Calcium mediated nitric oxide responses: Acquisition of nickel stress tolerance in cyanobacterium Nostoc muscorum ATCC 27893

Calcium (Ca(2+)) and nitric oxide (NO) are potentially active and multitasking signaling molecules which are known to regulate abiotic stresses in plants, but their interactive role in the acquisition of metal stress tolerance in cyanobacteria remains elusive. In current study the signaling role of Ca(2+) (800 μM) and NO (10 μM SNP) on key physiological and biochemical attributes of the agriculturally and economically important cyanobacterium Nostoc muscorum ATCC 27893 subjected to Ni stress (2 μM) was examined. Results revealed that Ni at elevated level caused severe damages to the test organism but exogenous supplementation of Ca(2+) and NO efficiently mitigated its toxic effects and up-regulated the growth, pigment contents, rate of photosynthesis (whole cell oxygen evolution and Chl a fluorescence indices: Kinetic traits: ΦP(0,) Ψ(0), ΦE(0) and PI(ABS), along with Fv/F(0)), nitrogen metabolism (NO(3)‾ and NO(2)‾ uptake, nitrate:NR and NiR; and ammonia:GS and GOGAT; assimilating enzymes), and boosted the enzymatic (SOD, POD, CAT and GST) along with non-enzymatic (proline, cysteine and NP-SH) antioxidants. Whereas the increased values of energy flux traits: (ABS/RC, TR(0)/RC, DI(0)/RC and ET(0)/RC) along with F(0)/Fv, rate of respiration, oxidative stress biomarkers (SOR, H(2)O(2) and MDA), and activity of GDH enzyme exhibited lowering trends with application of Ca(2+) and NO. Further, addition of EGTA (Ca(2+) scavenger) and PTIO (NO scavenger) reversed the positive impacts of Ca(2+) and NO and worsened the toxicity of Ni on test cyanobacterium, but the damages were more pronounced under PTIO application that demonstrated Ca(2+) mediated signaling role of NO in Ni toxicity alleviation.