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Toxoplasma gondii can infect almost all the warm-blooded animals including human beings with broad medical and agricultural significance.Key to the asexual lifestyle of T.gondii tachyzoites is to replicate in and egress from the infected host cell,move through the tissues and reinvade another,thus extending infection.Mitogen-activated protein kinases(MAPKs)participate in diverse important physiological events including mediating the development of inflammatory and tumor.Two novel MAPK homologues,TgMAPK1 and TgERK7,have been identified in T.gondii,yet the function of TgERK7 is to be elucidated.The objectives of the present study were to create ΔTgERK7 knockout strain,and examine the biological function of TgERK7.Knockout strain ΔTgERK7 was created using double homologous recombinant method,and was used to evaluate the virulence in BALB/c mice compared to wild-type parasites.To understand the role of TgERK7 in T.gondii,complementation strain pUC/TgERK7 with chloramphenicol resistance was constructed,and was used as control to estimate effect on the asexual life cycle of ΔTgERK7 parasites.We show that putative cell-cycle-associated protein kinase TgERK7,which mainly localizes on the plasma membrane of the parasite tails,is essential to the virulence of tachyzoites for BALB/c mice.We also demonstrate that TgERK7,the orthologue of eukaryotic ERK2,participates in the overproduction of inflammatory-related cytokines such as TNF-α,IL6,IFN-γ and MCP-1,which is the main reason causing the acute death of T.gondii-infected mice.Our data showed that TgERK7 regulates the intracellular replication of the tachyzoits,but not host cell invasion or egress from parasite-infected cells.Our results therefore suggest that TgERK7 is an important novel virulence factor regulating the intracellular replication of T.gondii,with the overproduction of inflammatory-related cytokines,the main reason leading T.gondii-infected mice to acute death.