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Senthil-Kumar, M.

Publications and source records attributed to Senthil-Kumar, M..

3 recordsLinked to original sources

SWEET11 and SWEET12 transporters function in tandem to modulate sugar flux in Arabidopsis: An account of the underlying unique structure-function relationship

Sugar will eventually be exported transporters (SWEETs) have been identified as a unique class of sugar efflux transporters in all biological kingdoms. AtSWEET11 and AtSWEET12 in Arabidopsis act synergistically to perform distinct physiological roles, particularly in apoplasmic phloem loading, seed filling, and sugar level alteration at the site of pathogen infection. Plasma membrane-localized AtSWEET11 and AtSWEET12 transporters exclusively facilitate sucrose transport along the concentration gradient. This article examines the sucrose binding pocket of AtSWEET11 and AtSWEET12 using docking studies, and how they act synergistically in various functions throughout plant development and during abiotic and biotic stresses. Further, we highlight the phylogenetic and the in-silico analyses of AtSWEET11 and AtSWEET12 orthologs from 39 economically important plant species that could provide new platforms for future studies on sugar allocation mechanisms across the different plant families. In-depth understanding of these transporters and their molecular regulatory mechanisms could be harnessed for crop improvement and crop protection.

plant biology↗

Sweet revenge: AtSWEET12 in plant defense against bacterial pathogens by apoplastic sucrose limitation

Depriving bacterial pathogens of sugars is a potential plant defense strategy. The relevance of SUGARS WILL EVENTUALLY BE EXPORTED TRANSPORTERS (SWEETs) in plant susceptibility to pathogens has been established, but their role in plant defense remains unknown. We identified Arabidopsis thaliana SWEETs (AtSWEETs) involved in defense against nonhost and host Pseudomonas syringae pathogens through reverse genetic screening of atsweet1-17 mutants. Double/triple mutant, complementation, and overexpression line analysis, and apoplastic sucrose estimation studies revealed that AtSWEET12 suppresses pathogen multiplication by limiting sucrose availability in the apoplast. Localization studies suggested that plant defense occurred via increased plasma membrane targeting of AtSWEET12 with concomitant AtSWEET11 protein reduction. Moreover, the heterooligomerization of AtSWEET11 and AtSWEET12 was involved in regulating sucrose transport. Our results highlight a PAMP-mediated defense strategy against foliar bacterial pathogens whereby plants control AtSWEET11-mediated sucrose efflux in the apoplast through AtSWEET12. We uncover a fascinating new mechanism of pathogen starvation as a broad-spectrum disease resistance mechanism in parallel with existing immune pathways. One sentence summaryThe transporter AtSWEET12 restricts bacterial pathogen multiplication by regulating sucrose availability to pathogens in the apoplast.

plant biology↗

CaProDH2-mediated modulation of proline metabolism confers tolerance to Ascochyta in chickpea under drought

Drought and leaf blight caused by the fungus Ascochyta rabiei often co-occur in chickpea (Cicer arietinum)-producing areas. While the responses of chickpea to either drought or A. rabiei infection have been extensively studied, their combined effect on plant defense mechanisms is unknown. Fine modulation of stress-induced signaling pathways under combined stress is an important stress adaptation mechanism that warrants a better understanding. Here we show that drought facilitates resistance against A. rabiei infection in chickpea. The analysis of proline levels and gene expression profiling of its biosynthetic pathway under combined drought and A. rabiei infection revealed the gene encoding proline dehydrogenase (CaProDH2) as a strong candidate conferring resistance to A. rabiei infection. Transcript levels of CaProDH2, pyrroline-5-carboxylate (P5C) quantification, and measurement of mitochondrial reactive oxygen species (ROS) production showed that fine modulation of the proline-P5C cycle determines the observed resistance. In addition, CaProDH2-silenced plants lost basal resistance to A. rabiei infection induced by drought, while overexpression of the gene conferred higher resistance to the fungus. We suggest that the drought-induced accumulation of proline in the cytosol helps maintain cell turgor and raises mitochondrial P5C contents by a CaProDH2-mediated step, which results in ROS production that boosts plant defense responses and confers resistance to A. rabiei infection. Our findings indicate that manipulating the proline-P5C pathway may be a possible strategy for improving stress tolerance in plants suffering from combined drought and A. rabiei infection.

plant biology↗