Role of acetylcholine and acetylcholinesterase in improving abiotic stress resistance/tolerance.

Abiotic stress that plants face may impact their growth and limit their productivity. In response to abiotic stress, several endogenous survival mechanisms get activated, including the synthesis of quaternary amines in plants. Acetylcholine (ACh), a well-known quaternary amine, and its components associated with cholinergic signaling are known to contribute to a variety of physiological functions. However, their role under abiotic stress is not well documented. Even after several studies, there is a lack of a comprehensive understanding of how cholinergic components mitigate abiotic stress in plants. Acetylcholine hydrolyzing enzyme acetylcholinesterase (AChE) belongs to the GDSL lipase/acylhydrolase protein family and has been found in several plant species. Several studies have demonstrated that GDSL members are involved in growth, development, and abiotic stress. This review summarizes all the possible mitigating effects of the ACh-AChE system on abiotic stress tolerance and will try to highlight all the progress made so far in this field.

Acetylcholine suppresses shoot formation and callusing in leaf explants of in vitro raised seedlings of tomato, Lycopersicon esculentum Miller var. Pusa Ruby.

We present experimental evidence to show that acetylcholine (ACh) causes decrease in shoot formation in leaf explants of tomato (Lycopersicon esculentum Miller var Pusa Ruby) when cultured on shoot regeneration medium. The optimum response was obtained at 10(-4) M ACh-enriched medium. ACh also causes decrease in percentage of cultures forming callus and reduces the callus mass. Inhibitors of enzymatic hydrolysis of ACh, neostigmine and physostigmine, also suppresses callogenesis and caulogenesis. On the other hand, the breakdown products of Ach, choline and acetate, do not alter the morphogenic response induced on the shoot regeneration medium. Neostigmine showed optimal reduction in shoot formation at 10(-5) M. The explants cultured on neostigmine augmented medium showed decline in the activity of ACh hydrolyzing enzyme acetylcholinesterase. ACh and neostigmine added together showed marked reduction in callus mass. These results strongly support the role of ACh as a natural regulator of morphogenesis in tomato plants.

Nicotine promotes rooting in leaf explants of in vitro raised seedlings of tomato, Lycopersicon esculentum Miller var. Pusa Ruby.

Nicotine promotes rooting in leaf explants of tomato (Lycopersicon esculentum Miller var. Pusa Ruby). Nicotine at 10(-9) to 10(-3) M concentrations was added to the MS basal medium. The optimum response (three-fold increase in rooting) was obtained at 10(-7) M nicotine-enriched MS medium. At the same level i.e. 10(-7) M Nicotine induced dramatic increase (11-fold) in the number of secondary roots per root. We have shown earlier that exogenous acetylcholine induces a similar response in tomato leaves. Since nicotine is an agonist of one of the two acetylcholine receptors in animals, its ability to simulate ACh action in a plant system suggests the presence of the same molecular mechanism operative in both, animal and plant cells.

Acetylcholine causes rooting in leaf explants of in vitro raised tomato (Lycopersicon esculentum Miller) seedlings.

The animal neurotransmitter acetylcholine (ACh) induces rooting and promotes secondary root formation in leaf explants of tomato (Lycopersicon esculentum Miller var. Pusa Ruby), cultured in vitro on Murashige and Skoog's medium. The roots originate from the midrib of leaf explants and resemble taproot. ACh at 10(-5) M was found to be the optimum over a wide range of effective concentrations between 10(-7) and 10(-3) M. The breakdown products, choline and acetate were ineffective even at 10(-3) M concentration. ACh appears to have a natural role in tomato rhizogenesis because exogenous application of neostigmine, an inhibitor of ACh hydrolysis, could mimic the effect of ACh. Neostigmine, if applied in combination with ACh, potentiated the ACh effect.