农作物耐盐创新科研平台:Nature Communications | 中农学者揭示植物重要抗盐碱机制
Nature Commun | 中国农业大学蒋才富课题组揭示植物重要抗盐碱机制
期刊:Nature Communications
主题:钙离子结合蛋白编码基因的自然变异赋予玉米耐盐碱性
标题:Natural variation of an EF-hand Ca2+-bindingprotein coding gene confers saline-alkaline tolerance in maize
影响因子:11.878
检测指标:Na+、H+流速
检测样品:玉米根分生区(距根尖约500μm)
Na+、H+流实验处理方法:
Na+:5日龄的玉米幼苗,100mM NaCl(pH 8.0)处理24h后,正常缓冲液/50μM阿米洛利处理30min
H+:5日龄的玉米幼苗碱处理(pH 8.0)24h/盐碱处理(100mM NaCl,pH 8.0)24h
Na+、H+流实验测试液成份:
0.1mM KCl,0.1mM CaCl2、Na+:0.1mM CaCl2、0.1mM KCl,0.3mM MES和0.5mM NaCl,pH 6.0
H+:0.1mM CaCl2、0.1mM KCl和0.3mM MES,pH 7.0
作者:中国农业大学蒋才富、曹一博
英文摘要
Sodium (Na+) toxicityis one of the major damages imposed on crops by saline-alkaline stress.
Here we show thatnatural maize inbred lines display substantial variations in shoot Na+ contentsand saline-alkaline (NaHCO3) tolerance, and reveal that ZmNSA1 (Na+ Contentunder Saline-Alkaline Condition) confers shoot Na+ variations under NaHCO3 condition by a genome-wide association study. Lacking of ZmNSA1 promotes shoot Na+ homeostasis by increasing root Na+ efflux. A naturally occurred 4-bpdeletion decreases the translation efficiency of ZmNSA1 mRNA, thus promotes Na+homeostasis.
We further show that,under saline-alkaline condition, Ca2+ binds to the EF-hand domain of ZmNSA1then triggers its degradation via 26S proteasome, which in turn increases thetranscripts levels of PM-H+-ATPases (MHA2 and MHA4), and consequently enhancesSOS1 Na+/H+ antiportermediated root Na+ efflux.
Our studies reveal themechanism of Ca2+-triggered saline-alkaline tolerance and provide an importantgene target for breeding saline-alkaline tolerant maize varieties.
中文摘要(谷歌机翻)
钠(Na+)毒性是盐碱胁迫对农作物造成的主要损害之一。
在这里,我们显示天然玉米自交系显示出芽Na+含量和盐碱(NaHCO3)耐受性的显着差异,并揭示了ZmNSA1(盐碱条件下的Na +含量)通过全基因组关联赋予了NaHCO3条件下芽Na+的变异。研究。ZmNSA1的缺乏通过增加根系Na+的流出而促进芽Na+稳态。自然发生的4 bp缺失会降低ZmNSA1 mRNA的翻译效率,从而促进Na+稳态。
我们进一步表明,在盐碱条件下,Ca2+结合到ZmNSA1的EF-手结构域,然后通过26S蛋白酶体触发其降解,这反过来又增加了PM-H+ -ATPases(MHA2和MHA4)的转录水平。增强SOS1 Na+ / H+反转运蛋白介导的根Na+外排。
我们的研究揭示了Ca2+触发的盐碱耐受性的机制,并为选育耐盐碱玉米品种提供了重要的基因靶标。