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 ...

Sugar-induced anthocyanin accumulation has been observed in many plant species. We observed that sucrose (Suc) is the most effective inducer of anthocyanin biosynthesis in Arabidopsis (Arabidopsis thaliana) seedlings. Other sugars and osmotic controls are either less effective or ineffective. Analysis of Suc-induced anthocyanin accumulation in 43 Arabidopsis accessions shows that considerable natural variation exists for this trait. The Cape Verde Islands (Cvi) accession essentially does not respond to Suc, whereas Landsberg erecta is an intermediate responder. The existing Landsberg erecta/Cvi recombinant inbred line population was used in a quantitative trait loci analysis for Suc-induced anthocyanin accumulation (SIAA). A total of four quantitative trait loci for SIAA were identified in this way. The locus with the largest contribution to the trait, SIAA1, was fine mapped and using a candidate gene approach, it was shown that the MYB75/PAP1 gene encodes SIAA1. Genetic complementation studies and analysis of a laboratory-generated knockout mutation in this gene confirmed this conclusion. Suc, in a concentration-dependent way, induces MYB75/PAP1 mRNA accumulation. Moreover, MYB75/PAP1 is essential for the Suc-mediated expression of the dihydroflavonol reductase gene. The SIAA1 locus in Cvi probably is a weak or loss-of-function MYB75/PAP1 allele. The C24 accession similarly shows a very weak response to Suc-induced anthocyanin accumulation encoded by the same locus. Sequence analysis showed that the Cvi and C24 accessions harbor mutations both inside and downstream of the DNA-binding domain of the MYB75/PAP1 protein, which most likely result in loss of activity.

Genes for trehalose metabolism are widespread in higher plants. Insight into the physiological role of the trehalose pathway outside of resurrection plant species is lacking. To address this lack of insight, we express Escherichia coli genes for trehalose metabolism in Arabidopsis thaliana, which manipulates trehalose 6-phosphate (T6P) contents in the transgenic plants. Plants

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Sugars have a central regulatory function in steering plant growth. This review focuses on information presented in the past 2 years on key players in sugar-mediated plant growth regulation, with emphasis on trehalose 6-phosphate, target of rapamycin kinase, and Snf1-related kinase 1 regulatory systems. The regulation of protein synthesis by sugars is fundamental to plant growth control, and recent advances in our understanding of the regulation of translation by sugars will be discussed.

SummaryDespite the recent discovery that trehalose synthesis is widespread in higher plants very little is known about its physiological signi®cance. Here we report on an Arabidopsis mutant (tps1), disrupted in a gene encoding the ®rst enzyme of trehalose biosynthesis (trehalose-6-phosphate synthase). The tps1 mutant is a recessive embryo lethal. Embryo morphogenesis is normal but development is retarded and stalls early in the phase of cell expansion and storage reserve accumulation. TPS1 is transiently up-regulated at this same developmental stage and is required for the full expression of seed maturation marker genes (2S2 and OLEOSN2). Sucrose levels also increase rapidly in seeds during the onset of cell expansion. In Saccharomyces cerevisiae trehalose-6-phosphate (T-6-P) is required to regulate sugar in¯ux into glycolysis via the inhibition of hexokinase and a de®ciency in TPS1 prevents growth on sugars (Thevelein and Hohmann, 1995). The growth of Arabidopsis tps1±1 embryos can be partially rescued in vitro by reducing the sucrose level. However, T-6-P is not an inhibitor of AtHXK1 or AtHXK2. Nor does reducing hexokinase activity rescue tps1±1 embryo growth. Our data establish for the ®rst time that an enzyme of trehalose metabolism is essential in plants and is implicated in the regulation of sugar metabolism/embryo development via a different mechanism to that reported in S. cerevisiae.

Timing of germination is presumably under strong natural selection as it determines the environmental conditions in which a plant germinates and initiates its postembryonic life cycle. To investigate how seed dormancy is controlled, quantitative trait loci (QTL) analyses has been performed in six Arabidopsis thaliana recombinant inbred line populations by analyzing them simultaneously using a mixed model QTL approach. The recombinant inbred line populations were derived from crosses between the reference accession Landsberg erecta (Ler) and accessions from different world regions. In total, 11 delay of germination (DOG) QTL have been identified, and nine of them have been confirmed by near isogenic lines (NILs). The absence of strong epistatic interactions between the different DOG loci suggests that they affect dormancy mainly by distinct genetic pathways. This was confirmed by analyzing the transcriptome of freshly harvested dry seeds of five different DOG NILs. All five DOG NILs showed discernible and different expression patterns compared with the expression of their genetic background Ler. The genes identified in the different DOG NILs represent largely different gene ontology profiles. It is proposed that natural variation for seed dormancy in Arabidopsis is mainly controlled by different additive genetic and molecular pathways rather than epistatic interactions, indicating the involvement of several independent pathways. recombinant inbred lines | quantitative trait loci analyses | near isogenic lines | transcriptome analyses S eed dormancy is an important adaptive trait that together with flowering time is a primary component of the different life history strategies of plants (1). Seasonal timing of germination might well be a stronger factor conditioning the flowering time of Arabidopsis in the field than variation in the genetic basis for flowering time itself (2). Seed dormancy controls the timing of germination by arresting growth and development, despite the presence of favorable environmental conditions to complete germination. Specific environmental and developmental triggers can overcome this arrest. Environmental factors can act during seed development on the mother plant, during seed storage (i.e., after-ripening; AR) and in mature imbibed seeds. The various aspects of seed dormancy and germination have been extensively reviewed recently (3-6). In addition, it has been shown that there is considerable variation for seed dormancy in nature (7-9). The identification of the genes underlying this natural variation for seed dormancy may help to further understand the mechanisms involved in this process. At the same time, it provides insight into the way nature shaped genetic variability for this trait during adaptive evolution. A common approach to discover genes that control quantitative traits is the use of whole-genome scans to identify quantitative trait loci (QTL). These analyses provide estimates of several genetic parameters that underlie phenotypic variation, including the number of loci, th...