The brassinosteroid signal transduction pathway

Steroids function as signaling molecules in both animals and plants. While animal steroid hormones are perceived by nuclear receptor family of transcription factors, brassinosteroids （BR） in plants are perceived by a cell surface receptor kinase, BRI 1. Recent studies have demonstrated that BR binding to the extracellular domain of BRI 1 induces kinase activation and dimerization with another receptor kinase, BAKI. Activated BRI 1 or BAKI then regulate, possibly indirectly, the activities of BIN2 kinase and/or BSU 1 phosphatase, which directly regulate the phosphorylation status and nuclear accumulation of two homologous transcription factors, BZRI and BES 1. BZRI and BES 1 directly bind to promoters of BR responsive genes to regulate their expression. The BR signaling pathway has become a paradigm for both receptor kinase signaling in plants and steroid signaling by cell surface receptors in general.

A positive feedback regulation of SnRK1 signaling by autophagy in plants

SnRK1,an evolutionarily conserved heterotrimeric kinase complex that acts as a key metabolic sensor in maintaining energy homeostasis in plants,is an important upstream activator of autophagy that serves as a cellular degradation mechanism for the healthy growth of plants.However,whether and how the autophagy pathway is involved in regulating SnRK1 activity remains unknown.In this study,we identified a clade of plant-specific and mitochondria-localized Fcs-like zinc finger(FLZ)proteins as currently unknown ATG8-interacting partners that actively inhibit SnRK1 signaling by repressing the T-loop phosphorylation of the catalyticαsubunits of SnRK1,thereby negatively modulating autophagy and plant tolerance to energy deprivation caused by long-term carbon starvation.Interestingly,these AtFLZs are transcriptionally repressed by low-energy stress,and AtFLZ proteins undergo a selective autophagy-dependent pathway to be delivered to the vacuole for degradation,thereby constituting a positive feedback regulation to relieve their repression of SnRK1 signaling.Bioinformatic analyses show that the ATG8-FLZ-SnRK1 regulatory axis first appears in gymnosperms and seems to be highly conserved during the evolution of seed plants.Consistent with this,depletion of ATG8-interacting ZmFLZ14 confers enhanced tolerance,whereas overexpression of ZmFLZ14 leads to reduced tolerance to energy deprivation in maize.Collectively,our study reveals a previously unknown mechanism by which autophagy contributes to the positive feedback regulation of SnRK1 signaling,thereby enabling plants to better adapt to stressful environments.