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. 2025 May:222:109689.
doi: 10.1016/j.plaphy.2025.109689. Epub 2025 Feb 25.

SLR1-LPA1 signal regulates sheath blight resistance and lamina joint angle in rice

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SLR1-LPA1 signal regulates sheath blight resistance and lamina joint angle in rice

Hongyao Zhu et al. Plant Physiol Biochem. 2025 May.

Abstract

Previous studies have suggested that Dense and Erect Panicle 1 (DEP1) interacts with Lose Plant Architecture 1 (LPA1) to regulate auxin transport by which DEP1-LPA1 modulates rice sheath blight (ShB) resistance. In this study, we identified that dep1 and lpa1 exhibited semi-dwarfism and dep1/lpa1 was shorter than the single mutant. LPA1 OX displayed higher height, whereas DEP1 OX exhibited similar height with wild-type. The gibberellic acid (GA)-dependent shoot growth was inhibited in dep1 and lpa1 while activated in LPA1 OX, suggesting that LPA1 may play a role in GA signaling transduction. Yeast two-hybrid screening revealed that slender rice 1 (SLR1), a GA signaling negative regulator, interacted with LPA1. Additionally, slr1 was less susceptible to ShB, whereas the GA signaling positive regulator DWARF1 mutant d1 was more susceptible to ShB. This suggested that GA signaling positively regulates rice resistance to ShB. Furthermore, slr1 was similar to LPA1 OX in terms of reduced lamina joint angle, whereas d1 did not show any difference. This implied that SLR1 may regulate LPA1 dependent signaling to control the lamina joint angle via a mechanism that was independent of GA signaling. Transcriptome data indicated that GA signaling and catabolic genes were regulated by LPA1. Transient and ChIP assays suggested that LPA1 bound to the promoter of gibberellin 2-beta-dioxygenase, a GA catabolic gene, to activate its expression. These findings indicated that LPA1 modulated GA homeostasis and SLR1 interacted with and inhibited LPA1 to regulate ShB resistance and lamina joint angle in rice.

Keywords: LPA1; Lamina joint angle; Rice; SLR1; Sheath blight.

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Conflict of interest statement

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

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