Biological factors driving YCS
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Yellow Canopy Syndrome (YCS) was first observed in 2012 in the Central and Northern cane-growing regions in Australia and has since spread much further south. The 2015 season is particularly bad in the Mackay and Proserpine regions. YCS is still an undiagnosed condition and is not correlated to mineral nutrient deficiency or any known sugarcane pathogens. When the severity of YCS expression is high and appears several times during the season, more than 50% crop loss can occur. In this project, we have established that expression of YCS is associated with an increase in soluble sugars, especially sucrose, glucose, fructose, and trehalose in the leaves. There is also a significant suppression of leaf photosynthesis, reduced stomatal conductance, increased variable fluorescence, and accumulation of abscisic acid. This disturbance in leaf metabolism is evident throughout the canopy even in the absence of visual yellowing. It is a common comment from growers and productivity services staff that YCS is associated with a slowdown in growth and sometimes the crop does not respond at all to rainfall and other favourable growth conditions. In many ways, this is typical of the reduced growth phenomenon (RGP). There cannot be any doubt of yield loss occurring when YCS symptoms appear. We have identified more than 200 metabolites from an extraction cohort of more than 1500. The most striking differences relate to changes in sugars. However, there are additional changes that could be very important. Firstly, there are significant levels of mannitol, kestose, and lactose in the samples prepared from YCS expressing tissues. These are indicative of microorganisms (Leuconostoc) that normally associate with injured tissue, especially where there are significant available carbohydrates. Secondly, there are increases in various organic and amino acids, some of which are indicative of abiotic stress. Thirdly, there are significant increases in several stress related metabolites, such as caffeoyl/chlorogenic type compounds, which are indicative of wounding and activation of plant defence systems. We have sequenced the transcriptome of control and YCS symptomatic leaves. The results indicate YCS has a wide impact on primary, secondary, and regulatory metabolism. Close to 4000 genes are upregulated greater than 5 fold in the YCS symptomatic leave tissue. We have ascribed a putative identity to 3191 of these sequences. More than 500 of the sequences are upregulated greater than 100 fold. These genes include those involved in protease regulation, sugar metabolism and transport, responses to auxin and abscisic acid (ABA) levels, chloroplast and heat shock protein production, regulation of ubiquitin conjugating enzymes and several cytochrome P450 genes. More than 2000 genes are down regulated in the YCS symptomatic leaves. A putative identity has been ascribed to 1263 of these. More than 150 of these are down regulated more than 100 fold. Functions associated include those of chloroplast structural and function genes, senescence related genes, transcription factors, phosphofructokinases, glycolytic enzymes, pathogenesis related genes, trehalose metabolism genes, and primary carbon fixation genes. The metabolome and transcriptome databases that were developed in this project will form the core of continued work on YCS. In addition, this will be an invaluable database for any further research on sugarcane responses to stress and sugar level control. Based on the results obtained in this study we propose that the development of YCS symptoms in sugarcane is driven by an accumulation of sucrose, glucose and fructose. The increase in sugars is already evident in leaf 3 and older while symptom expression mostly occurs much lower in the canopy. The pattern of yellowing shows remarkable resemblance with those in maize mutants that are defective in sucrose loading of the phloem and phloem translocation of sugars in the minor veins. The accumulation of sucrose at the site of phloem loading in the minor vein is likely to create feedback inhibition on photosynthesis, as well as partially disrupt electron transport, which then leads to enhanced sucrose levels at the stomata. This would result in partial stomata closure, which further compromises photosynthetic efficiency and evaporative cooling. This combination of reduced stomatal conductance together with electron transport inefficiency will make the crop particularly vulnerable to environmental stresses such as water and heat. In older leaves where photosynthesis and metabolism is already reduced to natural leaf senescence, these stress events are enough to ‘push’ the metabolism over a threshold where photo-oxidation and the disruption of metabolism triggers yellowing.