Methyl-coenzyme M reductase-dependent endogenous methane enhances plant tolerance against abiotic stress and alters ABA sensitivity in Arabidopsis thaliana.

Our study firstly elaborated the underlying mechanism of endogenous CH4-induced abiotic tolerance, along with an alteration of ABA sensitivity by mimicking the endogenous CH4 production in MtMCR transgenic Arabidopsis. Endogenous methane (CH4) production and/or emission have been ubiquitously observed in stressed plants. However, their physiological roles remain unclear. Here, the methyl-coenzyme M reductase gene from Methanobacterium thermoautotrophicum (MtMCR), encoding the enzyme of methanogenesis, was expressed in Arabidopsis thaliana, to mimic the production of endogenous CH4. In response to salinity and osmotic stress, MtMCR expression was up-regulated in transgenic plants, resulting in significant increase of endogenous CH4 levels. Similar results were observed in abscisic acid (ABA) treatment. The functions of endogenous CH4 were characterized by the changes in plant phenotypes related to stress and ABA sensitivity during the germination and post-germination periods. When challenged with osmotic stress, a reduction in water loss and stomatal closure, were observed. Redox homeostasis was reestablished during osmotic and salinity stress, and ion imbalance was also restored in salinity conditions. The expression of several stress/ABA-responsive genes was up-regulated, and ABA sensitivity, in particularly, was significantly altered in the MtMCR transgenic plants. Together, our genetic study for the first time elaborated the possible mechanism of endogenous CH4-enhanced salinity and osmotic tolerance, along with an alteration of ABA sensitivity. These findings thus provided novel cues for understanding the possible roles of endogenous CH4 in plants.