ABSTRACT
Capsicum annuum L. Bugang exhibits a hypersensitive response against Tobacco mosaic virus (TMV) P(0) infection. The C. annuumUDP-glucosyltransferase 1 (CaUGT1) gene was upregulated during resistance response to TMV and by salicylic acid, ethephon, methyl viologen, and sodium nitroprusside treatment. When the gene was downregulated by virus-induced gene silencing, a delayed HR was observed. In addition, free and total SA concentrations in the CaUGT1-downregulated hot pepper were decreased by 52% and 48% compared to that of the control plants, respectively. This suggested that the CaUGT1 gene was involved in resistance response against TMV infection by controlling the accumulation of SA.
Subject(s)
Capsicum/enzymology , Glucosyltransferases/genetics , Plant Diseases/virology , Salicylic Acid/metabolism , Tobacco Mosaic Virus/pathogenicity , Capsicum/virology , Cell Death , DNA, Complementary/metabolism , Immunity, Innate/genetics , Phenotype , RNA, Messenger/metabolism , Signal Transduction , Transcription, GeneticABSTRACT
A series of microarray analyses employing the expressed sequence tags (ESTs) of hot pepper was conducted in an effort to elucidate the molecular mechanisms inherent to hypersensitive response (HR) by viral or bacterial pathogens. There were 2535 ESTs exhibiting differential expression (over 2-fold changes) among about 5000 ESTs during viral or bacterial response. Further, via virus-induced gene silencing (VIGS) and TMV-infection studies, we were able to isolate several ESTs, which may be relevant to defense response against TMV. Of these ESTs, Capsicum annuum fatty acid desaturase 1 (CaFAD1) showed the distinct phenotype against TMV infection and thus was subjected to further study. CaFAD1-silenced plants showed weaker resistance against TMV-P0 infection compared to TRV2 control plants. Also the suppression of FAD1 expression caused blocking of cell death induced by Bcl2-associated X (Bax) protein in tobacco plants. Therefore, this report presents that both microarray and VIGS approaches are feasible in hot pepper plants and the TMV-induced CaFAD1 plays a role in HR response.
Subject(s)
Capsicum/enzymology , Capsicum/virology , Fatty Acid Desaturases/genetics , Gene Expression Regulation, Plant , Gene Silencing , Tobacco Mosaic Virus/metabolism , Cloning, Molecular , Expressed Sequence Tags , Oligonucleotide Array Sequence Analysis/methods , Phenotype , Plant Leaves/metabolism , Reverse Transcriptase Polymerase Chain Reaction , Rhizobium/metabolism , Signal Transduction , Nicotiana/metabolismABSTRACT
Hot pepper (Capsicum annuum L. cv. Bugang) plants exhibit a hypersensitive response (HR) upon infection by Tobacco mosaic virus (TMV) pathotype P(0). Previously, to elucidate molecular mechanism that underlies this resistance, hot pepper cv. Bugang leaves were inoculated with TMV-P(0) and genes specifically up-regulated during the HR were isolated by microarray analysis. One of the clones, Capsicum annuum cytosolic pyruvate kinase 1 (CaPK(c)1) gene was increased specifically in the incompatible interaction with TMV-P(0). The expression of CaPK(c)1 gene was also triggered not only by various hormones such as salicylic acid (SA), ethylene, and methyl jasmonate (MeJA), but also NaCl and wounding. These results suggest that CaPK(c)1 responds to several defense-related abiotic stresses in addition to TMV infection.
