Abstract Background and Aims Soil salinization severely limits crop productivity worldwide. Halophytes provide important biological resources for identifying genes that confer salinity tolerance. Salt glands, specialized epidermal structures in recretohalophytes like Limonium bicolor, excrete excess Na⁺, yet their developmental and functional regulation remains poorly understood. Methods We focused on LbSTICHEL (LbSTI), a homolog of the Arabidopsis trichome regulator STI, and investigated its function and upstream regulation in L. bicolor. Key Results LbSTI was found to be specifically expressed in the salt glands of L. bicolor, as determined by RNA in situ hybridization and GUS histochemical staining driven by LbSTI promoter. The function of LbSTI was further investigated in L. bicolor. In L. bicolor, plants overexpressing LbSTI produced more salt glands, exhibited increased salt secretion and greater tolerance to salinity stress compared to nontransformed controls. Conversely, LbSTI-knockdown plants generated by virus-induced gene silencing showed opposite phenotypes. Meanwhile, LbSTI increased the trichome development and salinity tolerance in wild-type plants and a sti mutant of Arabidopsis, which indicated the conservation across species. Furthermore, the upstream regulatory transcription factor LbMUSTANG3 (LbMUG3) was identified to bind to the LbSTI promoter and inhibit the transcription of LbSTI using a yeast one-hybrid and dual-luciferase reporter assay. Further functional validation revealed that LbMUG3 delayed salt gland development in L. bicolor. Additionally, the expression of LbSTI was significantly upregulated in LbMUG3-silence lines. Conclusions The current LbMUG3-LbSTI module may be a useful tool to cultivate salinity tolerance plants.
Zhu et al. (Fri,) studied this question.
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