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Influence of Bacillus subtilis strain on abscisic acid content in ABA-deficient barley mutant and its wild type

The ability to produce phytohormones and influence their metabolism in plants is an important property of rhizosphere bacteria that determines their plant growth promoting effect. Since abscisic acid (ABA) reduces stomatal conductance and increases the ability of tissues to conduct water, maintenance of water balance in lettuce plants on the background of activation of their growth was associated with the accumulation of ABA under the influence of bacteria. The aim of the study is to test the hypothesis that the growth-stimulating effect of bacteria on plants depends on their ability to synthesize the hormone ABA. The plants were grown on a light platform; seedlings were treated with a bacterial suspension simultaneously with planting. The ABA content, the relative water content, the chlorophyll content, the level of non-photochemical quenching, the leaf area and the weight of the shoots were measured. The level of transcripts of the HvNCED1, HvNCED2, and HvCYP707A1 genes responsible for ABA metabolism in barley was assessed using real-time PCR. Comparison of the ABA-deficient mutant of barley and plants of its wild type revealed the stimulation of the growth of plants of both genotypes upon bacterial treatment. The shoot mass and leaf area of the untreated mutant with bacteria were about 30 % less compared to Steptoe. The stimulating effect of bacteria was manifested in an increase in leaf area by 15 % in Steptoe and by 35 % in Az 34; shoot mass – by 18 % and 41 %, respectively. As a result, the phenotype difference between plants of two genotypes decreased. In the deficient mutant, the ABA level increased under the influence of Bacillus subtilis IB-22 more than twice. It was due to the ability of bacteria to produce ABA and reduce the activity of ABA degradation in barley plants. The results obtained in this study indicate that certain bacterial strains are able to increase the level of ABA in plants, compensating for the genetically determined deficiency of this hormone.