4.7 Article

Synthetic strigolactone (rac-GR24) alleviates the adverse effects of heat stress on seed germination and photosystem II function in lupine seedlings

期刊

PLANT PHYSIOLOGY AND BIOCHEMISTRY
卷 155, 期 -, 页码 965-979

出版社

ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.plaphy.2020.07.043

关键词

Antioxidant enzymes; Chlorophyll a fluorescence; Germination indices; Glyoxalase system; GR24; Heat stress tolerance; JIP-Test; Strigolactones; PSII thermotolerance

资金

  1. Internal Grant Agency of PalacI47 University, Olomouc [IGA_PrF_2020_021]
  2. European Regional Development Fund-Project Plants as a tool for sustainable global development [CZ.02.1.01/0.0/0.0/16_019/0000827]

向作者/读者索取更多资源

There is increasing experimental evidence that strigolactones, a class of carotenoid-derived sesquiterpenoid hormones, and their downstream signal components play a role in plant resilience to abiotic stress. Strigolactones positively influence plant coping mechanisms in response to abiotic stressors like drought and high salinity. In this study, we examined the effects of rac-GR24 (a synthetic strigolactone analog) and strigolactone inhibitors on the physiological and molecular responses associated with thermotolerance during seed germination and seedling development in Lupinus angustifolius under heat stress. Photosystem I & II functions were also evaluated via Chl a fluorescence transient analysis in heat stressed lupine seedlings. Our results suggest a putative role for GR24 in mediating tolerance to heat stress during seed germination and seedling development albeit these responses appeared independent of D14-mediated signalling. Seeds primed with GR24 had the highest of all germination indices, enhanced praline content and reduced pemxidation of lipids. GR24 also enhanced the activities of enzymes of the antioxidant and glyoxalase systems in lupine seedlings. The JIP-test indicated that GR24 conferred resistance to heat stress-induced damage to the oxygen evolution complex while also preventing the inactivation of PSII reaction centres thus ensuring PSII thermotolerance.

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