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Birch lab at the University of Dundee's Division of Plant Sciences discover new knowledge in fight against potato blight disease


United Kingdom
July 30, 2018


Phytophthora infestans in potato leaves (c) James Hutton Institute
 

"This study reveals that protecting the host protein SWAP70 by reducing the activity of NRL1, a negative regulator of immunity, could provide a method to combat late blight disease"        

Potato blight, caused by the water mould Phytophthora infestans, is the major disease of potatoes worldwide and is thus a threat to food security. New research from the Birch lab in the University of Dundee's Division of Plant Sciences, based at the James Hutton Institute, has discovered a mechanism that could combat late blight disease in potato crops. The findings have been published in Proceedings of the National Academy of Sciences (PNAS).

Professor Paul Birch, Head of the Division of Plant Sciences, said: “To be a successful pathogen, microbes need to suppress or otherwise manipulate host defences. To do this they use virulence determinants called ‘effector’ proteins that are delivered inside plant cells where they re-programme defences and metabolism to the pathogen’s benefit.

“This latest research, primarily conducted by Dr Qin He and Dr Shaista Naqvi in my lab, found that the infamous potato blight pathogen delivers an effector protein into its host which targets a negative regulator of immunity, NRL1, which is a ubiquitin E3 ligase. The effector promotes the activity of NRL1 in removing the host protein SWAP70, which is a positive regulator of immunity.

"In effect, the pathogen is using the plant against itself - promoting endogenous processes that negatively regulate immunity in order to create a susceptible environment. This study reveals that protecting SWAP70 by reducing the activity or availability of NRL1 could provide a method to combat late blight disease.”



More solutions from:
    . James Hutton Institute
    . University of Dundee


Website: http://www.hutton.ac.uk

Published: August 6, 2018


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