Adenovirus is a double-stranded DNA virus that causes localized infections. The virus takes over the host cell through commanding control of replication machinery and inactivating repair and degradation activities. The adenovirus E411k protein functions in turning off host protein synthesis and turning on late viral gene expression. E4 11k is also known to disrupt P-bodies, cellular RNA processing bodies, through an interaction with the P-body protein, Ddx6. We hypothesize that the disruption of P-bodies is the mechanism by which E4 11k disrupts gene expression. Our goal is to identify the binding site on Ddx6 for the E4 11k protein. Ddx6 deletion mutants were created in order to remove the possible binding site from E4 11k, and a co-Immunoprecipitation will be performed to determine the specific binding site of E4 11k on Ddx6. When the identification of the binding site is narrowed down to a single amino acid or single sequence of amino acids, the true function of the binding of E4 11k with Ddx6 during adenovirus infection can be identified in human cells. Additional P-body functions can be identified and could prove to be applicable in studying other viruses.
