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ARS Home » Research » Publications at this Location » Publication #349120

Title: Genetic analysis of salinity responses in Medicago genotypes

Author
item Sandhu, Devinder
item CORNACCHIONE, MONICA - National Institute Of Agricultural Technology(INTA)
item Pudussery, Manju
item KAUNDAL, AMITA - University Of California
item Ferreira, Jorge
item Suarez, Donald

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 1/15/2018
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Reduced availability of clean water in arid and semi-arid regions will require the use of low-quality/alternative waters for irrigation. The main consideration for using low-quality/alternative waters is often their salt concentration. Plants respond to salinity stress through a complex network of physiological, biochemical, and ecological strategies. Although several genomes have been sequenced and putative genes have been annotated, the functional characterization of genes involved in salt tolerance is still lacking. Studies on alfalfa (Medicago sativa) showed that the most salt-tolerant genotypes that were top performers for biomass accumulated low Na+ and Cl-. Salinity reduced foliar area and stomatal conductance. Several genes that are known to play important roles in different components of the salt tolerance mechanism were upregulated during salt stress. Gene expression analyses allowed us to classify genotypes based on component traits. Some Na+/H+ exchangers (NHX) that are known to play important role in salt tolerance in Arabidopsis thaliana also played critical role in alfalfa. Bioinformatics and phylogenetic analyses of Arabidopsis genes enabled us to characterize corresponding genes in Medicago truncatula. Na+ exclusion was found to be responsible for the relatively smaller increase in Na+ concentration compared to Cl-, in roots under salt stress. This new knowledge gained from M. truncatula may become instrumental in characterizing salt tolerance responses in alfalfa.