Plants encounter a number of environmental stresses throughout their life cycles, most of which activate mitogen activated protein kinase (MAPK) pathway. The MAPKs show crosstalks at several points but the activation and the final response is known to be specific for particular stimuli that in-turn activates specific set of downstream targets. Interestingly, reactive oxygen species (ROS) is an important and common messenger produced in various environmental stresses and is known to activate many of the MAPKs. ROS activates a similar MAPK in different environmental stimuli, showing different downstream targets with different and specific responses. In animals and yeast, the mechanism behind the specific activation of MAPK by different concentration and species of ROS is elaborated, but in plants this aspect is still unclear. This review mainly focuses on the aspect of specificity of ROS mediated MAPK activation. Attempts have been made to review the involvement of ROS in abiotic stress mediated MAPK signaling and how it differentiates with that of biotic stress.

Plants confront multifarious environmental stresses widely divided into abiotic and biotic stresses, of which heavy metal stress represents one of the most damaging abiotic stresses. Heavy metals cause toxicity by targeting crucial molecules and vital processes in the plant cell. One of the approaches by which heavy metals act in plants is by over production of reactive oxygen species (ROS) either directly or indirectly. Plants act against such overdose of metal in the environment by boosting the defense responses like metal chelation, sequestration into vacuole, regulation of metal intake by transporters, and intensification of antioxidative mechanisms. This response shown by plants is the result of intricate signaling networks functioning in the cell in order to transmit the extracellular stimuli into an intracellular response. The crucial signaling components involved are calcium signaling, hormone signaling, and mitogen activated protein kinase (MAPK) signaling that are discussed in this review. Apart from signaling components other regulators like microRNAs and transcription factors also have a major contribution in regulating heavy metal stress. This review demonstrates the key role of MAPKs in synchronously controlling the other signaling components and regulators in metal stress. Further, attempts have been made to focus on metal transporters and chelators that are regulated by MAPK signaling.

MYC2, a bHLH TF, acts as regulatory hub within several signaling pathways by integration of various endogenous and exogenous signals which shape plant growth and development. However, its involvement in salt stress regulation is still elusive. This study has deciphered a novel role of MYC2 in imparting salt stress intolerance by regulating delta1 ‐pyrroline‐5‐carboxylate synthase1 (P5CS1) gene and hence proline synthesis. P5CS1 is a rate‐limiting enzyme in the biosynthesis of proline. Y‐1‐H and EMSA studies confirmed the binding of MYC2 with the 5′UTR region of P5CS1. Transcript and biochemical studies have revealed MYC2 as a negative regulator of proline biosynthesis. Proline is necessary for imparting tolerance toward abiotic stress; however, its overaccumulation is toxic for the plants. Hence, studying the regulation of proline biosynthesis is requisite to understand the mechanism of stress tolerance. We have also studied that MYC2 is regulated by mitogen‐activated protein kinase (MAPK) cascade mitogen‐activated protein kinase kinase 3‐MPK6 and vice versa. Altogether, this study demonstrates salt stress‐mediated activation of MYC2 by MAPK cascade, regulating proline biosynthesis and thus salt stress.

Mitogen-activated protein kinase (MAPK) pathways are involved in several signal transduction processes in eukaryotes. Light signal transduction pathways have been extensively studied in plants; however, the connection between MAPK and light signaling pathways is currently unknown. Here, we show that MKK3-MPK6 is activated by blue light in a MYC2-dependent manner. MPK6 physically interacts with and phosphorylates a basic helix-loop-helix transcription factor, MYC2, and is phosphorylated by a MAPK kinase, MKK3. Furthermore, MYC2 binds to the MPK6 promoter and regulates its expression in a feedback regulatory mechanism in blue light signaling. We present mutational and physiological studies that illustrate the function of the MKK3-MPK6-MYC2 module in Arabidopsis thaliana seedling development and provide a revised mechanistic view of photomorphogenesis.

Mitogen-activated protein kinase (MAPK) signal transduction networks have been extensively explored in plants; however, the connection between MAPK signalling cascades and submergence tolerance is currently unknown. The ethylene response factor-like protein SUB1A orchestrates a plethora of responses during submergence stress tolerance in rice. In the present study, we report that MPK3 is activated by submergence in a SUB1A-dependent manner. MPK3 physically interacts with and phosphorylates SUB1A in a tolerant-allele-specific manner. Furthermore, the tolerant allele SUB1A1 binds to the MPK3 promoter and regulates its expression in a positive regulatory loop during submergence stress signalling. We present molecular and physiological evidence for the key role of the MPK3-SUB1A1 module in acclimation of rice seedlings to the adverse effects of submergence. Overall, the results provide a mechanistic understanding of submergence tolerance in Oryza sativa.