The DNA loop release factor WAPL suppresses Epstein-Barr virus latent membrane protein expression to maintain the highly restricted latency I program.

The DNA loop release factor WAPL suppresses Epstein-Barr virus latent membrane protein expression to maintain the highly restricted latency I program.

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Epstein-Barr virus (EBV) uses latency programs to colonize the memory B-cell reservoir, and each program is associated with human malignancies.However, knowledge animed aniflex complete remains incomplete of epigenetic mechanisms that maintain the highly restricted latency I program, present in memory and Burkitt lymphoma cells, in which EBNA1 is the only EBV-encoded protein expressed.Given increasing appreciation that higher order chromatin architecture is an important determinant of viral and host gene expression, we investigated roles of Wings Apart-Like Protein Homolog (WAPL), a host factor that unloads cohesin to control DNA loop size and that was discovered as an EBNA2-associated protein.WAPL knockout (KO) in Burkitt cells de-repressed LMP1 and LMP2A expression, but not other EBV oncogenes, to yield a viral program swisse high strength magnesium powder berry reminiscent of EBV latency II, which is rarely observed in B-cells.WAPL KO also increased LMP1/2A levels in latency III lymphoblastoid cells.

WAPL KO altered EBV genome architecture, triggering formation of DNA loops between the LMP promoter region and the EBV origins of lytic replication (oriLyt).Hi-C analysis further demonstrated that WAPL KO reprogrammed EBV genomic DNA looping.LMP1 and LMP2A de-repression correlated with decreased histone repressive marks at their promoters.We propose that EBV coopts WAPL to negatively regulate latent membrane protein expression to maintain Burkitt latency I.