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Dehydrin MtCAS31 promotes autophagic degradation under drought stress

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NIAID Data Ecosystem2026-03-11 收录
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https://figshare.com/articles/dataset/Dehydrin_MtCAS31_promotes_autophagic_degradation_under_drought_stress/9178736
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Drought stress seriously affects crop yield, and the mechanism underlying plant resistance to drought stress via macroautophagy/autophagy is not clear. Here, we show that a dehydrin, Medicago truncatula MtCAS31 (cold acclimation-specific 31), a positive regulator of drought response, plays a key role in autophagic degradation. A GFP cleavage assay and treatment with an autophagy-specific inhibitor indicated that MtCAS31 participates in the autophagic degradation pathway and that overexpressing MtCAS31 promotes autophagy under drought stress. Furthermore, we discovered that MtCAS31 interacts with the autophagy-related protein ATG8a in the AIM-like motif YXXXI, supporting its function in autophagic degradation. In addition, we identified a cargo protein of MtCAS31, the aquaporin MtPIP2;7, by screening an M. truncatula cDNA library. We found that MtPIP2;7 functions as a negative regulator of drought response. Under drought stress, MtCAS31 facilitated the autophagic degradation of MtPIP2;7 and reduced root hydraulic conductivity, thus reducing water loss and improving drought tolerance. Taken together, our results reveal a novel function of dehydrins in promoting the autophagic degradation of proteins, which extends our knowledge of the function of dehydrins. Abbreviations: AIM: ATG8-interacting motif; ATG: autophagy-related; ATI1: ATG8-interacting protein1; BiFC: Biomolecular fluorescence complementation; CAS31: cold acclimation-specific 31; ConcA: concanamycin A; DSK2: dominant suppressor of KAR2; ER: endoplasmic reticulum; ERAD: ER-associated degradation; NBR1: next to BRCA1 gene 1; PM: plasma membrane; PIPs: plasma membrane intrinsic proteins; TALEN: transcription activator-like effector nuclease; TSPO: tryptophan-rich sensory protein/translocator; UPR: unfolded protein response; VC: vector control
创建时间:
2019-07-31
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