Yellow Canopy Syndrome (YCS) is a condition affecting sugarcane production in Australia. It is not evident whether biotic or abiotic factors trigger the onset of YCS development. The presentation will focus on the phenology of YCS development and the accompanying changes in physiology, the metabolome, transcriptome and proteome. Evidently, the development of YCS is a failure to export adequate amounts of sucrose and an inability to prevent sucrose accumulation in the leaf by redirecting carbon to starch. Expression of the sucrose transporters and SWEET proteins suggest that the failure to export sucrose is not linked to inadequate loading of the phloem. A conceptual model of the sequence of events occurring in leaf metabolism will be discussed. Early stages in sucrose accumulation triggers a reduction in CO2 fixation in the cytosol of the mesophyll cells through a reduction in PEPC expression and suppression of PEP regeneration by reducing PPDK in the mesophyll chloroplast. At the same time triose phosphate is preferentially allocated to starch synthesis. These reactions cause reduced electron flow through the ETC and increased ROS production. Initially it is primarily photosystem II in the mesophyll chloroplasts that are affected with most of the genes encoding the structural and function components of PSII downregulated. In addition to a redirection of carbon flow to starch, an upregulation of the phenylpropanoid and ascorbate synthesis pathways is a likely responseto reduce damage from ROS. As sucrose continue to build up in both the cytosol and apoplast, chloroplast metabolism in all compartments is suppressed and photoreaction centres are uncoupled from electron transport. This, linked to stomatal closure as a result of the increased sucrose levels, leads to elevated leaf temperatures, accelerated senescence and cell death.