Synthetic biology plays a pivotal role in improving crop traits and increasing bioproduction through the use of engineering principles that purposefully modify plants through "design, build, test, and learn" cycles, ultimately resulting in improved bioproduction based on an input genetic circuit (DNA, RNA, and proteins). Crop synthetic biology is a new tool that uses circular principles to redesign and create innovative biological components, devices, and systems to enhance yields, nutrient absorption, resilience, and nutritional quality. In the digital age, artificial intelligence (AI) has demonstrated great strengths in design and learning. The application of AI has become an irreversible trend, with particularly remarkable potential for use in crop breeding. However, there has not yet been a systematic review of AI-driven synthetic biology pathways for plant engineering. In this review, we explore the fundamental engineering principles used in crop synthetic biology and their applications for crop improvement. We discuss approaches to genetic circuit design, including gene editing, synthetic nucleic acid and protein technologies, multi-omics analysis, genomic selection, directed protein engineering, and AI. We then outline strategies for the development of crops with higher photosynthetic efficiency, reshaped plant architecture, modified metabolic pathways, and improved environmental adaptability and nutrient absorption; the establishment of trait networks; and the construction of crop factories. We propose the development of SMART (self-monitoring, adapted, and responsive technology) crops through AI-empowered synthetic biotechnology. Finally, we address challenges associated with the development of synthetic biology and offer potential solutions for crop improvement.

Plant roots perceive heat stress (HS) and adapt their architecture accordingly, which in turn influence the yield in crops. Investigating their heterogeneity and cell type-specific response to HS is essential for improving crop resilience. Here, we generate single-cell transcriptional landscape of maize (Zea mays) roots in response to HS. We characterize 15 cell clusters corresponding to 9 major cell types and identify cortex as the main root cell type responsive to HS with the most differentially expressed genes and its trajectory being preferentially affected upon HS. We find that cortex size strongly correlated with heat tolerance that is experimentally validated by using inbred lines and genetic mutation analysis of one candidate gene in maize, providing potential HS tolerance indicator and targets for crop improvement. Moreover, interspecies comparison reveals conserved root cell types and core markers in response to HS in plants, which are experimentally validated. These results provide a universal atlas for unraveling the transcriptional programs that specify and maintain the cell identity of maize roots in response to HS at a cell type-specific level.

Dihydromyricetin (DMY), an important flavanone found in Ampelopsis grossedentata, possesses antioxidative properties that ameliorate skeletal muscle insulin sensitivity and exert a hepatoprotective effect. However, little is known about the effects of DMY in the context of high-fat diet (HFD)-induced hepatic insulin resistance. Male Sprague-Dawley(SD) rats were fed a HFD(60% fat) supplemented with DMY for 8 weeks. The administration of DMY to the rats with HFD-induced insulin resistance reduces hyperglycemia, plasma levels of insulin, and steatosis in the liver. Furthermore, DMY treatment modulated 24 metabolic pathways, including glucose metabolism, the TCA cycle. DMY significantly enhanced glucose uptake and improved the translocation of glucose transporter 1. The specificity of DMY promoted the phosphorylation of AMP-activated protein kinase (AMPK). In addition, the exposure of HepG2 cells to high glucose concentrations impaired the insulin-stimulated phosphorylation of Akt2 Ser474 and insulin receptor substrate-1 (IRS-1) Ser612, increased GSK-3β phosphorylation, and upregulated G6Pase and PEPCK expression. Collectively, DMY improved glucose-related metabolism while reducing lipid levels in the HFD-fed rats. These data suggest that DMY might be a useful drug for use in type 2 diabetes insulin resistance therapy and for the treatment of hepatic steatosis.

Background/Aims: Cajaninstilbene acid (3-hydroxy-4-prenyl-5-methoxystilben-2 -carboxylic acid, CSA), a natural stilbene isolated from the leaves of Cajanus cajan, has attracted considerable attention for its wide range of pharmacological activities. This study investigated whether CSA protects against corticosterone (CORT)-induced injury in PC12 cells and examined the potential mechanisms underlying this protective effect. Methods: Cell viability and cytotoxicity were detected using a 3-(4,5-desethyithiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and a lactate dehydrogenase (LDH) assay kit, respectively. PC12 cell apoptosis was measured using Hoechst 33342 staining and a DNA fragmentation assay kit, and intracellular Ca²⁺ concentrations were assessed by fluorescent labelling. Next, the mitochondrial permeability transition pores (mPTPs) and mitochondrial membrane potentials (∆Ψm) were detected using a colorimetric mPTP detection kit and a 5,5',6,6'-tetrachloro-1,1',3,3'- tetraethylbenzimidazolyl-carbocyanine iodide (JC-1) kit, respectively. Finally, cytochrome c, caspase-3 and inhibitor of caspase-activated deoxyribonuclease (ICAD) expression levels were monitored by western blot analysis. Results: Treatment with 100 µmol/l CORT induced cytotoxicity in PC12 cells. However, CSA dose-dependently increased cell viability and decreased LDH release as well as CORT-induced apoptosis. Mechanistically, compared with the CORT-treated group, CSA strongly attenuated intracellular Ca²⁺ overload and restored mitochondrial functions, including mPTPs and ∆Ψm. Furthermore, the down-regulation of cytochrome c and ICAD protein expression and the blockage of caspase-3 activity were observed upon CSA treatment. Conclusions: In summary, our data are the first to show that the in vitro antidepressant-like effect of CSA may be attributed to the cytoprotection of neurons and that such neuroprotective mechanisms are correlated with intracellular Ca²⁺ homeostasis and mitochondrial apoptotic pathways.