Single-celled organisms living freely in nature, such as yeasts, face large variations in their natural environment. Environmental conditions that threaten the survival of a cell, or at least prevent it from performing optimally, are commonly referred to as cell stress. These environmental changes may be of a physical or chemical nature: temperature, radiation, concentrations of solutes and water, presence of certain ions, toxic chemical agents, pH and nutrient availability. In nature, yeast cells often have to cope with fluctuations in more than one such growth parameter simultaneously (Hohman & Mager, 2003). In industry, yeast stress has several very important practical implications. In brewing, for example, if yeast is nutrient-starved during extended periods of storage, certain cell surface properties such as flocculation capability are deleteriously affected (Walker, 1998).

Carotenogenic yeasts are considered to be ubiquitous due to its world-wide distribution in terrestrial, freshwater and marine habitats, and to its ability to colonize a large variety of substrates. They can assimilate various carbon sources, including waste materials as cheap substrates. The red yeast is able to grow under a wide range of initial pH conditions from 2.5 to 9.5 and over a wide range of temperatures from 5 to 26°C (Libkind et al., 2008; Latha et al., 2005). The most important consenquence of environmental stress in red yeast is stimulation of carotenoid and other secondary (as well as primary) metabolite production. Changes of ergosterol production, lipid content, glycerol and trehalose as well as membrane remodeling are described as a response to stress (Hohman & Mader, 2003). Carotenoid pigments accumulation in most yeasts starts in the late logarithmic phase and continues in the stationary phase and is highly variable. Carotenoid production depends on differences between strains of the same species and is strongly influenced by the cultivation conditions. Addition of stress factors into cultivation medium led to different changes of growth according to the yeast species, type of stress factor or growth phase, in which stress factors were added (Marova et al., 2004).

Carotenogenesis in many organisms is regulated by light. However, the intensity and protocol of illumination varies with the microorganism. Temperature is another important factor affecting the performance of cells and product formation. The effect of temperature depends on the species specificity of the microorganism and often manifests itself in quantity variations of synthesized carotenoids. It was reported that lower temperatures (25°C) seemed to favor synthesis of P-carotene and torulene, whereas higher temperatures (35°C) positively influenced torularhodin synthesis by R. glutinis (Frengova & Beshkova,

2007) . The effect of aeration is dependent on the species of the microorganism. The aeration influenced not only the amount of carotenoids produced, but also the composition of individual pigments making up the total carotenoids (Simova et al., 2004). At higher aeration, the concentration of total carotenoids increased relative to the biomass and fatty acids in R. glutinis, but the composition of carotenoids (torulene > p-carotene > y-carotene > torularhodin) remained unaltered. In contrast, S. roseus responds to enhanced aeration by a shift from the predominant p-carotene to torulene and torularhodin (Davoli, 2004). Also other inducers of oxidative stress such as irradiation and free radical generators have a significant effect on the carotenoid production. By UV mutagenesis of the pink yeast R. glutinis the yellow colored mutant 32 was obtained which produced 24-fold more total carotenoids (2.9 mg/ g dry cells) and 120-fold more p-carotene than the wild-type in a much shorter time (Bhosale & Gadre, 2001). Production of carotenoids by Rhodotorula glutinis cells grown under oxidative stress was about 5-6 times higher than in wild-type (Marova et al., 2004; Marova et al., 2010).

Tolerance to deleterious factors (e. g., low pH) refers to a microorganism’s ability to survive a stress. This phenomenon is described as adaptive response, induced tolerance, habituation, acclimatization or stress hardening. Once cells have been challenged with a mild stress, they become more resistant to severe stress. Also exposure to one type of stress has been demonstrated to lead to tolerance to other types of stress as well (cross-protection) (Hohman & Mager, 2003). When cells are shifted to stress environments, they respond with changes in the expression of hundreds or thousands of genes, revealing the plasticity of genomic expression. Some of the expression changes are specific to each new environment, while others represent a common response to environmental stress. Comparative analysis of the genomic expression responses to diverse environmental changes revealed that the expression of roughly 900 genes (around 14% of the total number of yeast genes) is stereotypically altered following stressful environmental transitions. The functions of these gene products may protect critical aspects of the internal milieu, such as energy reserves, the balance of the internal osmolarity and oxidation-reduction potential, and the integrity of cellular structures. The protection of these features by the stress gene products likely contributes to the cross-resistance of yeast cells to multiple stresses, in which cells exposed to a mild dose of one stress become tolerant of an otherwise-lethal dose of a second stressful condition (Hohman & Mager, 2003; Gasch & Werner-Washburne, 2002; Gasch et al., 2000).

A critical component of cell survival is maintaining a viable energy source. Glucose is the preferred carbon source in yeast, and upon stress, the cell induces a variety of genes that affect glucose metabolism. This includes genes encoding glucose transporters that serve to import external glucose into the cell and glucose kinases that activate the sugar for subsequent catabolism. In response to stressful environments, the fate of glucose is divided between trehalose synthesis, glycogen storage, ATP synthesis through glycolysis, and NADPH regeneration by the pentose phosphate shuttle (Hohman & Mager, 2003).