DOI：http://dx.doi.org/10.1016/j.cell.2016.08.029
本篇文獻翻譯還參考了中國水稻研究所倪建平老師發表在《中國稻米》雜誌上的對朱健康院士綜述「Abiotic Stress Signaling and Responses in Plants」的譯文。
ABA strongly activates SnRK2.2, SnRK2.3, and SnRK2.6/OST1 and weakly activates SnRK2.7 and SnRK2.8. The snrk2.2/3/6 triple mutant in Arabidopsis is extremely insensitive to ABA in seed germination, seedling growth, stomatal closure, and gene regulation.
strongly activates 強烈激活
weakly activates 微弱激活
ABA強烈激活SnRK2.2、SnRK2.3和SnRK2.6/OST1，也微弱激活SnRK2.7 和SnRK2.8。擬南芥snrk2.2/3/6 三突變體表現出在種子萌發、幼苗生長、氣孔關閉、基因調控等方面對ABA極不敏感。
Many effector proteins of ABA responses are direct substrates of SnRK2 kinases. bZIP transcription factors such as ABI5 and ABFs (ABA-responsive element-binding factors) are phosphorylated by the SnRK2s.
許多ABA應答中的效應蛋白是SnRK2激酶的直接底物。bZIP家族轉錄因子如ABI5和ABFs（ABA 響應元件結合因子）能被SnRK2s磷酸化。
Much of the ABA signaling occurs at the plasma membrane. The association of PYLs with the plasma membrane is mediated by their interaction with C2 domain proteins.
大部分ABA信號發生在質膜上。PYLs與質膜的結合是通過它們與C2結構域蛋白的互作所介導的。
Plasma-membrane proteins such as the anion channel SLAC1 are SnRK2 substrates that mediate ABA-induced stomatal closure and reduce transpirational water loss under drought stress.
質膜蛋白如陰離子通道SLAC1，是介導ABA誘導的氣孔關閉和減少乾旱脅迫下蒸騰失水的SnRK2的底物。
Recent phosphoproteomic studies identified dozens of additional SnRK2 substrate proteins, including several proteins important for chloroplast function, flowering time control, miRNA and chromatin regulation, and RNA splicing.
phosphoproteomic 磷酸化蛋白組學
chromatin 染色質
RNA splicing RNA拼接
最近磷酸化蛋白組學研究鑑定了數十個新的SnRK2的底物蛋白，包括一些調控葉綠體功能、開花時間、miRNA和染色質調節、RNA拼接相關的重要蛋白質。
The PYL-PP2C-SnRK2 core ABA-signaling module activates a MAPK cascade comprised of the MAP3Ks MAP3K17/18, the MAP2K MKK3, and the MAPKs MPK1/2/7/14, which may regulate many ABA effector proteins through phosphorylation.
PYL-PP2C-SnRK2核心ABA信號途徑激活一個由MAP3Ks MAP3K17/18、MAP2K MKK3以及MAPKsMPK1/2/7/14組成的MAPK級聯，後者可能通過磷酸化調節許多ABA的效應蛋白。
ABA-activated SnRK2s also phosphorylate the plasma-membrane NADPH oxidase RbohF, which when phosphorylated generates O2- in the apoplastic space. The O2- subsequently forms H2O2, a signaling molecule that mediates various ABA responses, including stomatal closure.
ABA激活的SnRK2s還磷酸化質膜NADPH氧化酶RbohF，磷酸化發生時在質外體空間產生O2- 。O2-隨後形成H2O2，作為信號分子調節包括氣孔關閉在內的各種ABA應答過程。
ABA induction of ROS in guard cells is impaired in Arabidopsis pip2;1 mutant plants, indicating that apoplastic H2O2 can enter cells via the aquaporin PIP2;1.
guard cells 保衛細胞
aquaporin 水通道蛋白
在擬南芥pip2;1突變體中，ABA誘導保衛細胞ROS產生減弱，表明質外的H2O2可以通過水通道蛋白PIP2;1進入細胞。
The MAP kinases MPK9 and MPK12 function redundantly in anion-channel regulation in guard cells downstream of ROS and affect ABA
regulation of stomatal closure.
MAP激酶MPK9和MPK12在ROS下遊保衛細胞的陰離子通道調節中和影響氣孔關閉的ABA調節中功能冗餘。
Another important component that connects ABA signaling and ROS is the plasma-membrane RLK GHR1. GHR1 interacts with and activates SLAC1. GHR1 is critical for ABA and ROS regulation of stomatal closure. Interestingly, GHR1 function is antagonized by ABI2 but not by ABI1.
另一個連接ABA信號和ROS的重要組件是質膜類受體蛋白激酶GHR1。GHR1與SLAC1互作並激活後者，GHR1對ABA和ROS調節的氣孔關閉至關重要。有趣的是，GHR1的功能被ABI2拮抗但不受ABI1影響。
H2O2 could also modulate the calcium signal to affect ABA responses, and GHR1 is required for H2O2 activation of plasma-membrane Ca2+channel.
H2O2也可以調節鈣信號從而影響ABA的應答，H2O2活化質膜鈣離子通道也需要GHR1的介導。
Calcium signaling is critical for ABA regulation of stomatal closure, and
mutant plants defective in four redundant calcium-dependent protein kinases, CPK5, CPK6, CPK11, and CPK23, are incapable of closing stomata in response to ABA.
鈣信號轉導對ABA調節氣孔關閉至關重要，ABA不能誘導缺失CPK5、CPK6、CPK11、CPK23四個功能冗餘的鈣依賴蛋白激酶的四突變體氣孔關閉。
Like the SnRK2s, CPKs can phosphorylate effectors (including SLAC1) of ABA responses in guard cells.
與SnRK2s一樣,CPKs可以磷酸化保衛細胞ABA響應的效應蛋白(包括SLAC1) 。
Furthermore, ABA-triggered calcium signal can activate the CBL1/9-CIPK26 module to cause phosphorylation of effector proteins such as RbohF.
此外，ABA引起的鈣信號可以激活CBL1/9-CIPK26模塊，導致RbohF等效應蛋白的磷酸化。
In addition to inducing H2O2 and calcium signals, ABA triggers the generation of nitric oxide (NO) and phospholipids such as phosphatidic acid.
除誘導H2O2和鈣信號外，ABA還觸發一氧化氮(NO)和磷脂(如磷脂酸)的產生。
NO causes the S-nitrosylation of a cysteine residue adjacent to the catalytic site of SnRK2s, resulting in inactivation of the kinases.
the S-nitrosylation of a cysteine residue
半胱氨酸殘基的巰基亞硝基化
adjacent 鄰近的
catalytic site 催化點，催化中心
NO導致鄰近SnRK2s的催化中心的半胱氨酸殘基的巰基亞硝基化，最終導致該激酶（SnRK2s）失活。
NO also causes tyrosine nitration and S-nitrosylation of cysteine residues in PYLs.
NO也導致PYLs蛋白的酪氨酸硝基化和半胱氨酸殘基的巰基亞硝基化。
Tyrosine nitration inhibits PYL activity and also accompanies polyubiquitylation and proteasome-mediated degradation of PYLs. Phosphatidic acid contributes to ABA signaling by binding to and activating RbohD and RbohF.
polyubiquitylation 多聚泛素化
proteasome-mediated 蛋白酶體介導的
酪氨酸硝基化抑制PYL活性並伴隨多聚泛素化和蛋白酶體介導的PYLs的降解。磷脂酸通過結合和激活RbohD和RbohF，參與ABA信號轉導。
Therefore, the in vivo regulation of SLAC1, Rbohs, and other effectors of ABA responses in plants requires a network of signaling pathways that include not only the PYL-PP2C-SnRK2 core pathway but also other pathways that involve calcium, ROS, NO, phospholipids, and the other kinases described above.
the in vivo regulation 體內調控
因此，植物中SLAC1、Rbohs以及其他ABA響應效應蛋白的體內調節依賴於一個包括PYL-PP2C-SnRK2核心途徑以及鈣、ROS、NO、磷脂和上述其他蛋白激酶途徑的複雜的調控網絡。
刷上去看看英文原文再複習一遍看能看還能看懂多少。