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Involvement of MEK1 MAPKK, NTF6 MAPK, WRKY/MYB transcription factors, COI1 and CTR1 in N ‐mediated resistance to tobacco mosaic virus
Author(s) -
Liu Yule,
Schiff Michael,
DineshKumar S. P.
Publication year - 2004
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2004.02085.x
Subject(s) - wrky protein domain , tobacco mosaic virus , biology , gene silencing , gene , transcription factor , tobacco rattle virus , genetics , gene expression , microbiology and biotechnology , virus , transcriptome
Summary The tobacco N gene, a member of the Toll‐interleukin 1 homology region/nucleotide binding site/leucine‐rich repeat (TIR–NBS–LRR) class of resistance ( R ) genes, confers resistance to tobacco mosaic virus (TMV). We used a candidate gene approach to identify known defense genes that were also involved in N signaling. The requirement for these genes was determined by downregulating their expression using the well‐established tobacco rattle virus (TRV)‐based virus‐induced gene silencing (VIGS). Silencing of genes encoding a mitogen‐activated protein kinase (MAPK) NTF6/NRK1, or an MAPK kinase (MAPKK) MEK1/NQK1 , attenuated N ‐mediated resistance to TMV. We also found that N resistance is compromised in plants in which expression of WRKY1–WRKY3 and MYB1 transcription factors were downregulated. In addition, suppression of jasmonic acid (JA) signaling component COI1 ortholog affected N function. However, downregulation of expression of CTR1 ortholog leads to more rapid hypersensitive response (HR). The involvement of these genes in N ‐ and other R ‐gene‐mediated defense provides further evidence for the convergence of downstream signaling pathways of different R genes.