In strawberry, sucrose is the major form of carbohydrate translocated from the leaves to the fruits and plays an important role in fruit ripening. As a conserved energy sensor, sucrose nonfermenting-1 (SNF1)-related kinase 1 (SnRK1) plays an important role in plant carbon metabolism. However, evidence that SnRK1 regulates sucrose accumulation in fruits is lacking. In this study, we transiently expressed FaSnRK1α in strawberry fruits and found that overexpression (OE) of the FaSnRK1α gene significantly increased the sucrose content, whereas repression of FaSnRK1α by RNA interference (RNAi) decreased the sucrose content. Further analysis revealed that FaSnRK1α increased the expression of FaSUS1 and FaSUS3 as well as the activity of sucrose synthase (SUS; EC 2.4.1.13) and that FaSPS1 expression and sucrose phosphate synthase (SPS; EC 2.4.1.14) activity were strongly downregulated, which decreased the accumulation of sucrose. However, the expression of FaSPS3, which is reported to contribute to sucrose accumulation, was induced by FaSnRK1α, and FaNI expression and invertase (INV; EC 3.2.1.26) activity were upregulated by FaSnRK1α. In addition, FaSnRK1α positively upregulated the expression of the sucrose transporter (SUT) genes FaSUT1 and FaSUT5 and interacted with FaSUS1, FaSPS1 and FaSPS3 proteins but not with FaSUS3, FaNI, FaSUT1 or FaSUT5 proteins. Overall, FaSnRK1α systematically regulates the expression of the genes and activities of key enzymes involved in the sucrose metabolic pathway and promotes the long-distance transport of sucrose, thereby increasing sucrose accumulation and ultimately promoting fruit ripening. However, the mechanisms by which sucrose transport and degradation are regulated by SnRK1 warrant additional research.
Sucrose nonfermenting-1-related protein kinase 1 (SnRK1) is a central integrator of plant stress and energy starvation signalling pathways. We found that the FaSnRK1α-overexpression (OE) roots had a higher respiratory rate and tolerance to waterlogging than the FaSnRK1α-RNAi roots, suggesting that FaSnRK1α plays a positive role in the regulation of anaerobic respiration under waterlogging. FaSnRK1α upregulated the activity of anaerobic respiration-related enzymes including hexokinase (HK), phosphofructokinase (PFK), pyruvate kinase (PK), pyruvate decarboxylase (PDC), alcohol dehydrogenase (ADH) and lactate dehydrogenase (LDH). FaSnRK1α also enhanced the ability to quench reactive oxygen species (ROS) by increasing antioxidant enzyme activities. We sequenced the transcriptomes of the roots of both wild-type (WT) and FaSnRK1α-RNAi plants, and the differentially expressed genes (DEGs) were clearly enriched in the defence response, response to biotic stimuli, and cellular carbohydrate metabolic process. In addition, 42 genes involved in glycolysis and 30 genes involved in pyruvate metabolism were significantly regulated in FaSnRK1α-RNAi roots. We analysed the transcript levels of two anoxia-related genes and three ERFVIIs, and the results showed that FaADH1, FaPDC1, FaHRE2 and FaRAP2.12 were upregulated in response to FaSnRK1α, indicating that FaSnRK1α may be involved in the ethylene signalling pathway to improve waterlogging tolerance. In conclusion, FaSnRK1α increases the expression of ERFVIIs and further activates anoxia response genes, thereby enhancing anaerobic respiration metabolism in response to low-oxygen conditions during waterlogging.
Plants suffer from a variety of environmental stresses during their growth and development. The evolutionarily conserved sucrose nonfermenting kinase 1-related protein kinase 1 (SnRK1) plays a central role in the regulation of energy homeostasis in response to stresses. In plant cells, autophagy is a degradation process occurring during development or under stress, such as nutrient starvation. In recent years, SnRK1 signaling has been reported to be an upstream activator of autophagy. However, these studies all focused on the regulatory effect of SnRK1 on TOR signaling and the autophagy-related gene 1 (ATG1) complex. In this study, overexpression of the gene encoding the Prunus persica SnRK1 α subunit (PpSnRK1α) in tomato improved the photosynthetic rates and enhanced the resistance to low nutrient stress (LNS). Overexpression of PpSnRK1α increased autophagy activity and upregulated the expression of seven autophagy-related genes (ATGs). The transcriptional levels of SlSnRK2 family genes were altered significantly by PpSnRK1α, signifying that PpSnRK1α may be involved in the ABA signaling pathway. Further analysis showed that PpSnRK1α not only activated autophagy by inhibiting target of rapamycin (TOR) signaling but also enhanced ABA-induced autophagy. This indicates that PpSnRK1α regulates the photosynthetic rate and induces autophagy, and then responds to low nutrient stress.