Arabidopsis AtSUC2 and AtSUC4, encoding sucrose transporters, are required for abiotic stress tolerance in an ABA‐dependent pathway

Sucrose transporters (SUCs or SUTs) play a central role, as they orchestrate sucrose allocation both intracellularly and at the whole plant level. Previously, we found AtSUC4 mutants changing sucrose distribution under drought and salt stresses. Here, we systematically examined the role of Arabidops...

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Veröffentlicht in:Physiologia plantarum 2015-01, Vol.153 (1), p.119-136
Hauptverfasser: Gong, Xue, Liu, Mingli, Zhang, Lijun, Ruan, Yanye, Ding, Rui, Ji, Yuqi, Zhang, Ning, Zhang, Shaobin, Farmer, John, Wang, Che
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Sprache:eng
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Zusammenfassung:Sucrose transporters (SUCs or SUTs) play a central role, as they orchestrate sucrose allocation both intracellularly and at the whole plant level. Previously, we found AtSUC4 mutants changing sucrose distribution under drought and salt stresses. Here, we systematically examined the role of Arabidopsis AtSUC2 and AtSUC4 in response to abiotic stress. The results showed significant induction of AtSUC2 and AtSUC4 in salt, osmotic, low temperature and exogenous abscisic acid (ABA) treatments by public microarray data and real‐time quantitative reverse transcription polymerase chain reaction (qRT‐PCR) analyses. The loss‐of‐function mutation of AtSUC2 and AtSUC4 led to hypersensitive responses to abiotic stress and ABA treatment in seed germination and seedling growth. These mutants also showed higher sucrose content in shoots and lower sucrose content in roots, as compared with that in wild‐type plants, and inhibited the ABA‐induced expression of many stress‐ and ABA‐responsive genes, especially ABFs and ABF‐downstream and upstream genes. The loss‐of‐function mutant of AtSUC3, a unique putative sucrose sensor, reduced the expression of AtSUC2 and AtSUC4 in response to abiotic stresses and ABA. These findings confirmed that AtSUC2 and AtSUC4 are important regulators in plant abiotic stress tolerance that use an ABA signaling pathway, which may be crossed with sucrose signaling.
ISSN:0031-9317
1399-3054
DOI:10.1111/ppl.12225