The perception of wine flavor and aroma is the result of a multitude of interactions between a large number of chemical compounds and sensory receptors. Compounds interact and combine and show synergistic (i.e., the presence of one compound enhances the perception of another) and antagonistic (a compound suppresses the perception of another) interactions. The chemical profile of a wine is derived from the grape, the fermentation microflora (in particular the yeast Saccharomyces cerevisiae), secondary microbial fermentations that may occur, and the aging and storage conditions. Grape composition depends on the varietal and clonal genotype of the vine and on the interaction of the genotype and its phenotype with many environmental factors which, in wine terms, are usually grouped under the concept of "terroir" (macro, meso and microclimate, soil, topography). The microflora, and in particular the yeast responsible for fermentation, contributes to wine aroma by several mechanisms: firstly by utilizing grape juice constituents and biotransforming them into aroma- or flavor-impacting components, secondly by producing enzymes that transform neutral grape compounds into flavor-active compounds, and lastly by the de novo synthesis of many flavor-active primary (e.g., ethanol, glycerol, acetic acid, and acetaldehyde) and secondary metabolites (e.g., esters, higher alcohols, fatty acids). This review aims to present an overview of the formation of wine flavor and aroma-active components, including the varietal precursor molecules present in grapes and the chemical compounds produced during alcoholic fermentation by yeast, including compounds directly related to ethanol production or secondary metabolites. The contribution of malolactic fermentation, ageing, and maturation on the aroma and flavor of wine is also discussed.

Pseudohyphal differentiation in Saccharomyces cerevisiae was first described as a response of diploid cells to nitrogen limitation. Here we report that haploid and diploid starch-degrading S. cerevisiae strains were able to switch from a yeast form to a filamentous pseudohyphal form in response to carbon limitation in the presence of an ample supply of nitrogen. Two genes, MSSIO and MUCI, were cloned and shown to be involved in pseudohyphal differentiation and invasive growth. The deletion of MSSIO resulted in extremely reduced amounts of pseudohyphal differentiation and invasive growth, whereas the deletion of MUCI abolished pseudohyphal differentiation and invasive growth completely. MsslO appears to be a transcriptional activator that responds to nutrient limitation and coregulates the expression of MUCI and the STAI-3 glucoamylase genes, which are involved in starch degradation. MUCI encodes a 1367-amino acid protein, containing several serine/threonine-rich repeats. Mucd is a putative integral membrane-bound protein, similar to mammalian mucin-like membrane proteins that have been implicated to play a role in the ability of cancer cells to invade other tissues.

Mutations in genes necessary for survival in stationary phase were isolated to understand the ability of wild-type Saccharomyces cerevisiae to remain viable during prolonged periods of nutritional deprivation. Here we report results concerning one of these mutants, rvsl67, which shows reduced viability and abnormal cell morphology upon carbon and nitrogen starvation. The mutant exhibits the same response when cells are grown in high salt concentrations and other unfavorable growth conditions. The RVS167 gene product displays significant homology with the Rvs161 protein and contains a SH3 domain at the C-terminal end. Abnormal actin distribution is associated with the mutant phenotype. In addition, while the budding pattern of haploid strains remains axial in standard growth conditions, the budding pattern of diploid mutant strains is random. The gene RVS167 therefore could be implicated in cytoskeletal reorganization in response to environmental stresses and could act in the budding site selection mechanism.In Saccharomyces cerevisiae, nutrient availability coordinates cell growth and proliferation. In medium containing all essential growth elements, yeast cells proliferate and cell growth and division are held in balance by the necessity of a minimum cell size before beginning a new division cycle (36). If one of the essential elements, for example, carbon or nitrogen, becomes exhausted, yeast cells stop division in the nonbudding G1 phase of the cell cycle (81). The culture then is in stationary phase, and cells can remain in the living state for prolonged periods under conditions which are not propitious for growth. Indeed, in their natural environment, yeast cells spend only a small fraction of their existence in exponential growth, because of the limited availability of nutriments.The transition from exponentially growing cells to arrested stationary-phase cells following nutrient starvation is accompanied by a number of molecular and physiological changes. At the molecular level, accumulation of glycogen and trehalose (48) is observed. The global analysis of proteins synthesized under starvation conditions reveals a subset of proteins whose synthesis increases in nutritional deprivation (9, 32). In addition, synthesis of most of the proteins expressed during exponential phase ceases (9). Physiological changes concern a higher resistance to heat shock (60), to lytic enzymes (20), and to a large number of other environmental stresses.There are mainly two questions related to stationaryphase entry. The first question concerns the mechanisms implied in cell proliferation control in response to the nutrient starvation. Some of the molecular regulatory elements of cell proliferation control are now relatively well-known in S. cerevisiae. Thus a multitude of observations has been taken as evidence that the cyclic AMP (cAMP) pathway could be a signal-transmitting pathway for growth arrest following nutrient exhaustion (35,50,77 sponding to the nutritional environment. Genetic evidence for the existence of at least...

The actin cytoskeleton cells is altered in rvs161 mutant yeast, with the defect becoming more pronounced under unfavorable growth conditions, as described for the rvs167 mutant. The cytoskeletal alteration has no apparent effect on invertase secretion and polarized growth. Mutations in RVS161, just as in RVS167, lead to a random budding pattern in a/alpha diploid cells. This behavior is not observed in a/a diploid cells homozygous for the rvs161-1 or rvs167-1 mutations. In addition, sequence comparisons revealed that amphiphysin, a protein first found in synaptic vesicles of chicken and shown to be the autoantigen of Stiff Man syndrome, presents similarity with both Rvs proteins. Furthermore, limited similarities with myosin heavy chain and tropomyosin alpha chain from higher eukaryotic cells allow for the definition of a possible consensus sequence. The finding of related sequences suggests the existence of a function for these proteins that is conserved among eukaryotic organisms.