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Little is known about the tolerance mechanisms that reduce the negative effects of microbial infection on host fitness. Here, we demonstrate that the histone H3 lysine 9 methyltransferase  G9a  regulates tolerance to virus infection by shaping the response of the evolutionary conserved Jak-Stat pathway in  Drosophila .  G9a -deficient mutants are more sensitive to RNA virus infection and succumb faster to infection than wild-type controls, which was associated with strongly increased Jak-Stat dependent responses, but not with major differences in viral load. Genetic experiments indicate that hyperactivated Jak-Stat responses are associated with early lethality in virus-infected flies. Our results identify an essential epigenetic mechanism underlying tolerance to virus infection.

The Epigenetic Regulator G9a Mediates Tolerance to RNA Virus Infection in Drosophila