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Soil salinity pose a significant challenge to global agriculture, threatening crop yields and food security. Understanding the salt tolerance mechanisms of plants is crucial for improving their survival under salt stress. AFP2, a negative regulator of ABA signaling, has been shown to play a crucial role in salt stress tolerance during seed germination. Mutations in AFP2 gene lead to increased sensitivity to salt stress. However, the underline mechanisms by which AFP2 regulates seed germination under salt stress remain elusive. In this study, we identified a protein interaction between AFP2 and SOS2, a Ser/Thr protein kinase known to play a critical role in salt stress response. Using a combination of genetic, biochemical, and physiological approaches, we investigated the role of the SOS2-AFP2 module in regulating seed germination under salt stress. Our findings reveal that SOS2 physically interacts with AFP2 and stabilizes it, leading to the degradation of the ABI5 protein, a negative transcription factor in seed germination under salt stress. This study sheds light on previously unknown connections within salt stress and ABA signaling, paving the way for novel strategies to enhance plant resilience against environmental challenges., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Heat shock proteins (HSPs) are stress-responsive proteins that are conserved across all organisms. Heat shock protein 101 (HSP101) has an important role in thermotolerance owing to its chaperone activity. However, if and how it functions in development under nonstress conditions is not yet known. By using physiological, molecular, and genetic methods, we investigated the role of HSP101 in the control of flowering in Arabidopsis (Arabidopsis thaliana (L.) Heynh.) under nonstress conditions. Knockout and overexpression of HSP101 cause late and early flowering, respectively. Late flowering can be restored by rescue of HSP101. HSP101 regulates the expression of genes involved in the six known flowering pathways; the most negatively regulated genes are FLOWERING LOCUS C (FLC) and SHORT VEGETATIVE PHASE (SVP); downstream integrators of the flowering pathways are positively regulated. The late-flowering phenotype of loss-of-HSP101 mutants is suppressed by both the mutations of FLC and SVP. The responses of flowering time to exogenous signals do not change in HSP101 mutants. HSP101 is also found in nonspecific regions according to subcellular localization. We found that HSP101 promotes flowering under nonstress conditions and that this promotion depends on FLC and SVP. Our data suggest that this promotion could occur through a multiple gene regulation mechanism., (© American Society of Plant Biologists 2021. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

The remodelling of membrane lipids contributes to the tolerance of plants to stresses, such as freezing and deprivation of phosphorus. However, whether and how this remodelling relates to tolerance of PEG-induced osmotic stress has seldom been reported. Thellungiella salsuginea is a popular extremophile model for studies of stress tolerance. In this study, it was demonstrated that T. salsuginea was more tolerant to PEG-induced osmotic stress than its close relative Arabidopsis thaliana. Lipidomic analysis indicated that plastidic lipids are more sensitive to PEG-induced osmotic stress than extra-plastidic ones in both species, and that the changes in plastidic lipids differed markedly between them. PEG-induced osmotic stress led to a dramatic decrease in levels of plastidic lipids in A. thaliana, whereas the change in plastidic lipid in T. salsuginea involved an adaptive remodelling shortly after the onset of PEG-induced osmotic stress. The two aspects of this remodelling involved increases in (1) the level of plastidic lipids, especially digalactosyl diacylglycerol, and (2) the double bond index of plastidic lipids. These remodelling steps could maintain the integrity and improve the fluidity of plastidic membranes and this may contribute to the PEG-induced osmotic stress tolerance of T. salsuginea., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

At the cellular level, the remodelling of membrane lipids and production of heat shock proteins are the two main strategies whereby plants survive heat stress. Although many studies related to glycerolipids and HSPs under heat stress have been reported separately, detailed alterations of glycerolipids and the role of HSPs in the alterations of glycerolipids still need to be revealed. In this study, we profiled the glycerolipids of wild-type Arabidopsis and its HSP101-deficient mutant hot-1 under two types of heat stress. Our results demonstrated that the alterations of glycerolipids were very similar in wild-type Arabidopsis and hot-1 during heat stress. Although heat acclimation led to a slight decrease of glycerolipids, the decrease of glycerolipids in plants without heat acclimation is more severe under heat shock. The contents of 36:x monogalactosyl diacylglycerol (MGDG) were slightly increased, whereas that of 34:6 MGDG and 34:4 phosphatidylglycerol (PG) were severely decreased during moderate heat stress. Our findings suggested that heat acclimation could reduce the degradation of glycerolipids under heat shock. Synthesis of glycerolipids through the prokaryotic pathway was severely suppressed, whereas that through the eukaryotic pathway was slightly enhanced during moderate heat stress. In addition, HSP101 has a minor effect on the alterations of glycerolipids under heat stress. [ABSTRACT FROM AUTHOR]