Cross-talk between ABA and sugar signaling is mediated by the ACGT core and CE1 element reciprocally in OsTIP3;1 promoter.

Recently, much effort has been made to determine the molecular links and cross-talk between sugar and abscisic acid (ABA) signaling pathways. ABA-inducible expression of OsTIP3;1, encoding a rice tonoplast intrinsic protein, was enhanced by sugar depletion. Such a stimulatory increase in OsTIP3;1 expression under sugar-starvation is possibly not owing to changes in endogenous ABA content. The transient expression assay indicated that the 5' flanking region of OsTIP3;1 delivered similar collaborative responsiveness to starvation and ABA, suggesting that this gene promoter could be a good molecular probe to examine the interaction between sugar and ABA signaling pathways. Targeted mutagenesis demonstrated that disruption of ACGT cores decreased the induction of OsTIP3;1 promoter activity under either starvation or ABA, whereas mutation of coupling element 1 (CE1), which is an ABI4 binding site, reversely increased it, suggesting that those two distinct cis-regulatory elements reciprocally regulate the responsiveness of this promoter to both sugar and ABA. Consistent with this result, antisense inhibition of ABI4 increased the OsTIP3;1 promoter activity. ABI4 expression was also enhanced by sugars and repressed by ABA, suggesting that reduced ABI4 binding to CE1 in the absence of sugar and presence of ABA could increase ABA-induction of the OsTIP3;1 promoter activity.