Please use this identifier to cite or link to this item: http://223.31.159.10:8080/jspui/handle/123456789/698
Title: Functional involvement of a mitogen activated protein kinase module, OsMKK3-OsMPK7-OsWRK30 in mediating resistance against Xanthomonas oryzae in rice
Authors: Jalmi, Siddhi Kashinath
Sinha, Alok Krishna
Keywords: Biotic
Plant signalling
Xanthomonas oryzae
Rice
Mitogen Activated Protein Kinase Module
Issue Date: 2016
Publisher: Nature Publishing Group
Citation: Scientific Reports, 6: 37974
Abstract: Mitogen-activated protein kinases (MAPKs) are highly conserved signaling modules in eukaryotes, transmitting signals from upstream receptor to downstream target by phosphorelay mechanism. Here we report involvement of a poorly characterized group C MAPK of rice namely, OsMPK7 along with its upstream MAPK kinase, OsMKK3 and downstream target, OsWRKY30 during Xanthomonas oryzae infection, a causal agent of leaf blight disease in rice. X. oryzae infection resulted in induction of OsMPK7 and OsMKK3. OsMKK3 was found to physically interact and phosphorylate OsMPK7. Overexpression of OsMPK7 and OsMKK3, individually and in combinations resulted in inhibition of disease symptoms caused by X. oryzae, however silencing of OsMPK7 resulted in disease susceptibility. Furthermore, OsWRKY30 was identified as downstream target of OsMPK7 through protein-protein interaction techniques and was found to be a positive regulator of defence response against X. oryzae pathogen. The overexpression of OsMKK3-OsMPK7 upregulated genes involved in pathogenesis, cell wall structure maintenance and cell metabolism indicating possible mechanism of disease resistance. These leaves also showed restricted movement of the pathogen from the point of infection to uninfected area. Taken together, this work suggests a positive involvement of OsMKK3-OsMPK7-OsWRKY30 module in imparting disease resistance against X. oryzae infection in rice.
Description: Accepted date: 03 November 2016
URI: http://59.163.192.83:8080/jspui/handle/123456789/698
ISSN: 2045-2322
Appears in Collections:Institutional Publications

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