Tag: Xiao H. L.

Ca(2+) plays dual and distinctive roles in the crosstalk between BL and NO signaling in stomata

 

Nitric oxide blocks blue light-induced K+ influx by elevating the cytosolic Ca2+ concentration in Vicia faba L. guard cells.

Zhao X., Li Y. Y., Xiao H. L., Xu C. S., Zhang X. (2013)

Zhao X1, Li YY, Xiao HL, Xu CS, Zhang X.
Institute of Plant Stress Biology, State Key Laboratory of Cotton Biology, College of Life Sciences, Henan University, Kaifeng 475004, China.

in Journal of Integrative Plant Biology 55, 527–536. -doi: 10.1111/jipb.12038 –

| CrossRef | CAS | PubMed | –

https://www.ncbi.nlm.nih.gov/pubmed?cmd=Retrieve&list_uids=23384172&dopt=Abstract

Abstract

Ca(2+) plays a pivotal role in nitric oxide (NO)-promoted stomatal closure. However, the function of Ca(2+) in NO inhibition of blue light (BL)-induced stomatal opening remains largely unknown.

Here, we analyzed the role of Ca(2+) in the crosstalk between BL and NO signaling in Vicia faba L. guard cells. Extracellular Ca(2+) modulated the BL-induced stomatal opening in a dose-dependent manner, and an application of 5 μM Ca(2+) in the pipette solution significantly inhibited BL-activated K(+) influx.

Sodium nitroprusside (SNP), a NO donor, showed little effect on BL-induced K(+) influx and stomatal opening response in the absence of extracellular Ca(2+), but K(+) influx and stomatal opening were inhibited by SNP when Ca(2+) was added to the bath solution.

Interestingly, although both SNP and BL could activate the plasma membrane Ca(2+) channels and induce the rise of cytosolic Ca(2+), the change in levels of Ca(2+) channel activity and cytosolic Ca(2+) concentration were different between SNP and BL treatments.

SNP at 100 μM obviously activated the plasma membrane Ca(2+) channels and induced cytosolic Ca(2+) rise by 102.4%. In contrast, a BL pulse (100 μmol/m(2) per s for 30 s) slightly activated the Ca(2+) channels and resulted in a Ca(2+) rise of only 20.8%.

Consistently, cytosolic Ca(2+) promoted K(+) influx at 0.5 μM or below, and significantly inhibited K(+) influx at 5 μM or above.

Taken together, our findings indicate that Ca(2+) plays dual and distinctive roles in the crosstalk between BL and NO signaling in guard cells, mediating both the BL-induced K(+) influx as an activator at a lower concentration and the NO-blocked K(+) influx as an inhibitor at a higher concentration.