NOS-derived NO modulates photosynthetic integrity, carbon metabolism and cellular homeostasis in the cyanobacterium Aphanizomenon flos-aquae under methyl viologen stress.

Photosynthetic organisms often face environmental challenges that disrupt cellular homeostasis. Of the various protective mechanisms, nitric oxide (NO) is a crucial signaling molecule with diverse regulatory functions. In mammalian cells, NO is enzymatically synthesized by nitric oxide synthase (NOS) and regulates several physiological processes such as neuronal differentiation, vascular relaxation, synaptic signaling, and immune regulation. Although recent studies have reported the presence of canonical NOS homologs in photosynthetic microorganisms, their function is yet to be elucidated. Hence, this study investigated the role of NOS-derived NO in mitigating the detrimental effects of the herbicide methyl viologen (MV) in the filamentous cyanobacterium Aphanizomenon flos-aquae 2012/KM1/D3. The findings revealed that NOS-derived NO regulated nonphotochemical quenching and alleviated photoinhibition, supporting photosynthetic efficiency under MV stress. At the cellular level, NOS-derived NO curbed lipid peroxidation and preserved membrane integrity, reinforcing structural defenses. Furthermore, it sustained photosystem gene expression and pigment biosynthesis, ensuring that the light-capture machinery remained intact. These protective effects were absent in L-NG-nitroarginine methyl ester-treated cells, in which the expression of gluconeogenic and pentose phosphate pathway enzymes was increased, likely compensating for the deficit in reducing power. Together, these findings establish the multifaceted role of NOS-derived NO signaling in reinforcing photosynthetic resilience.