Cao Jing, Maitirouzi Ayixianmuguli, Feng Yudan, Zhang Hua, Heng Youqiang, Zhang Jinbo, Wang Yan
Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, 830046, China.
Xinjiang Institute of Ecology and Geography, Chinese Academy of Sciences, Urumqi, 830011, China.
Plant Mol Biol. 2024 Dec 13;115(1):5. doi: 10.1007/s11103-024-01536-8.
Pathogenesis-related proteins (PR), whose expressions are induced by biotic and abiotic stress, play important roles in plant defense. Previous research identified the salt-induced HcPR10 gene in the halophyte Halostachys caspica as a regulator of plant growth and development through interactions with cytokinin. However, the mechanisms by which HcPR10 mediates resistance to abiotic stress remain poorly understood. In this study, we found that the heterologous expression of HcPR10 significantly enhanced salt and drought tolerance in Arabidopsis, likely by increasing the activity of antioxidant enzyme systems, allowing for effective scavenging of reactive oxygen species (ROS) and thus protecting plant cells from oxidative damage. Additionally, the overexpression of HcPR10 also activated the expression of stress-related genes in Arabidopsis. Furthermore, using yeast two-hybrid technology, five proteins (HcLTPG6, HcGPX6, HcUGT73B3, HcLHCB2.2, and HcMSA1) were identified as potential interacting partners for HcPR10, which could positively regulate the salt stress response mediated by HcPR10. Our findings lay the foundation for a better understanding of the molecular mechanisms of HcPR10 in response to abiotic stress and reveal additional candidate genes for improving crop salt tolerance through genetic engineering.
病程相关蛋白(PR)的表达受生物和非生物胁迫诱导,在植物防御中发挥重要作用。先前的研究确定,盐生植物盐穗木中盐诱导的HcPR10基因通过与细胞分裂素相互作用,作为植物生长发育的调节因子。然而,HcPR10介导非生物胁迫抗性的机制仍知之甚少。在本研究中,我们发现HcPR10的异源表达显著增强了拟南芥的耐盐性和耐旱性,可能是通过提高抗氧化酶系统的活性,有效清除活性氧(ROS),从而保护植物细胞免受氧化损伤。此外,HcPR10的过表达还激活了拟南芥中与胁迫相关基因的表达。此外,利用酵母双杂交技术,鉴定出五种蛋白质(HcLTPG6、HcGPX6、HcUGT73B3、HcLHCB2.2和HcMSA1)作为HcPR10的潜在相互作用伙伴,它们可以正向调节HcPR10介导的盐胁迫反应。我们的研究结果为更好地理解HcPR10响应非生物胁迫的分子机制奠定了基础,并揭示了通过基因工程提高作物耐盐性的其他候选基因。