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. 2019 Apr 24;116(19):9568–9577. doi: 10.1073/pnas.1818401116

Fig. 6.

Fig. 6.

Search for additional Vpr-antagonized components that restrict HIV-1 replication in CEM.SS T cells. PRCA with HIV-1.mRFP.vpr.wt and HIV-1.RFP.vpr.Q8* was performed in CEM.SS T cells. Percentages of cell-associated HIV-1 DNA of the competing viruses at 7 dpi are shown. INPUT, percentages of the competing viruses in the initial inoculum. (A) TET2 and cGAS sensing pathway. CEM.SS T cells were subjected to NT RNAi using two different shRNAs (NT1 and NT2) or RNAi targeting cGAS or TET2. The cells were infected with HIV-1 3 d after initiation of RNAi. (B) cGAS and TET2 levels in cell extracts at the time of HIV-1 infection were revealed by immunoblotting. SF2 and lamin B1 provided loading controls. Results representative of two biological replicate experiments are shown. (C) Epigenetic modifiers. CEM.SS T cells were cultured in the presence of SAHA (200 nM), TSA (1 nM), GSK343 (0.7 μM), EX527 (10 μM), SGC0946 (2 μM), C646 (3 μM), and UNC0638 (1 μM), starting 12 h before HIV-1 infection until 7 dpi. Results representative of three biological replicate experiments are shown. (D) HUSH complex. CEM.SS T cells were subjected to NT RNAi (CT1), or shRNAs targeting TASOR. The cells were infected with HIV-1 3 dpi of RNAi. TASOR levels in cell extracts at the time of HIV-1 infection were revealed by immunoblotting. Lamin B1 provided a loading control. Results representative of two biological replicate experiments are shown.