Xu Zijian, Sun Mengli, Jiang Xuefei, Sun Huapeng, Dang Xuanmin, Cong Hanqing, Qiao Fei
Hainan Key Laboratory for Sustainable Utilization of Tropical Bioresources, Institute of Tropical Agriculture and Forestry, Hainan University, Haikou, China.
Key Laboratory of Crop Gene Resources and Germplasm Enhancement in Southern China, Ministry of Agriculture, Danzhou, China.
Front Plant Sci. 2018 Oct 12;9:1469. doi: 10.3389/fpls.2018.01469. eCollection 2018.
Glycinebetaine is an important non-toxic osmoprotectant, which is accumulated in higher plants under various stresses. The biosynthesis of glycinebetaine achieved via is a two-step oxidation from choline and betaine aldehyde, catalyzed by choline monooxygenase (CMO) and betaine aldehyde dehydrogenase (BADH), respectively. Up-regulated gene expression of BADH and CMO induced by stress is clearly observed, but the signal transduction is poorly understood. Here, glycinebetaine accumulation in response to osmotic stress and growth recovery induced by exogenous glycinebetaine were observed in a watermelon cell line. When tracing back to the genome sequence of watermelon, it shows that there exists only one member of or corresponding to glycinebetaine biosynthesis. Both genes harbor a CGTCA-motif in their promoter region which is involved in methyl jasmonate (MeJA)-responsiveness. Amongst MeJA, Ethephon, abscisic acid (ABA), and salicylic acid (SA), MeJA was most effective in gene inducing the expression of and , and the accumulation of glycinebetaine could also reach an amount comparable to that after osmotic stress by mannitol. Moreover, when ibuprofen (IBU), a JA biosynthesis inhibitor, was pre-perfused into the cells before osmotic stress, glycinebetaine accumulation was suppressed significantly. Interestingly, newly grown cells can keep a high content of glycinebetaine when they are sub-cultured from osmotic stressed cells. This study suggests that osmotic stress induced glycinebetaine biosynthesis occurs via JA signal transduction and not only plays a key role in osmotic stress resistance but also contributes to osmotic stress hardening.
甘氨酸甜菜碱是一种重要的无毒渗透保护剂，在各种胁迫条件下高等植物中会积累该物质。甘氨酸甜菜碱的生物合成是通过胆碱和甜菜碱醛的两步氧化反应实现的，分别由胆碱单加氧酶（CMO）和甜菜碱醛脱氢酶（BADH）催化。胁迫诱导的BADH和CMO基因表达上调现象明显，但信号转导机制尚不清楚。在此，我们在一个西瓜细胞系中观察到了渗透胁迫诱导的甘氨酸甜菜碱积累以及外源甘氨酸甜菜碱诱导的生长恢复情况。追溯西瓜的基因组序列发现，对应甘氨酸甜菜碱生物合成的CMO或BADH只有一个成员。这两个基因在其启动子区域都含有一个CGTCA基序，该基序参与茉莉酸甲酯（MeJA）应答反应。在MeJA、乙烯利、脱落酸（ABA）和水杨酸（SA）中，MeJA在诱导CMO和BADH基因表达方面最有效，甘氨酸甜菜碱的积累量也能达到与甘露醇渗透胁迫后相当的水平。此外，当在渗透胁迫前将JA生物合成抑制剂布洛芬（IBU）预先灌注到细胞中时，甘氨酸甜菜碱的积累会受到显著抑制。有趣的是，从渗透胁迫细胞中继代培养得到的新生长细胞能够保持较高的甘氨酸甜菜碱含量。本研究表明，渗透胁迫诱导的甘氨酸甜菜碱生物合成通过JA信号转导发生，不仅在渗透胁迫抗性中起关键作用，而且有助于渗透胁迫驯化。
