Complementactivationviatheclassical,themannanbindinglectinorthealternativepathwayleadstotheformationoftheterminalcomplementcomplex(TCC).C7playsanimportantroleintheterminalcomplementcascade,sinceC7incorporationintotheTCCallowsitshydrophilic-amphiphilictransition,whichsubsequentlyleadstothedirectbindingofthecomplextotargetcellmembranes.Todate,C7hasbeenclonedonlyfromtheOncorhynchusmykissParalichthysolivaceusHypophthalmichthysmolitrixC7showedthehighestsequenceidentity(82%)withthoseofC7,similartoC7reportedforotherteleostspecies,displayedmanyconservedstructuralmotifs,suchasTSP1,LDLRa,MACPF,EGF,TSP1andCCP.Thismayindicatethattoattacktheexogenousbacteria.WithintheH.molitrixsynonymousmutation,andidentifiedsixalleles.RT-PCRwasconductedtodetecttheexpressionoftheC7geneinvarioustissuesofhealthyAeromonashydrophilaH.molitrix,buttheexpressionofthetargetgeneinthebrain,gill,heart,kidney,liver,intestineandspleenincreasedafter12hofchallengewith.Withtheremovalofpathogens,theexpressiongraduallyreduceduntilacompletedisappearance.ThisresultindicatedthatC7maybean