TOR-mediated translational control of cytokinin homeostasis in shoot apical meriSTEM

Objective

Plant growth and organogenesis depend on the ability of meristems to integrate metabolic signals with developmental pathways. The shoot apical meristem (SAM) is a key developmental hub where nutrient availability and hormonal cues, particularly cytokinin, coordinate cell proliferation and organ initiation. The conserved kinase Target of Rapamycin (TOR) acts as a central regulator of these inputs, and its activity is essential for meristem activation and stem cell maintenance. Work from the host lab has shown that light and sugar activate TOR, which in turn promotes expression of the stem cell regulator WUSCHEL (WUS) and enables proper SAM function. Recent findings further reveal that TOR sustains shoot growth by repressing the translation of CKX transcripts, which encode cytokinin-degrading enzymes, thereby preserving cytokinin levels required for WUS expression and meristem activity. However, the mechanism behind this selective translational control remains unknown. TORcySTEM (TOR–cytokinin–merisSTEM axis) will dissect this regulatory pathway through three objectives: 1) Identify TOR-sensitive cis-regulatory elements within CKX transcripts; 2) Discover TOR-regulated trans-acting effector proteins; 3) Establish how this control shapes cytokinin signaling and SAM function. Together, these aims will uncover how TOR-dependent translational control fine-tunes cytokinin homeostasis and stem cell activity, providing a mechanistic link between metabolism and shoot development.