scholarly journals Mitogen-Activated Protein Kinase Phosphatases Affect UV-B-Induced Stomatal Closure via Controlling NO in Guard Cells

2016 ◽  
Vol 173 (1) ◽  
pp. 760-770 ◽  
Author(s):  
Feng-Chen Li ◽  
Jing Wang ◽  
Mi-Mi Wu ◽  
Cai-Ming Fan ◽  
Xuan Li ◽  
...  
2012 ◽  
Vol 25 (12) ◽  
pp. 1639-1653 ◽  
Author(s):  
Huajian Zhang ◽  
Deqing Li ◽  
Meifang Wang ◽  
Jiewen Liu ◽  
Wenjun Teng ◽  
...  

Many bacterial, fungal, and oomycete species secrete necrosis and ethylene-inducing peptide 1 (Nep1)-like proteins (NLP) that trigger programmed cell death (PCD) and innate immune responses in dicotyledonous plants. However, how NLP induce such immune responses is not understood. Here, we show that silencing of the MAPKKKα–MEK2–WIPK mitogen-activated protein kinase (MAPK) cascade through virus-induced gene silencing compromises hydrogen peroxide accumulation and PCD induced by Nep1Mo from Magnaporthe oryzae. WIPK interacts with NbWRKY2, a transcription factor in Nicotiana benthamiana, in vitro and in vivo, suggesting an effector pathway that mediates Nep1Mo-induced cell death. Unexpectedly, salicylic acid–induced protein kinase (SIPK)- and NbWRKY2-silenced plants showed impaired Nep1Mo-induced stomatal closure, decreased Nep1Mo-promoted nitric oxide (NO) production in guard cells, and a reduction in Nep1Mo-induced resistance against Phytophthora nicotianae. Expression studies by real-time polymerase chain reaction suggested that the MEK2–WIPK–NbWRKY2 pathway regulated Nep1Mo-triggered NO accumulation could be partly dependent on nitrate reductase, which was implicated in NO synthesis. Taken together, these studies demonstrate that the MAPK cascade is involved in Nep1Mo-triggered plant responses and MAPK signaling associated with PCD exhibits shared and distinct components with that for stomatal closure.


2008 ◽  
Vol 56 (4) ◽  
pp. 347 ◽  
Author(s):  
Xiaoping She ◽  
Xigui Song

By using pharmacological approaches and laser scanning confocal microscopy (LSCM) based on 4, 5-diaminofluorescein diacetate (DAF-2 DA), the roles of MAPKK/CDPK and their effects on nitric oxide (NO) levels of guard cells during darkness-induced stomatal closure in broad bean were investigated. The results indicated that both 2′-amino-3′-methoxyflavone (PD98059) (an inhibitor of mitogen-activated protein kinase kinase, MAPKK) and trifluoperazine (TFP) (a specific inhibitor of calcium-dependent protein kinase, CDPK) reduced the levels of NO in guard cells and significantly reversed darkness-induced stomatal closure, implying that MAPKK/CDPK mediate darkness-induced stomatal closure by enhancing NO levels in guard cells. In addition, as with NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO), but not with nitric oxide synthase inhibitor NG-nitro-L-Arg-methyl ester (L-NAME), PD98059 and TFP not only reduced 4,5-diaminofluorescein diacetate (DAF-2 DA) fluorescence in guard cells by sodium nitroprusside (SNP) in light, but also abolished NO that had been generated during a dark period, and reversed stomatal closure by SNP and by darkness, suggesting MAPKK and CDPK are probably related to restraining the NO scavenging to elevate NO levels in guard cells, during darkness-induced stomatal closure. The results also showed that both PD98059 and TFP reduced stomatal closure by SNP, implying that the possibility of MAPKK and CDPK acting as the target downstream of NO should not be ruled out. There may be a causal and interdependent relationship between MAPKK/CDPK and NO in darkness-induced stomatal closure, and in the process this cross-talk may lead to the formation of a self-amplification loop about them.


1998 ◽  
Vol 3 (1) ◽  
pp. 23-27 ◽  
Author(s):  
Kathryn Z Guyton ◽  
Myriani Gorospe ◽  
Xiantao Wang ◽  
Yolanda D Mock ◽  
Gertrude C Kokkonen ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document