The N-terminus of AtMSL10 interacts with its own C- terminus (bioRxiv)

Plants are equipped with multiple mechanosensitive (MS) ion channels that respond to external and internal mechanical perturbations. When one of these, AtMSL10, is overexpressed it leads to a cell death phenotype, although there is no discernible phenotype associated with its loss of function. Recently Basu et al. demonstrated a novel activation mechanism of AtMSL10 when transducing the effect of increased membrane tension: when the ion channel opened in response to membrane tension, a conformational change at MSL10 C-terminus occurred. This structural rearrangement causes the dephosphorylating of the N-terminus of AtMSL10, activated it and triggering MSL10-directed cell death. The authors also showed that AtMSL10 activation induces expression of several stress-responsive genes. This study is interesting for proposing a mechanism involving the intra- and/intermolecular interaction between N- and C- termini of the same protein and it also sheds lights on the process of how plants perceive and respond to stress. (Summary by Nanxun Qin) bioRxiv 10.1101/726521