The role of nitric oxide (NO) in plant responses to disturbed zinc homeostasis

Zinc (Zn) is an essential trace element for living organisms including plants, and sub- or supraoptimal amounts of available Zn induce stress responses. Nitric oxide (NO) signal molecule and its reaction products, the reactive nitrogen species (RNS) are involved in the regulation of numerous abiotic stress responses. Our knowledge regarding Zn deficiency is incomplete, thus in a preliminary experiment we showed that there is a correlation between the capability of mild Zn deficiency tolerance and the capability of root NO production. Additionally, in the case of severe Zn deficiency, the NO level responses proved to be species-dependent. Our computational analysis highlighted that among Arabidopsis Zn transporter proteins (ZIPs, MTPs, HMAs) there are numerous targets of NO-dependent S-nitrosation and tyrosine nitration indicating the regulatory role of NO in plant Zn transport. These observations support the putative role of NO in Zn deficiency responses, but further experimental confirmation is needed. Regarding excess Zn, the previously described oxidative stress processes have been supplemented by recent research which found that also RNS metabolism is affected and RNS-related signaling is increased in plants grown in the presence of supraoptimal Zn supply, but the alterations depend on the sensitivity of the plant species, the Zn concentration, and the duration of the treatment. According to the available data, the stress-relieving effect of exogenous NO is mediated by several mechanisms, such as the alleviation of oxidative stress due to the activation of antioxidants and the reduction of in planta Zn accumulation. Similar to the bulk form, nano-ZnO induces nitro-oxidative stress in plants in a way dependent on plant species, concentration, and particle size. Moreover, exogenous application of NO improves the performance of ZnO nanoparticle-treated plants by decreasing Zn ion accumulation, improving photosynthesis, and reducing oxidative stress due to the upregulation of antioxidants.