ArticlePlant biotechnology journal2024
BpGRP1 acts downstream of BpmiR396c/BpGRF3 to confer salt tolerance in Betula platyphylla.
Article in Plant biotechnology journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- The E3 ubiquitin ligase RHB1A and the transcription factor GRF1 form a regulatory module that orchestrates the trade-off between photosynthetic growth and salt tolerance in poplar.Plant communications · 2026Article
- Article
- Rice RING E3 Ligase OsRMT1 Negatively Regulates Salt Tolerance by Degrading the Canonical Salt-Responsive Protein OsMBL1.Plant biotechnology journal · 2025Article
- The Regulatory Roles of RNA-Binding Proteins in Plant Salt Stress Response.Plants (Basel, Switzerland) · 2025Review
- Identification and expression analysis of the RBOH gene family of Isatis indigotica Fort. and the potential regulation mechanism of RBOH gene on HPlant cell reports · 2025Article
- The Class I HD-ZIP transcription factor PagHB7a functions as a positive regulator of salt tolerance inForestry research · 2025Article
- Molecular mechanism of salinity and waterlogging tolerance in mangroveFrontiers in plant science · 2024Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Glycine-rich RNA-binding proteins (GRPs) have been implicated in the responses of plants to environmental stresses, but the function of GRP genes involved in salt stress and the underlying mechanism remain unclear. In this study, we identified BpGRP1 (glycine-rich RNA-binding protein), a Betula platyphylla gene that is induced under salt stress. The physiological and molecular responses to salt tolerance were investigated in both BpGRP1-overexpressing and suppressed conditions. BpGRF3 (growth-regulating factor 3) was identified as a regulatory factor upstream of BpGRP1. We demonstrated that overexpression of BpGRF3 significantly increased the salt tolerance of birch, whereas the grf3-1 mutant exhibited the opposite effect. Further analysis revealed that BpGRF3 and its interaction partner, BpSHMT, function upstream of BpGRP1. We demonstrated that BpmiR396c, as an upstream regulator of BpGRF3, could negatively regulate salt tolerance in birch. Furthermore, we uncovered evidence showing that the BpmiR396c/BpGRF3 regulatory module functions in mediating the salt response by regulating the associated physiological pathways. Our results indicate that BpmiR396c regulates the expression of BpGRF3, which plays a role in salt tolerance by targeting BpGRP1.
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Registered trials
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