Synchronised regulation of disease resistance in primed finger millet plants against the blast disease

同步调控促发穗谷子植株对稻瘟病的抗病性

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作者:Savita Veeranagouda Patil, Belur Satyan Kumudini, Hosur Gnanaprakash Pushpalatha, Savitha De Britto, Shin-Ichi Ito, Surya Sudheer, D P Singh, Vijai Kumar Gupta, Sudisha Jogaiah

Abstract

Plants, being sessile, are exposed to an array of abiotic and biotic stresses. To adapt towards the changing environments, plants have evolved mechanisms that help in perceiving stress signals wherein phytohormones play a critical role. They have the ability to network enabling them to mediate defense responses. These endogenous signals, functioning at low doses are a part of all the developmental stages of the plant. Phytohormones possess specific functions as they interact with each other positively or negatively through cross-talks. In the present study, variations in the amount of phytohormones produced during biotic stress caused due to Magnoporthe grisea infection was studied through targeted metabolomics in both primed and control finger millet plants. Histochemical studies revealed callose deposition at the site of pathogen entry in the primed plants indicating its role during plant defense. The knowledge on the genetic makeup during infection was obtained by quantification of MAP kinase kinases 1 and 2 (MKK1/2) and lipoxygenase (LOX) genes, wherein the expression levels were high in the primed plants at 6 hours post-inoculation (hpi) compared to mock-control. Studies indicate the pivotal role of mitogen-activated protein kinase (MAPK or MAP kinases) during defense signalling. It is the first report to be studied on MAPK role in finger millet-blast disease response. Temporal accumulation of LOX enzyme along with its activity was also investigated due to its significant role during jasmonate synthesis in the plant cells. Results indicated its highest activity at 12 hpi. This is the first report on the variation in phytohormone levels in fingermillet - M. grisea pathosystem upon priming which were substantiated through salicylic acid (SA) pathway.

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