中科院华南植物园屈红霞-蒋国祥团队在Plant J发表研究论文《Energy homeostasis mediated by the LcSnRK1α–LcbZIP1/3 signaling pathway modulates litchi fruit senescence》。
细胞能量状态是决定园艺作物衰老进程的关键因素。尽管保守能量主调节因子蔗糖非发酵 1 (SNF1) 相关蛋白激酶 1 (SnRK1) 在植物发育中的作用已确立，但其在调控果实衰老中的作用机制和相关信号通路仍然未知。
在本研究中，作者证明能量缺乏会加速果实衰老，而外源性ATP处理会延迟衰老进程。荔枝果实中LcSnRK1的瞬时沉默抑制了能量代谢相关基因的表达，而其在番茄中的异源表达促进了成熟和高能量水平。
生化分析表明，LcSnRK1与转录因子LcbZIP1和LcbZIP3相互作用并使其磷酸化，直接与启动子结合，激活DARK INDUCIBLE 10 (LcDIN10)、天冬酰胺合成酶1 (LcASN1) 和花青素合成酶 (LcANS) 的表达，从而提高-调整代谢重编程以确保能量和氧化还原稳态。
总之，这些观察结果揭示了一种翻译后修饰机制，LcSnRK1介导的LcbZIP1 和LcbZIP3磷酸化调节代谢重编程相关基因的表达，从而调节荔枝果实的衰老。
Cellular energy status is a key factor deciding the switch-on of the senescence of horticultural crops. Despite the established significance of the conserved energy master regulator sucrose nonfermenting 1 (SNF1)-related protein kinase 1 (SnRK1) in plant development, its working mechanism and related signaling pathway in the regulation of fruit senescence remain enigmatic. Here, we demonstrate that energy deficit accelerates fruit senescence, whereas exogenous ATP treatment delays it. The transient suppression of LcSnRK1α in litchi fruit inhibited the expression of energy metabolism-related genes, while its ectopic expression in tomato promoted ripening and a high energy level. Biochemical analyses revealed that LcSnRK1α interacted with and phosphorylated the transcription factors LcbZIP1 and LcbZIP3, which directly bound to the promoters to activate the expression of DARK INDUCIBLE 10 (LcDIN10), ASPARAGINE SYNTHASE 1 (LcASN1), and ANTHOCYANIN SYNTHASE (LcANS), thereby fine-tuning the metabolic reprogramming to ensure energy and redox homeostasis. Altogether, these observations reveal a post-translational modification mechanism by which LcSnRK1α-mediated phosphorylation of LcbZIP1 and LcbZIP3 regulates the expression of metabolic reprogramming-related genes, consequently modulating litchi fruit senescence.
