Plants retain the remarkable ability to continually adapt their development in response to nutrient availability, to maximise survival and fitness in a changing environment. The TARGET OF RAPAMYCIN (TOR) kinase has been characterised as a master regulator of the nutrition sensing pathway in all eukaryotes. TOR kinase senses nutrient and energy status to direct growth and development. Understanding of plant TOR complex components (TOR, LST8 and RAPTOR) and upstream and downstream targets has advanced tremendously in the past decade and TOR signalling has been implicated in a myriad of plant developmental processes. However, there is a significant lack of TOR characterisation beyond model plant species. KalanchoÃ« daigremontiana has evolved the ability to regain totipotency in the serrations of the leaf margin, from which develop plantlets. The mechanism behind the unique phenomenon of plantlet formation remains elusive but is known to recruit key regulators of organogenesis and embryogenesis and respond to favourable environmental conditions. We propose TOR kinase as the central regulator of plantlet formation, integrating external signals and developmental pathways to first trigger pluripotency, then direct plantlet development. Here we show that KdTOR inhibition both chemically (Torin2 application) and genetically (generation of 35S::KdTORantisense lines) significantly reduces plantlet formation. Downregulation of KdTOR also produces mutant phenotypes in the plantlets. We show, by qRT-PCR analysis and generation of KdTORp::GUS lines, that KdTOR is expressed during plantlet development. Taken together, expression and functional analyses suggest that KdTOR signalling is most crucial at the earliest stages of plantlet formation (to trigger pluripotency) and again at the initiation of the plantlet at the leaf pedestal. This work reveals the recruitment of the conserved TOR signalling pathway to a novel plant developmental process.