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The Role Of MAPK Signaling Pathway In Whitefly-geminiviruses Interaction

Posted on:2017-03-15Degree:MasterType:Thesis
Country:ChinaCandidate:J J ZhaoFull Text:PDF
GTID:2283330485462459Subject:Plant protection
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As the only known vector of Begomovirus, whitefly Bemisia tacbaci (Gennadius) plays a critical role in the spread of these virus. With serious damage of whitefly and begomovirus around the world, more and more attention have been drew to the mechanism of interaction between them. Previously, we have shown that TYLCV infection can induce immune response in whitefly, such as autophagy; on the other hand, activation of autophagy supresses the accumulation of virus in whitefly. Inscets including whitefly rely on innate immune response to cope with pathogen infections, however in whitefly, the realted immune response to begomovirus infection remains largely unknown. Understanding the immune response of whitefly to begomovirus infection will advance our knowledge about the mechanism underlying whitefly-begomovirus interaction.In the present study, we examined the impact of TYLCV, TYLCCNV and PaLCuCNV infection on the activation of MAPK signaling pathway to explore the role of MAPK signaling pathway in the whitefly-begomovirus interaction. As a member of MAPK signaling cascade, JNK is found to be extensively involved in organize-virus interation. To verify the role of JNK signaling pathway in whitelfy-TYLCV interaction, we used specific inhibitors and RNAi to manipulate whitefly JNK signaling pathway and examined the viral accumulation and virus transmission capacity in whitefly. At last, we also used specific inhibitors to explore the relationship between JNK signaling pathway and apoptosis in whitefly, thus providing information for the research of apoptosis in whitefly. These results are as follows:(1) TYLCV infection activated JNK signaling pathway in MEAM1 whiteflyThe phosphorylation of JNK and the downstrem transcription factor c-Jun increased after the infection of TYLCV in whitefly as shown by Western Blot. Besides, c-Jun translocated into nuclear of midgut cells after TYLCV infection. These results snow tnat IYCLV intection in MEAMI wnitefiy activates the JNK signaling pathway.(2) The role of JNK signaling pathway in TYLCV accumulation in MEAM1 whiteflyApplication of specific inhibitor against JNK signaling cascade decreased DNA and coat protein of TYLCV as well as the virus transmission rate. And anisomycin, inducer of JNK signaling cascade resulted in the opposite effect. Besides, RNAi against JNK and the downstream transcription factor c-Jun reduced the density of virus in midgut accordding to immune-fluroence.These results show that JNK signaling pathway promotes the accumulation of TYLCV in MEAM1 whitefly.(3) Impact of TYLCCNV and PaLCuCNV infection on MAPK signaling pathwayWestern blot showed that TYLCCNV and PaLCuCNV infection induced the phosphorylation of JNK, ERK, p38 in MEAM1 whitefly. These results suggest that a general involvement of JNK signaling pathway in the whitelfy-begomovirus interaction.(4) Relationship between JNK signaling pathway and apoptosisApplication of specific inhibitor against JNK signaling pathway resulted in enhanced apoptosis in whitefly midgut as shown by TUNEL, which indicates that JNK signaling pathway supresses apoptosis in MEAM1 whitwfly.
Keywords/Search Tags:Whitelfy, Tomato Yellow Leaf Curl Virus, Tomato Yellow Leaf Curl China Virus, Papaya Leaf Curl China Virus, JNK, MAPK
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