Defining the role of the ABI4 transcription factor in the sugar regulated control of storage oil breakdown in Arabidopsis

All living organisms maintain constant levels of soluble carbohydrates in their cells, and use these to support respiration and growth. In order to achieve this carbohydrate concentration is sensed and appropriate metabolic pathways are activated and repressed to increase or decrease the flow of carbon through essential processes as required. This process is known as metabolic feedback. Failure to regulate carbohydrate levels can lead to slow development or even disease, such as in the case of diabetes. In plants this process regulates the accumulation of stored reserves, which form much of the food we eat. Plants sense the intracellular concentration of soluble sugars and in times of excess up-regulate reserve deposition, such as starch synthesis, and in times of depletion up-regulate reserve breakdown, either from starch, fatty acids or amino acids from proteins. During early seedling development plants are dependent on the breakdown of stored fatty acids for their energy source, as they have not yet developed the apparatus for fixing carbon from the atmosphere through photosynthesis. Fatty acid catabolism can be inhibited by the provision of sugars, making this an excellent model system to study metabolic feedback networks in plants. We have recently shown that the ABI4 gene represses lipid breakdown in the model plant Arabidopsis. ABI4 encodes a transcription factor, meaning that it's function is to control the activity of other genes. Many of the known target genes of ABI4 are subject to regulation by metabolic status, suggesting a role in metabolic feedback control. ABI4 also functions in the response to the plant hormone ABA which is well known to play a role in plant sugar responses. This work aims to understand how metabolic feedback control works in plants, how ABI4 action is regulated and how ABI4 can turn off fatty acid catabolism in response to sugar levels.

Post-germinative fatty acid catabolism is inhibited by both sugars and ABA in a tissue specific fashion, and we have recently discovered that the APETALA2 transcription factor ABI4 mediates this regulation in Arabidopsis (Penfield et al., 2006, Plant Cell 18, 1887-1899). This is one of only a handful of cases where a specific regulatory protein has been linked to the regulation of primary carbon metabolism in plants. ABI4 and ABA control multiple sugar regulated metabolic processes in plants, suggesting that the function of ABI4 is of central importance in the feedback regulation of plant metabolism by sugar status. However, little is known of how ABI4 function is coupled with sugar signalling pathways, and few important primary targets of ABI4 have been identified. We have complemented the abi4-1 mutant with a construct overexpressing an epitope tagged ABI4 protein and show here that its protein abundance is regulated by soluble sugar levels. This important result demonstrates that ABI4 links sugar regulated gene expression directly to plant sugar sensing pathways, and suggests that ABI4 is a core component of the carbohydrate homeostatic feedback mechanism in plants. This project builds on existing strengths in the Graham lab in plant signalling and metabolism, and aims to elucidate how ABI4 protein abundance is coupled to soluble sugar levels and to understand in detail the ABI4 mediated feedback control of lipid breakdown by sugars.