H2O2, NO, and H2S networks during root development and signalling under physiological and challenging environments: Beneficial or toxic?

Hydrogen peroxide (H2O2) is a reactive oxygen species (ROS) and a key modulator of the development and architecture of the root system under physiological and adverse environmental conditions. Nitric oxide (NO) and hydrogen sulphide (H2S) also exert myriad functions on plant development and signalling. Accumulating pieces of evidence show that depending upon the dose and mode of applications, NO and H2S can have synergistic or antagonistic actions in mediating H2O2 signalling during root development. Thus, H2O2-NO-H2S crosstalk might essentially impart tolerance to elude oxidative stress in roots. Growth and proliferation of root apex involve crucial orchestration of NO and H2S-mediated ROS signalling which also comprise other components including mitogen-activated protein kinase, cyclins, cyclin-dependent kinases, respiratory burst oxidase homolog (RBOH), and Ca2+ flux. This assessment provides a comprehensive update on the cooperative roles of NO and H2S in modulating H2O2 homoeostasis during root development, abiotic stress tolerance, and root-microbe interaction. Furthermore, it also analyses the scopes of some fascinating future investigations associated with strigolactone and karrikins concerning H2O2-NO-H2S crosstalk in plant roots.

Automated summary

Hydrogen peroxide (H2O2) plays a crucial role in modulating root development and architecture under both normal and adverse environmental conditions. Nitric oxide (NO) and hydrogen sulphide (H2S) also have diverse functions in plant development and signaling. Depending on the dosage and application mode, NO and H2S can synergistically or antagonistically mediate H2O2 signaling during root development, thus enhancing tolerance to oxidative stress. This assessment provides a comprehensive update on the cooperative roles of NO and H2S in modulating H2O2 homeostasis during root development, abiotic stress tolerance, and root-microbe interaction.