English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

In plant glycobiology, free “metabolic” carbohydrates consist of small sugars (glucose, fructose, sucrose, trehalose), sucrose-derived oligosaccharides (fructans, Raffinose Family Oligosaccharides), starch and its breakdown products (Van den Ende, 2013). All these carbohydrates are directly or indirectly derived from photosynthesis. Plants typically accumulate higher carbohydrate levels as compared with other multicellular eukaryotes, especially when (milder) stresses compromise growth more than photosynthesis (Van den Ende and El-Esawe, in press). In a historical perspective, the central role of sugars was already suggested many decades ago, with proposed roles in overall plant growth and development (Allsopp, 1954), disease susceptibility (Horsfall and Dimond, 1957), flowering (Kraus and Kraybill, 1918) and apical dominance (Loeb, 1924). The latter two processes were suggested to be regulated by the “nutrient diversion hypothesis” (Gregory and Veale, 1957; Corbesier et al., 1998). This theory, narrowed down to sugar nutrients, states that a minimal level of sugar assimilates needs to reach the apex (flowering) or lateral bud (removal of apical dominance) before floral transition or lateral bud outgrowth is initiated. The discovery that indole-3-acetic acid (IAA) repressed lateral bud outgrowth in decapitated shoots (Thimann, 1937) boosted plant hormone research at the expense of sugar-centered research. However, things changed when small sugars, similar to hormones, were considered as important signals in plants (Moore et al., 2003). Since then, a renewed and strongly increasing worldwide interest in sugar signaling, sensing and metabolism was noticed (Ruan, 2014; Smeekens and Hellmann, 2014). Mason et al. (2014) focused on the underlying mechanisms involved during apical dominance in pea. The authors challenge a long-held dogma in plant physiology, proposing that sugar signals, and not IAA, initiates lateral bud outgrowth after apex decapitation. For decades, textbooks declare that phloemmediated IAA transport fluxes down the stem decrease after decapitation, relieving the IAA-mediated inhibition on bud outgrowth. However, the discovery that stem IAA cannot enter the bud, and the fact that IAA application on decapitated stems cannot always prevent bud burst, suggested that a positive signal could overrule IAA-mediated inhibitory effects (Mason et al., 2014). Buds from the decapitated apex could be released starting from 2.5 h post-decapitation as shown by timelapse photography (Mason et al., 2014). Importantly, this was not accompanied by a measurable IAA depletion in the adjacent stem. However, a much slower bud release was reported before (Wardlaw and Mortimer, 1970). Mason et al. (2014) designed an elegant set of physiological experiments demonstrating that leaves are the source of a rapid decapitation induced signal that promotes bud release. They reasoned that sucrose could be a candidate for this signaling role. Subsequently, [11C] CO2 was fed to leaves and the movement of [11C] photo-assimilates was monitored along the stem. They found a speed of 150 cm h−1, which agreed with the timing of bud burst and phloem-mediated transport. Exogenous sucrose applications promoted bud burst. Moreover, in plants decapitated low on the stem, leaf removal caused a serious delay in bud release, and this could be rescued by feeding sucrose, but not sorbitol, via the petiole. Unfortunately, the sucrose-specific character of this response was not tested. Comparing glucose and sucrose responses could be informative to discriminate between glucoseor sucrose-mediated signaling events. These data strongly suggest that a minimal threshold sucrose level is required to sustain lateral bud outgrowth. Initiation of bud outgrowth would not make much sense if not enough C would be available to sustain the later stages of bud growth. However, this leaves us with a remaining question: is there still room for hormone signaling events in this process? I speculate that the answer on this question is “yes.” Internal sugar/IAA ratios within lateral buds or within the adjacent stem may be somehow integrated prior to lateral bud outgrowth initiation. In my opinion further studies should answer the following crucial questions (i) Are increased sugar levels associated with changed hormone levels in buds and how does this change over time? (ii) Do bud IAA levels depend on IAA biosynthesis from tryptophan within the bud, or is indol-3-aldehyde, a phloem-mobile lateral bud inhibitor (Nakajima et al., 2002), involved via a

Sugars take a central position in plant growth, development and, stress responses. A focus on apical dominance