Impaired KIN10 function restores developmental defects in the Arabidopsis trehalose 6‐phosphate synthase1 (tps1) mutant

Abstract

Sensing carbohydrate availability is essential for plants to coordinate their growth and development. In Arabidopsis thaliana, TREHALOSE 6-PHOSPHATE SYNTHASE 1 (TPS1) and its product, trehalose 6-phosphate (T6P), are important for the metabolic control of development. tps1 mutants are embryo-lethal and unable to flower when embryogenesis is rescued. T6P regulates development in part through inhibition of SUCROSE NON-FERMENTING1 RELATED KINASE1 (SnRK1).Here, we explored the role of SnRK1 in T6P-mediated plant growth and development using a combination of a mutant suppressor screen and genetic, cellular and transcriptomic approaches.We report nonsynonymous amino acid substitutions in the catalytic KIN10 and regulatory SNF4 subunits of SnRK1 that can restore both embryogenesis and flowering of tps1 mutant plants. The identified SNF4 point mutations disrupt the interaction with the catalytic subunit KIN10.Contrary to the common view that the two A. thaliana SnRK1 catalytic subunits act redundantly, we found that loss-of-function mutations in KIN11 are unable to restore embryogenesis and flowering, highlighting the important role of KIN10 in T6P signalling.

SnRK1 inhibits anthocyanin biosynthesis through both transcriptional regulation and direct phosphorylation and dissociation of the MYB/bHLH/TTG1 MBW complex

“…Consistent with negative regulation of SnRK1 activity by T6P (Zhang et al, 2009), the tps1 mutant, deficient in the major T6P synthase TPS1 (Eastmond et al, 2002; Van Dijken et al, 2004), shows significantly reduced anthocyanin accumulation and MYB75 and DFR expression in sucrose-rich medium (Figure 2C,D). Moreover, the recently described tps1 suppressor mutants with additional mutations in the SnRK1α1 catalytic site (160-1: G178R, 199-6: R259Q, 232-2: G162D) and concomitant restoration of embryogenesis and transition to flowering (Zacharaki et al, 2022) showed a fully restored sucrose-induced anthocyanin biosynthesis and MYB75 and DFR expression (Figure 2E,F). Together, our results confirm that SnRK1 is an important negative regulator of sucrose-induced anthocyanin biosynthesis, at least in part by transcriptional repression of MYB75 , a key factor in controlling expression of DFR , an essential enzyme for anthocyanin biosynthesis.…”

“…Arabidopsis thaliana mutant lines were in the Col-0 or Ler background. The Ler SnRK1α1 OX, SnRK1α1 RNAi (Baena-González et al, 2007), dfr1 ( tt3-1 ; NASC NW84) and Col-0 pap1-D (Borevitz et al, 2000), myb75 RNAi (Jover-Gill et al, 2014), ttg1-21 (GK-580A05; NASC N2105595), ttg1-22 (GK-286A06; NASC N330696), tps1 (Van Dijken et al, 2004), tps1 suppressor (Zacharaki et al, 2022) and NLS-SnRK1α1 and βMYR-SnRK1α1 (Ramon et al, 2019) mutants and transgenic lines have been described previously.…”

Comparative Analysis on the Evolution of Flowering Genes in Sugar Pathway in Brassicaceae

“…TRIOSE PHOSPHATE ISOMERASE (TPI) promotes the transition of plants from heterotrophic growth to autotrophic growth [ 62 ]. The Arabidopsis snf4 mutation disrupts the interaction of SNF4 with SNRK1 and thus affects the role of SNRK1 in the T6P-mediated signaling pathway [ 63 ].…”

Integrated Transcriptome and Targeted Metabolite Analysis Reveal miRNA-mRNA Networks in Low-Light-Induced Lotus Flower Bud Abortion

“…Tre and its precursor T6P have diverse and vital functions in plants, linking growth and development to carbon status [ 30 , 31 ]. As an important enzyme in T6P synthesis, TPS1 is also essential for normal vegetative growth and transition to flowering, and the deletion of TPS1 prevents floral transition in Arabidopsis [ 32 , 33 ]. They were reported to play important roles in maize early kernel development and events leading to stress-induced kernel abortion [ 34 ].…”