KEGG里面和盐胁迫相关Pathway信息
https://www.genome.jp/kegg-bin/show_pathway?map=ath04016&show_description=show
关于盐胁迫的信号转导通路
小麦耐盐机制的总结与展望—《The Crop Journal》special issue
https://mp.weixin.qq.com/s/IWYBwnBuvcOY58qcOaXo1A
Fig. 7. The suggested model depicting ionic mechanisms contributing to K+ retention in leaf mesophyll in barley. Upon NaCl exposure, the plasma membrane is depolarized by the massive entry of external Na+ via non-selective cation channel (NSCC) and results in K+ loss mediated by depolarization-activated K+ outward rectifying channel (KOR) channels. Cytosolic K+ homeostasis is disrupted. The accompanied production of ROS has detrimental effects of leaf photochemistry in chloroplasts and, in severe cases, could trigger PCD or lead to necrosis. ROS also activate NSCC exacerbating K+ loss from cytosol. Compared with salt sensitive genotypes, higher vacuolar K+ pool in the leaf mesophyll in salt tolerant barley genotypes allows plants to maintain cytosolic K+ homeostasis by releasing vacuolar K+ into cytosol; this process is mediated by tonoplast K+- permeable channels (TPK in the model). It is also suggested that tolerant varieties may have higher Na+/H+ NHX exchanger activity and, thus, can replace vacuolar K+ by Na+ to maintain its osmotic pressure in vacuole. As K+ uptake by AKT1 into leaf mesophyll is inhibited by the membrane depolarization, plants should rely on high affinity K+ uptake to restore cytosolic K+ homeostasis (a HAK/KUP family K+/H+ co-transporter in the model). A concurrent K+ and H+ uptake through HAK/KUP exchanger results in a +2 net charge transfer and may further depolarise the plasma+ membrane, resulting in a futile cycle of K . This process is partially compensated by higher ATPase- driven H+-pumping activity in sensitive varieties.
