Information concerning the sugar status of plant cells is of great importance during a11 stages of the plant life cycle. The availability of or lack of sugars triggers many metabolic and developmental responses, and it is not surprising, therefore, that sugars profoundly affect the expression of a large number of genes (for review, see Koch, 1996;Graham, 1996). Sugar sensing occurs at the level of individual cells and the responses of such cells must be integrated at the tissue, organ, and plant level. Therefore, sugar-induced signals will interact with other sensing and signaling pathways. The mechanisms used by plant cells to sense sugars and to process this information are essentially unknown, and only recently are these questions being addressed experimentally. This lack of knowledge contrasts with the situation in yeast and bacteria, in which the molecular and physiological analysis of mutants have yielded extensive information about sugar perception (Trumbly, 1992;Ronne, 1995;Saier et al., 1995).
SUGAR SENSING IN YEAST A N D ANIMALSYeast (Sacckauomyces ceuevisiae) serves as a model for investigating many basic biological questions about eukaryotes and is also an important paradigm for sugar sensing in plants. In yeast the availability of the preferred sugar substrate Glc signals the Glc repression phenomenon (for review, see Trumbly, 1992;Ronne, 1995;Thevelein and Hohmann, 1995). Glc repression dramatically alters yeast intermediary carbohydrate metabolism such that only Glc is being used as a carbon source, despite the presence of other readily accessible carbon sources. Glc is converted into Glu-6-P by HXK and is further metabolized via glycolysis. Genes involved in the metabolism of other carbon substrates are switched off, as are genes encoding key steps in gluconeogenic metabolism. A number of yeast mutants that are impaired in aspects of the Glc repression phenomenon have been isolated and their analysis has provided insight into the complexity of sugar sensing and signaling pathways. From these studies it was concluded that the Glc-phosphorylating enzyme HXK2 is a major Glc sensor responsible for sus- tained Glc repression. HXK2 activity initiates a signal transduction pathway that involves a number of different gene products (Fig. 1) and results in the repression of a large set of genes. Thus, the entry of Glc into glycolytic metabolism as mediated by HXK2 is a key step in Glc sensing.In the repression pathway the function of two protein complexes has been elucidated. These are the GLC7 type 1 protein phosphatase complex (Tu and Carlson, 1995, and refs. therein) and the SSN6/TUP1 complex, which functions as a general repressor of transcription through modulation of chromatin structure. Binding of the SSN6/TUP1 complex to specific sites is directed by the DNA-binding protein MIG1, and in this way genes that contain MIG1-binding sites are repressed. Exactly how the HXK2, GLC7, and SSNG/TUPl /MIG1 complexes are connected is unknown. For example, in the repression pathway no substrates for the REG1 ...