Lipid Metabolism Patterns In SPVD-infected Sweet Potato Leaves Under Different Temperature Regimes

Sweet potato(Ipomoea batatas(L.)Lam.)is important food,industry and energy crop and widely cultured all over the world.The cultivation area and production in China ranking the 1st in the world and this crop plays very important role in promoting food security in China.Recently,the outbreak of sweet potato virus disease(SPVD)caused incalculable economic loss in China.This complexion impacts the development of sweet potato industry.SPVD caused by the co-infection of two RNA viruses,e.g.Sweet potato feathery mottle virus(SPFMV,Potyvirus)and Sweet potato chlorotic stunt virus(SPCSV,Crinivirus).So far,the alterations of physiological and molecular responses of sweet potato upon the co-infection of SPFMV and SPCSV are largely unknown.Therefore,it is important and meaningful to investigate the viral and host interaction that can help us find some strategies to counteract the infection and prevalence of SPVD.RNA virus needs host factors to support their replication and host lipid components are necessities.However,how SPFMV and SPCSV co-infection affect host lipid metabolism is still unclear.In this dissertation,we investigated the lipid metabolism pattern in SPFMV and SPCSV co-infected(SPVD-infected)sweet potato(Xu 22,an elite sweet potato cultivar in China)leaves under different temperature regimes by using of untargeted lipidomics method and qRT-PCR.We revealed several important interactions between viruses and host.The main findings are as follows:Room temperature experiments(1)Compared with non-infected Xu 22,SPVD-infected Xu 22 exhibited obvious altered leaf lipidome.The phospholipids content was significantly enhanced after the infection of viruses,including PE,PA,PC and PI.However,the PG content was markedly decreased.In addition,the relative contents of sterol lipids,glycolipids and sphingolipids were all increased in SPVD-infected leaves.The total lipids showed no significant difference between the non-infected and SPVD-infected leaves.(2)The relative content of several lipid molecular species were significantly enhanced,such as PA(14:1/20:0)?PC(18:2/16:1)?PI(22:6/17:0)? PI3P(16:0/18:1)and so on.(3)qRT-PCR results showed that SPVD-infection altered gene expression pattern related to the lipid metabolism.The main change is the upregulation of PA,PE and PC synthesis genes(including PAH1,PAH2,DGK1,2,5,7,PLD?,CEK1,PECT1,CCT1,AAPT1,PSD1,PSD2)by SPVD-infection.Furthermore,we found two genes related to the synthesis of MGDG were also upregulated by the infection of the two viruses.(4)We further revealed that 1-butanol,which is a specific inhibitor of PLD and function as a blocker of PA production,significantly inhibited the accumulation of SPFMV-CP and SPCSV-RNase3 in SPVD-infected Xu 22 leaves.In addition,3-MA and E-64 D,which are two chemicals blocking the autophagy pathway in both animals and plants,obviously decreased the SPCSV-CP and SPCSV-RNase3 accumulation.High temperature experiments(5)During the high temperature of summer,the leaf lipidome of Xu 22 remodeled obviously when compared with room temperature condition.The main change was the accumulation of TG.SPVD-infected Xu 22 showed decreased TG accumulation and enhanced phospholipids accumulation(including PA,PE,PI,PC and PS).Most TG and phospholipids molecular species also showed the same trend with the lipid categories.Spearman coefficient proved that some TG molecular species showing significant negative correlation with some phospholipids molecular species.(6)Under high temperature condition,the expression level of genes required for the synthesis and breakdown of TG(PDAT1 and SDP1)were markedly enhanced in SPVD-infected Xu 22 leaves.In addition,some genes required for the synthesis of phospholipids were also upregulated.However,no obvious alterations were found in the genes required for the fatty acid synthesis.(7)Under high temperature condition,treatment of DMP,which is an inhibitor of TG breakdown and mobilization,caused obvious accumulation of lipid droplets and accompanied with the decrease of SPFMV accumulation.These evidence proved that phospholipids is required for the replication of SPFMV and SPCSV under regular temperature condition.However,the host autophagy pathway maybe required for the replication of SPCSV.Our work also highlights high-temperature induced TG as major resource to be utilized by SPFMV to synthesis membrane lipids that required for the replication of this virus.These findings provide novel insights into the ways of viruses exploiting host resources under specific environmental condition.In addition,this dissertation discovered several chemicals that have potential anti-SPVD applications in the field.