ArticleStress biology2022
NUA and ESD4 negatively regulate ABA signaling during seed germination.
Article in Stress biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Protein Post-Translational Modifications in Plant Abiotic Stress Responses.Plants (Basel, Switzerland) · 2025Review
- SIZ1 SUMOylates and stabilizes WRI1 to safeguard seed filling and fatty acid biosynthesis under high-temperature stress.The Plant cell · 2025Article
- SnRK2s: Kinases or Substrates?Plants (Basel, Switzerland) · 2025Review
- Allelic variation of TaABI5-A4 significantly affects seed dormancy in bread wheat.TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2024Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The phytohormone abscisic acid (ABA) plays important roles in plant growth, development and adaptative responses to abiotic stresses. SNF1-related protein kinase 2s (SnRK2) are key components that activate the ABA core signaling pathway. NUCLEAR PORE ANCHOR (NUA) is a component of the nuclear pore complex (NPC) that involves in deSUMOylation through physically interacting with the EARLY IN SHORT DAYS 4 (ESD4) SUMO protease. However, it is not clear how NUA functions with SnRK2 and ESD4 to regulate ABA signaling. In our study, we found that nua loss-of-function mutants exhibited pleiotropic ABA-hypersensitive phenotype. We also found that ABA-responsive genes remarkably up-regulated in nua by exogenous ABA. The nua snrk2.2 snrk2.3 triple mutant and nua abi5 double mutant partially rescued the ABA-hypersensitive phenotype of nua, thereby suggesting that NUA is epistatic to SnRK2s. Additionally, we observed that esd4-3 mutant was also ABA-hypersensitive. NUA and ESD4 were further demonstrated to physically interact with SnRK2s and negatively regulate ABA signaling by reducing SnRK2s stability. Taken together, our findings uncover a new regulatory mechanism that can modulate ABA signaling.
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