- Information
- Symbol: OsFRDL4
- MSU: LOC_Os01g69010
- RAPdb: Os01g0919100
- Publication
- An Al-inducible MATE gene is involved in external detoxification of Al in rice, 2011, Plant J.
- Retrotransposon-mediated aluminum tolerance through enhanced expression of the citrate transporter OsFRDL4., 2016, Plant Physiol.
- Hydrogen Sulfide Alleviates Aluminum Toxicity via Decreasing Apoplast and Symplast Al Contents in Rice., 2018, Front Plant Sci.
- OsGERLP: A novel aluminum tolerance rice gene isolated from a local cultivar in Indonesia, 2021, Plant Physiol Biochem.
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Genbank accession number
- Key message
- Taken together, our results show that OsFRDL4 is an Al-induced citrate transporter localized at the plasma membrane of rice root cells and is one of the components of high Al tolerance in rice
- Knockout of OsFRDL4 resulted in decreased Al tolerance and decreased citrate secretion compared with the wild-type rice, but did not affect citrate concentration in the xylem sap
- Furthermore, the OsFRDL4 expression was regulated by ART1, a C2H2-type zinc finger transcription factor for Al tolerance
- Furthermore, there is a positive correlation between OsFRDL4 expression level and the amount of citrate secretion in rice cultivars that are differing in Al tolerance
- The expression level of the OsFRDL4 gene in roots was very low in the absence of Al, but was greatly enhanced by Al after short exposure
- Immunostaining showed that OsFRDL4 was localized in all cells in the root tip
- Analysis with chromosome segment substitution lines (CSSL) derived from Nipponbare (high OsFRDL4 expression) and Kasalath (low OsFRDL4 expression) revealed that differential expression of OsFRDL4 is responsible for the QTL for Al tolerance detected previously on chromosome 1
- Connection
- ART1, OsFRDL4, An Al-inducible MATE gene is involved in external detoxification of Al in rice, Furthermore, the OsFRDL4 expression was regulated by ART1, a C2H2-type zinc finger transcription factor for Al tolerance
- OsFRDL2, OsFRDL4, Functional analysis of a MATE gene OsFRDL2 revealed its involvement in Al-induced secretion of citrate, but less contribution to Al tolerance in rice., A double mutant between osfrdl2 and osfrdl4 or osfrdl1 did not further decrease the Al-induced citrate secretion and Fe translocation compared with the single mutant
- ART1, OsFRDL4, Retrotransposon-mediated aluminum tolerance through enhanced expression of the citrate transporter OsFRDL4., 2-kb insertion in the OsFRDL4 promoter region in japonica subspecies is responsible for their higher expression level of OsFRDL4 due to the increased number of cis-acting elements of ART1
- OsFRDL4, OsWRKY22, Transcription factor WRKY22 promotes aluminum tolerance via activation of OsFRDL4 expression and enhancement of citrate secretion in rice Oryza sativa., We define the role of OsWRKY22 in response to Al stress in rice by using mutation and transgenic complementation assays, and characterize the regulation of OsFRDL4 by OsWRKY22 via yeas one-hybrid, electrophoretic mobility shift assay and ChIP-quantitative PCR
- OsFRDL4, OsWRKY22, Transcription factor WRKY22 promotes aluminum tolerance via activation of OsFRDL4 expression and enhancement of citrate secretion in rice Oryza sativa., We next show that OsWRKY22 is localized in the nucleus, functions as a transcriptional activator and is able to bind to the promoter of OsFRDL4 via W-box elements
- OsFRDL4, OsWRKY22, Transcription factor WRKY22 promotes aluminum tolerance via activation of OsFRDL4 expression and enhancement of citrate secretion in rice Oryza sativa., Finally, we find that both OsFRDL4 expression and Al-induced citrate secretion are significantly lower in art1 oswrky22 double mutants than in the respective single mutants
- OsFRDL4, OsWRKY22, Transcription factor WRKY22 promotes aluminum tolerance via activation of OsFRDL4 expression and enhancement of citrate secretion in rice Oryza sativa., We conclude that OsWRKY22 promotes Al-induced increases in OsFRDL4 expression, thus enhancing Al-induced citrate secretion and Al tolerance in rice
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