The loss of SR45 results in enhanced sensitivity to salt stress and changes in expression and splicing of genes involved in regulating salt stress response.Only the long isoform (SR45.1) rescued the salt-sensitive phenotype as well as the altered gene expression and splicing patterns in the mutant.
Data demonstrate that SR45 regulates alternative splicing of the Arabidopsis 5PTase13 gene which encodes an inositol polyphosphate 5-phosphatase previously shown to interact with and regulate the stability of SnRK1 in vitro thus providing a mechanistic link between SR45 function and the modulation of degradation of the SnRK1 energy sensor in response to sugars.
SR45 plays an unexpected role in mRNA processing of intronless genes and numerous abscisic acid (ABA) signaling genes are targeted for regulation at the posttranscriptional level.
SR45 recruits U1snRNP and U2AF to 5' and 3' splice sites respectively by interacting with pre-mRNA U1-70K and U2AF(35) and modulates alternative splicing (AS).
DNA methylation establishment and maintenance defects present in sr45-1 mutants are enhanced in dcl3-1 mutant background suggesting a synergistic cooperation between SR45 and DICER-LIKE3 (DCL3) in the RdDM pathway.
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