Regulatory role of Ca2+ and NO in salicylic acid (SA) induced signaling
against Ni2+-induced toxicity in Anabaena sp. PCC 7120
Abstract
Present study deals with the regulation of SA induced Ca2+-mediated NO
signaling in cyanobacterium Anabaena PCC 7120. Nickel (Ni2+)-toxicity
strongly inhibited growth (DW), exopolysaccharides, photosynthetic
pigments, PSII photochemistry (OJIP transient parameters: Fm, Fv, Fm/Fo,
Fv/Fo, Ψo, ФPo, ФEo, Area, N, and PIABS were suppressed; while Fo,
Fo/Fm, Fo/Fv, Sm, ФDo, ABS/RC, TRo/RC, ETo/RC and DIo/RC were raised),
nitrogen metabolism status and non-enzymatic antioxidant system by
increasing intracellular Ni2+ accumulation and excessive ROS production.
However, salicylic acid (SA), calcium (CaCl2) and sodium nitroprusside
(SNP) addition to the culture medium counteracted on negative impact of
Ni2+ thereby improving the growth. Further, to investigate the relation
between Ca2+ and NO, when c-PTIO was supplemented to Ni+SA+Ca and EGTA
to Ni+SA+NO treated culture medium, the recovery on above studied traits
caused due to Ca2+ and NO was arrested even in presence of SA to
Ni2+-stressed Anabaena cells thereby suggesting the signaling behavior
of Ca2+ and NO in SA induced pathway; however, the impact was worsened
under c-PTIO supplemented Ni+SA+Ca than EGTA supplemented Ni+SA+NO
treatment thereby suggesting key role of NO in SA-induced Ca2+-mediated
signaling. Additionally, NO accumulation, intracellular Ni2+
accumulation, ROS and indices, and non-enzymatic antioxidant system were
also examined that showed varied results.