Nitric oxide inhibits blue light-induced stomatal opening by regulating the K+ influx in guard cells

Abstract

Blue light (BL)-induced stomatal opening and nitric oxide (NO)-promoted stomatal closure comprise two main aspects of stomatal regulation. Stomatal movement depends on ion fluxion in guard cells, whereas the physiological roles of BL or NO in regulating ion channel activities remain largely unknown. For gaining further insights into NO function in mediating BL-induced stomatal opening, guard cell protoplasts (GCPs) were patch-clamped in a whole-cell configuration. The results showed that twice BL pulses (100μmolm−2s−1 for 30s) effectively activated inward rectifying K+ channels by 67% and 20% in Vicia GCPs, respectively. In contrast, Red light (RL) showed little effect on inward rectifying K+ channels. In accord with this, BL also increased inward K+ currents by 54% in Arabidopsis thaliana wild type gl1, but not in phot1-5 phot2-1 (BL receptor phototropin deletion mutant). Sodium nitroprusside (SNP, a NO donor), at 100μM, inhibited BL-dependent K+ influx and stomatal opening, which were abolished by c-PTIO (a specific NO scavenger). These results indicated that NO inhibits BL-induced stomatal opening maybe through restricting the K+ influx across plasma membrane in guard cells.