Figure 1.

A conceptual mechanistic basis for the interaction between fructans and hormones. This model explains how hormones may closely regulate both biosynthesis (A) and catabolism (B) of fructans. (A), The involvement of hormones in fructan biosynthesis. Suc-specific pathways involving transcription factors (MYB13), protein phosphatase (PP2A), and calcium (Ca²⁺) signaling closely mediate Suc-induction of fructan biosynthesis. In addition, these components are involved in hormones, abscisic acid (ABA), auxins (AUX), and ethylene (ET) biosynthesis as well as their homeostasis. A calcium sensor, CBL1, promotes ABA signaling by repressing the negative regulator of ABA signaling, PP2C. Ca²⁺/CaM module activates small AUX-up RNA proteins (SAURs) that control AUX levels. In contrast, AUX positively regulates SAURs. While Ca²⁺–dependent protein kinases (CDPKs) control the ET biosynthesis; PP2A tightly control ET biosynthesis by differentially regulating the turnover of ACC synthase (ACS5 and 6) isoforms. The presence of relatively stable, low levels of these hormones is important, and may form part of Suc-specific pathways positively regulating fructan biosynthesis via fine-tuning of FTs. (B), The hormonal network regulating fructan degradation. Stress-inducible ABA induces fructan catabolic enzymes, fructan exohydrolases (1-FEH), promoting fructan degradation in wheat. Suc is further hydrolysed by ABA-induced acid invertases (INVs). Part of the Fructose (Fru) would be used for Suc synthesis. While glucose (Glc) antagonizes ABA signaling, Fru antagonizes ET signaling, mediated by mitogen-activated protein kinases (MAPK3 and 6). It is known that ET counteracts ABA functions. In order to promote ET signaling, it is suggested here that both ET and AUX signaling that function synergistically may counteract ABA signaling and repress 1-FEH expression, thereby reducing glucose and fructose levels. The timing of fructan degradation may be a critical process affecting carbon availability and on-going physiological processes that could indeed alter the initiation of leaf senescence. Such AUX/ET signaling repression of 1-FEH might be mediated by a transcriptional complex MYB44-MYB77. This protein complex interacts with auxin response factors (ARFs) that bind to auxin responsive elements (AuxRE) of auxin responsive genes as was shown in arabidopsis. While ABA enhances Ca²⁺ levels, which in turn promotes ABA signaling and enhances FEH activity, Ca²⁺ signaling-based CDPKs (via ACS6 and 2) also promote ET biosynthesis. This suggests that a subtle hormonal balance governs biological processes more sensibly than could achieve by a single hormone. However, this conceptual model is largely constructed based on the knowledge from Arabidopsis; hence, this needs to be confirmed in fructan-accumulating species. Blue lines represent positive regulation while red lines indicate negative regulation. Gray lines depict degradation processes. See text for further explanations and the references.