1057 A viral histone H4 encoded in Cotesia plutellae bracovirus suppresses gene expression of host histone H4 using its prolonged N-terminal tail

Wednesday, November 19, 2008: 9:05 AM
Room A1, First Floor (Reno-Sparks Convention Center)
Wael Gad , Bioresource Sciennces, Andong National University, Andong City, Korea, Republic of (South)
Younggyun Kim , Bioresource Sciences, Andong National University, Andong, Korea, Republic of (South)
An endoparasitoid wasp, Cotesia plutellae, possesses a symbiotic bracovirus (CpBV) and parasitizes the diamondback moth, Plutella xylostella. A viral histone H4 gene has been found in CpBV genome and its gene product is known to impair an insect cellular immune response. Based on its high similarity to host H4 of P. xylostella except its prolonged N-terminal tail, it has been suspected to alter host gene expression by an epigenetic route. Histone subunits purified from the parasitized P. xylostella larvae contained both host and viral H4s, supporting the previous report. However, relative amounts of both histone H4s were varied with the parasitoid development in P. xylostella, where the host H4 level decreased in a constant level of the viral H4 level. The mRNA level of host H4 measured by quantitative RT-PCR showed significant decreases in the parasitized P. xylostella, but no change of host H4 in the nonparasitized. The decrease of host H4 expression was also observed by transient expression of the viral H4 in nonparasitized P. xylostella. Co-injection of the viral H4 and its specific double-stranded RNA recovered the host H4 expression level. The prolonged viral N-terminal H4 tail, as a functional domain, was assumed to play an important role in modulating specific gene expression. The truncated viral H4 by removing the N-terminal tail significantly lost its inhibitory actions against both host H4 expression and a host cellular immune response. This study suggests that the viral H4 encoded in CpBV can alter host gene expression with its prolonged N-terminal tail.

doi: 10.1603/ICE.2016.36306