Sugars are the primary products of photosynthesis and play multiple roles in plants. Although sugars are usually considered to be the building blocks of energy storage and carbon transport molecules, they have also gradually come to be acknowledged as signaling molecules that can initiate senescence. Senescence is an active and essential process that occurs at the last developmental stage and corresponds to programmed degradation of: cells, tissues, organs, and entire organisms. It is a complex process involving: numerous biochemical changes, transporters, genes, and transcription factors. The process is controlled by multiple developmental signals, among which sugar signals are considered to play a vital role; however, the regulatory pathways involved are not fully understood. The dynamic mechanistic framework of sugar accumulation has an inconsistent effect on senescence through the sugar signaling pathway. Key metabolizing enzymes produce different sugar signals in response to the onset of senescence. Diverse sugar signal transduction pathways and a variety of sugar sensors are involved in controlling leaf senescence. This review highlights the processes underlying initiation of sugar signaling and crosstalk between sugars and hormones signal transduction pathways affecting leaf senescence. This summary of the state of current knowledge across different plants aids in filling knowledge gaps and raises key questions that remain to be answered with respect to regulation of leaf senescence by sugar signaling pathways.

Leaf senescence is a genetically controlled process that involves the perception of extracellular signals and signal transduction. The receptor-like protein kinases (RLKs) are known to act as an important class of cell surface receptors and are involved in multiple biological processes such as development and stress responses. The functions of a number of RLK members have been characterized in Arabidopsis and other plant species, but only a limited number of RLK proteins have been reported to be associated with leaf senescence. In the present study, we have characterized the role of the somatic embryogenesis receptor kinase 4 (SERK4) gene in leaf senescence. The expression of SERK4 was up-regulated during leaf senescence and by several abiotic stress treatments in Arabidopsis. The serk4-1 knockout mutant was found to display a significant early leaf senescence phenotype. Furthermore, the results of overexpression analysis and complementary analysis supported the idea that SERK4 acts as a negative regulator in the process of leaf senescence.

Sucrose (Suc) accumulation is one of the key indicators of leaf senescence onset, but little is known about its regulatory role. Here, we found that application of high (120–150 mM) and low levels (60 mM) of Suc to young leaf (YL) and fully expanded leaf (FEL) discs, respectively, decreased chlorophyll content and maximum photosynthetic efficiency. Electrolyte leakage and malondialdehyde levels increased at high Suc concentrations (90–120 mM in YL and 60 and 150 mM in FEL discs). In FEL discs, the senescence-associated gene NtSAG12 showed a gradual increase in expression with increased Suc application; in contrast, in YL discs, NtSAG12 was upregulated with low Suc treatment (60 mM) but downregulated at higher levels of Suc. In YL discs, trehalose-6-phosphate (T6P) accumulated at a low half-maximal effective concentration (EC50) of Suc (1.765 mM). However, T6P levels declined as trehalose 6 phosphate synthase (TPS) content decreased, resulting in the maximum velocity of sucrose non-fermenting-1-related protein kinase (SnRK) and hexokinase (HXK) occurring at higher level of Suc. We therefore speculated that senescence was induced by hexose accumulation. In FEL discs, the EC50 of T6P occurred at a low concentration of Suc (0.9488 mM); T6P levels progressively increased with higher TPS content, which inhibited SnRK activity with a dissociation constant (K_d) of 0.001475 U/g. This confirmed that the T6P–SnRK complex induced senescence in detached FEL discs.