Volatile compounds from Alcaligenes faecalis JBCS1294 confer salt tolerance in Arabidopsis thaliana through the auxin and gibberellin pathways and differential modulation of gene expression in root and shoot tissues

Volatile compounds from rhizobacteria are known to elicit and regulate plant growth and defense against various biotic and abiotic stresses. In the present study, we elucidated the biological role of volatiles from Alcaligenes faecalis strain JBCS1294 on the growth performance of Arabidopsis thalian...

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Veröffentlicht in:Plant growth regulation 2015-01, Vol.75 (1), p.297-306
Hauptverfasser: Bhattacharyya, Dipto, Yu, Sang-Mi, Lee, Yong Hoon
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Sprache:eng
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Zusammenfassung:Volatile compounds from rhizobacteria are known to elicit and regulate plant growth and defense against various biotic and abiotic stresses. In the present study, we elucidated the biological role of volatiles from Alcaligenes faecalis strain JBCS1294 on the growth performance of Arabidopsis thaliana under salt stress. JBCS1294 volatiles promoted gains in fresh weight and shoot length of Arabidopsis Col-0 under salt stress by 61.5 and 45.8 %, respectively. Hexanedioic acid and butanoic acid were identified as major volatiles emitted from JBCS1294. However, volatiles from JBCS1294 were unable to induce salt tolerance in eir1 and gai-1 mutant lines of A. thaliana, or in auxin and gibberellin inhibitor-treated Col-0 plants. On the other hand, a significant increase of growth in cytokinin-, brassinosteroid-, and ethylene-defective mutant lines, or in respective inhibitor-treated Col-0, led us to conclude that the auxin and gibberellin pathways are mediators which confer salt tolerance in Arabidopsis upon introduction of JBCS1294 volatiles. Exposure to JBCS1294 volatiles did not alter proline content in gai-1 and gibberellin inhibitor-treated lines. Additionally, AtNHX1, AtHKT1, AtSOS1, AtAVP1, auxin and brassinosteroid pathway genes were upregulated in the roots after exposure of salt-stressed seedlings to JBCS1294 volatiles, suggesting tissue-specific remodeling of gene expression.
ISSN:0167-6903
1573-5087
DOI:10.1007/s10725-014-9953-5