当前位置: X-MOL 学术J. Exp. Bot. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
The protein kinase complex CBL10-CIPK8-SOS1 functions in Arabidopsis to regulate salt tolerance.
Journal of Experimental Botany ( IF 5.6 ) Pub Date : 2019-12-10 , DOI: 10.1093/jxb/erz549
Xiaochang Yin 1, 2 , Youquan Xia 1 , Qing Xie 1 , Yuxin Cao 1 , Zhenyu Wang 1 , Gangping Hao 2 , Jie Song 3 , Yang Zhou 1 , Xingyu Jiang 1
Affiliation  

Salt tolerance in plants is mediated by Na+ extrusion from the cytosol by the plasma membrane Na+/H+ antiporter SOS1. This is activated in Arabidopsis root by the protein kinase complex SOS2–SOS3 and in Arabidopsis shoot by the protein kinase complex CBL10–SOS2, with SOS2 as a key node in the two pathways. The sos1 mutant is more sensitive than the sos2 mutant, suggesting that other partners may positively regulate SOS1 activity. Arabidopsis has 26 CIPK family proteins of which CIPK8 is the closest homolog to SOS2. It is hypothesized that CIPK8 can activate Na+ extrusion by SOS1 similarly to SOS2. The plasma membrane Na+/H+ exchange activity of transgenic yeast co-expressing CBL10, CIPK8, and SOS1 was higher than that of untransformed and SOS1 transgenic yeast, resulting in a lower Na+ accumulation and a better growth phenotype under salinity. However, CIPK8 could not interact with SOS3, and the co-expression of SOS3, CIPK8, and SOS1 in yeast did not confer a significant salt tolerance phenotype relative to SOS1 transgenic yeast. Interestingly, cipk8 displayed a slower Na+ efflux, a higher Na+ level, and a more sensitive phenotype than wild-type Arabidopsis, but grew better than sos2 under salinity stress. As expected, sos2cipk8 exhibited a more severe salt damage phenotype relative to cipk8 or sos2. Overexpression of CIPK8 in both cipk8 and sos2cipk8 attenuated the salt sensitivity phenotype. These results suggest that CIPK8-mediated activation of SOS1 is CBL10-dependent and SOS3-independent, indicating that CIPK8 and SOS2 activity in shoots is sufficient for regulating Arabidopsis salt tolerance.

中文翻译:

蛋白激酶复合物 CBL10-CIPK8-SOS1 在拟南芥中发挥调节盐耐受性的作用。

植物的耐盐性是由质膜 Na + /H +逆向转运蛋白 SOS1从胞质溶胶中挤出 Na +介导的。这在拟南芥根中被蛋白激酶复合物 SOS2-SOS3 激活,在拟南芥芽中被蛋白激酶复合物 CBL10-SOS2 激活,SOS2 是这两个途径中的关键节点。sos1 突变体比 sos2 突变体更敏感,这表明其他伙伴可能正调节 SOS1 活性。拟南芥有 26 个 CIPK 家族蛋白,其中 CIPK8 是与 SOS2 最接近的同源物。假设 CIPK8 可以通过 SOS1 激活 Na +挤出,类似于 SOS2。质膜 Na + /H +共表达 CBL10、CIPK8 和 SOS1 的转基因酵母的交换活性高于未转化和 SOS1 转基因酵母,导致盐度下的 Na +积累更低,生长表型更好。然而,CIPK8 不能与 SOS3 相互作用,与 SOS1 转基因酵母相比,酵母中 SOS3、CIPK8 和 SOS1 的共表达并没有赋予显着的耐盐表型。有趣的是,cipk8 显示出较慢的 Na +流出,较高的 Na +水平,并且比野生型拟南芥更敏感的表型,但在盐胁迫下比 sos2 生长更好。正如预期的那样,相对于 cipk8 或 sos2,sos2cipk8 表现出更严重的盐害表型。CIPK8 在 cipk8 和 sos2cipk8 中的过表达减弱了盐敏感性表型。这些结果表明 CIPK8 介导的 SOS1 激活是 CBL10 依赖性和 SOS3 非依赖性的,表明 CIPK8 和 SOS2 在芽中的活性足以调节拟南芥的耐盐性。
更新日期:2020-03-26
down
wechat
bug