DDX5 potentiates HIV-1 transcription as a co-factor of Tat.

ABSTRACT:

Background

HIV-1 does not encode a helicase and hijacks those of the cell for efficient replication. We and others previously showed that the DEAD box helicase, DDX5, is an essential HIV dependency factor. DDX5 was recently shown to be associated with the 7SK snRNP. Cellular positive transcription elongation factor b (P-TEFb) is bound in an inactive form with HEXIM1/2 on 7SK snRNP. The Tat/P-TEFb complex is essential for efficient processivity of Pol II in HIV-1 transcription elongation and Tat competes with HEXIM1/2 for P-TEFb. We investigated the precise role of DDX5 in HIV replication using siRNA mediated knockdown and rescue with DDX5 mutants which prevent protein-protein interactions and RNA and ATP binding.

Results

We demonstrate a critical role for DDX5 in the Tat/HEX

SUBMITTER: Sithole N 

PROVIDER: S-EPMC7106839 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature