
Laguette N,Brégnard C,Hue P,Basbous J,Yatim A,Larroque M,Kirchhoff F,Constantinou A,Sobhian B,Benkirane Mdoi
10.1016/j.cell.2013.12.011subject
Has Abstractpub_date
2014-01-16 00:00:00pages
134-45issue
1-2eissn
0092-8674issn
1097-4172pii
S0092-8674(13)01545-6journal_volume
156pub_type
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