Abstract
The effect of glucose as a signaling molecule on induction of aliphatic glucosinolate biosynthesis was reported in our former study. Here, we further investigated the regulatory mechanism of indolic glucosinolate biosynthesis by glucose in Arabidopsis. Glucose exerted a positive influence on indolic glucosinolate biosynthesis, which was demonstrated by induced accumulation of indolic glucosinolates and enhanced expression of related genes upon glucose treatment. Genetic analysis revealed that MYB34 and MYB51 were crucial in maintaining the basal indolic glucosinolate accumulation, with MYB34 being pivotal in response to glucose signaling. The increased accumulation of indolic glucosinolates and mRNA levels of MYB34, MYB51, and MYB122 caused by glucose were inhibited in the gin2-1 mutant, suggesting an important role of HXK1 in glucose-mediated induction of indolic glucosinolate biosynthesis. In contrast to what was known on the function of ABI5 in glucose-mediated aliphatic glucosinolate biosynthesis, ABI5 was not required for glucose-induced indolic glucosinolate accumulation. In addition, our results also indicated that glucose-induced glucosinolate accumulation was due to enhanced sulfur assimilation instead of directed sulfur partitioning into glucosinolate biosynthesis. Thus, our data provide new insights into molecular mechanisms underlying glucose-regulated glucosinolate biosynthesis.
Highlights
0.204 ± 0.028a with adenylation to adenosine 5′-phosphosulfate (APS)
Our former study has demonstrated that glucose positively regulated aliphatic glucosinolate biosynthesis by hexokinase 1 (HXK1)-mediated signaling via transcription factors MYB28, MYB29, and abscisic acid (ABA)-insensitive 5 (ABI5)[59]
It was reported that different kinds of abiotic stresses including osmotic stress could affect glucosinolate content[60,61,62], so sorbitol was used as a osmotic stress control of glucose treatment
Summary
0.204 ± 0.028a with adenylation to adenosine 5′-phosphosulfate (APS). As a branching point of sulfate assimilation, APS can be reduced by APS reductase (APR) to sulfite, which is subsequently reduced to sulfide by sulfite reductase (SiR) and participates in the synthesis of cysteine and other sulfur-containing compounds. Our former study has demonstrated that glucose positively regulated aliphatic glucosinolate biosynthesis by HXK1-mediated signaling via transcription factors MYB28, MYB29, and ABA-insensitive 5 (ABI5)[59]. As another major kind of glucosinolates in Arabidopsis, indolic glucosinolate is synthesized via a distinct pathway from that of aliphatic glucosinolate. We investigated the regulatory mechanism of indolic glucosinolate by glucose signaling, and found that glucose promotes the accumulation of indolic glucosinolates through MYB34, MYB51, and MYB122, while MYB34 plays a key role This process is mediated by HXK1, but not by ABI5, suggesting that the mechanism underlying glucose-regulated indolic glucosinolates is distinct from that of aliphatic ones. We found that glucose-promoted accumulation of both aliphatic and indolic glucosinolates is associated with enhanced sulfur assimilation
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