Plant G-protein signaling cascade and host defense
3 Biotech, ISSN: 2190-5738, Vol: 10, Issue: 5, Page: 219
2020
- 13Citations
- 23Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations13
- Citation Indexes13
- 13
- CrossRef1
- Captures23
- Readers23
- 23
Review Description
The heterotrimeric guanine-nucleotide-binding proteins (G-proteins) play a crucial role in signal transduction and regulate plant responses against biotic and abiotic stresses. Necrotrophic pathogens trigger Gα subunit and, in contrast, sometimes Gβγ dimers. Beneficial microbes play a vital role in the activation of heterotrimeric G-proteins in plants against biotrophic and necrotrophic pathogens. The subunits of G-protein (α, β, and γ) are activated differentially against different kinds of pathogens which in turn regulates the entry of the pathogen in a plant cell. Defense mediated by G-proteins in plants imparts resistance against several pathogens. Activation of different G-protein subunits depends on the mode of nutrition of the pathogen. The current review discussed the role of the three subunits against various pathogens. It appeared to be specific in the individual host–pathogen system as well as the role of effectors in the induction of G-proteins. We also discussed the G-protein-mediated production of reactive oxygen species (ROS), including HO, activation of NADPH oxidases, hypersensitive response (HR), phospholipases, and ion channels in response to microorganisms.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85083975412&origin=inward; http://dx.doi.org/10.1007/s13205-020-02201-9; http://www.ncbi.nlm.nih.gov/pubmed/32355593; https://link.springer.com/10.1007/s13205-020-02201-9; https://dx.doi.org/10.1007/s13205-020-02201-9; https://link.springer.com/article/10.1007/s13205-020-02201-9
Springer Science and Business Media LLC
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