Sugar starvation activates the OsSnRK1a‐OsbHLH111/OsSGI1‐OsTPP7 module to mediate growth inhibition of rice

Sugar deficiency is the persistent challenge for plants during development. Trehalose‐6‐phosphate (T6P) is recognized as a key regulator in balancing plant sugar homeostasis. However, the underlying mechanisms by which sugar starvation limits plant development are unclear. Here, a basic helix–loop–helix (bHLH) transcription factor (OsbHLH111) was named starvation‐associated growth inhibitor 1 (OsSGI1) and the focus is on the sugar shortage of rice. The transcript and protein levels of OsSGI1 were markedly increased during sugar starvation. The knockout mutants sgi1‐1/2/3 exhibited increased grain size and promoted seed germination and vegetative growth, which were opposite to those of overexpression lines. The direct binding of OsSGI1 to sucrose non‐fermenting‐1 (SNF1)‐related protein kinase 1a (OsSnRK1a) was enhanced during sugar shortage. Subsequently, OsSnRK1a‐dependent phosphorylation of OsSGI1 enhanced the direct binding to the E‐box of trehalose 6‐phosphate phosphatase 7 (OsTPP7) promoter, thus rose the transcription inhibition on OsTPP7, then elevated trehalose 6‐phosphate (Tre6P) content but decreased sucrose content. Meanwhile, OsSnRK1a degraded phosphorylated‐OsSGI1 by proteasome pathway to prevent the cumulative toxicity of OsSGI1. Overall, we established the OsSGI1‐OsTPP7‐Tre6P loop with OsSnRK1a as center and OsSGI1 as forward, which is activated by sugar starvation to regulate sugar homeostasis and thus inhibits rice growth.