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The plasma membrane (PM)-localized Na+/H+ antiporter Salt Overly Sensitive1 (SOS1) is essential for plant salt tolerance through facilitating Na+ efflux; however, how SOS1 localization and protein accumulation is regulated in plants remains elusive. Here, we report that Sorting Nexin 1 (SNX1) is required for plant salt stress tolerance through affecting endosomal trafficking of SOS1 in Arabidopsis (Arabidopsis thaliana). Disruption of SNX1 caused salt hypersensitivity with increased Na+ accumulation and decreased Na+ efflux in Arabidopsis when challenged with high salinity stress. SNX1 co-localized and interacted with SOS1 in endosomes, promoting its PM localization and protein stability in plants under saline conditions. SOS1 overexpression promoted salt tolerance in the wild-type, whereas such effect was greatly compromised in the snx1-2 mutant. Pharmaceutical results showed that SOS1 recycling from the cytosol to the PM was largely blocked while its vacuolar degradation was accelerated in the snx1-2 mutant. Furthermore, salt-induced SOS1 phosphorylation enhanced its interaction and co-localization with SNX1, which is required for SOS1 PM localization in plants. Our study elucidates that SNX1 facilitates SOS1 PM localization and protein accumulation through endosomal trafficking, thereby enhancing salt tolerance in plants., (© The Author(s) 2024. Published by Oxford University Press on behalf of American Society of Plant Biologists. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Regulation of seed germination is important for plant survival and propagation. ABSCISIC ACID (ABA) INSENSITIVE5 (ABI5), the central transcription factor in the ABA signaling pathway, plays a fundamental role in the regulation of ABA-responsive gene expression during seed germination; however, how ABI5 transcriptional activation activity is regulated remains to be elucidated. Here, we report that C-type Cyclin1;1 (CycC1;1) is an ABI5-interacting partner affecting the ABA response and seed germination in Arabidopsis (Arabidopsis thaliana). The CycC1;1 loss-of-function mutant is hypersensitive to ABA, and this phenotype was rescued by mutation of ABI5. Moreover, CycC1;1 suppresses ABI5 transcriptional activation activity for ABI5-targeted genes including ABI5 itself by occupying their promoters and disrupting RNA polymerase II recruitment; thus the cycc1;1 mutant shows increased expression of ABI5 and genes downstream of ABI5. Furthermore, ABA reduces the interaction between CycC1;1 and ABI5, while phospho-mimic but not phospho-dead mutation of serine-42 in ABI5 abolishes CycC1;1 interaction with ABI5 and relieves CycC1;1 inhibition of ABI5-mediated transcriptional activation of downstream target genes. Together, our study illustrates that CycC1;1 negatively modulates the ABA response by interacting with and inhibiting ABI5, while ABA relieves the CycC1;1 interaction with and inhibition of ABI5 to activate ABI5 activity for the ABA response, thereby inhibiting seed germination., (© American Society of Plant Biologists 2022. All rights reserved. For permissions, please email: journals.permissions@oup.com.)