now...before everyone starts freaking out about this study not conducted on seawater bacteria...you're right!!! it is a study done on bacteria. do all bacteria metabolize...nope...but, hoepfully, this may end some speculation...
a little bit of digging and a little bit of scientific experience in skimming through a lot of research...
here's the whole thing if you want to skip my skimming...plus, i may have missed something...
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=387754
ABSTRACT:
We have discovered a microbial interaction between yeast, bacteria, and nematodes.
several natural isolates of Acinetobacter. This enhanced growth was due to a diffusible factor that was shown to be ethanol by chemical assays and evaluation of strains lacking ADH1, ADH3, and ADH5, as all three genes are involved in ethanol production by yeast. This effect is specific to ethanol: methanol, butanol, and dimethyl sulfoxide were unable to stimulate growth to any appreciable level. Low doses of ethanol not only stimulated growth to a higher cell density but also served as a signaling molecule: in the presence of ethanol,
Our results are consistent with the concept that ethanol can serve as a signaling molecule which can affect bacterial physiology and survival.
RESULTS:
The enhanced growth factor is ethanol. One compound that possesses all of the properties of the growth-enhancing factor (produced by late-log cultures of yeast, small, heat and protease resistant, volatile) is ethanol. Thus, we tested the ability of ethanol to affect the growth of AD321 (Fig. 3). A 95% ethanol solution was diluted in YPAD to various concentrations ranging from 0 to 9.5%. Acinetobacter strain AD321 growth was enhanced by 50% in medium containing low levels of ethanol (0.1%), and the bacterial cell density more than doubled in medium containing between 1 and 4% ethanol;
This enhanced-growth effect appears to be specific to ethanol, in that dimethyl sulfoxide or methanol did not enhance bacterial growth. In fact, these latter solvents inhibited bacterial growth by 8.5 to 17.9% at concentrations of up to 5%
We reasoned that if ethanol concentration were the primary determinant for enhancement of bacterial growth, then increasing the amount of ethanol produced by yeast should also result in an increase in bacterial growth enhancement up to a certain percentage,
YJM835 grown in the fermentable sugars glucose, fructose, or sucrose produced 0.93% ± 0.2% ethanol and enhanced bacterial growth by 53.6% ± 6.3%. Cells grown in glycerol neither produced significant amounts of ethanol (0.03% ± 0.1% ethanol) nor enhanced bacterial growth (−2.54% ± 2.97% growth enhancement), suggesting that yeast-derived ethanol may be the stimulatory component.
FIG. 5.
Ethanol is required for bacterial growth enhancement. (A) YJM835 cells were grown in YPAD or YP plus each of the carbon sources listed to a cell density of 5 Ã"” 107 to 7 Ã"” 107 cells/ml. Media were sterilized, and ethanol concentration was determined as described in Materialsand Methods. Bacteria were grown overnight in CY medium at room temperature, and cell densities were measured by the OD600. Cell densities are shown as the percent enhancement or inhibition compared to that of cells grown in YPAD alone. (B) Gene deletions were performed as described in Materials and Methods. Cells were grown in YPAD, conditioned media were sterilized, ethanol concentrations were determined, and bacteria were cultured as described above. (C) YJM835 cells were grown in YPAD or YP plus glucose at the concentrations listed to a cell density of 5Ã"” 107 to 7 Ã"” 107 cells/ml. Conditioned media were sterilized, ethanol concentrations were determined, and bacteria were cultured as described above. For all panels, columns represent bacterial growth enhancement and lines indicate ethanol concentration.
To determine if the ethanol produced by YJM835 is necessary to enhance the growth of AD321, we disrupted the genes responsible for ethanol production in an attempt to specifically remove ethanol from yeast-conditioned medium........
ADH1 is the cytoplasmic isoform of alcohol dehydrogenase and the major enzyme required for the conversion of acetaldehyde to ethanol ........
In our study, deletion of ADH1 resulted in a 50% decrease in the amount of ethanol produced and a reduction in bacterial growth-enhancing capacity
Ethanol induces a specific cell tolerance response. Along with salt and heat, ethanol is a commonly used stimulus to induce the general stress response in many bacteria (14, 30, 32). While the typical ethanol concentrations used for general stress stimulation are considerably higher than the concentrations produced by yeast in YPAD (4 versus 1%), it is possible that low concentrations of ethanol can also elicit a stress response. In low doses, ethanol might serve a signaling role by specifically altering the physiology of the bacterial cells.
To test this hypothesis directly, we incubated Acinetobacter cells in the presence of ethanol or butanol and challenged these cells with salt stress. As shown above, bacteria grown in 2.5% NaCl (or KCl) were inhibited from growing by 44.2%. However, medium supplemented with 0.1% ethanol resulted in a 196% increase in bacterial growth. In contrast, addition of 0.01% butanol (a concentration that induces a similar amount of plasma membrane desaturation as 0.1% ethanol in Acinetobacter spp. [19]) resulted in only a 59% increase in growth over cells grown in salt alone.
DISCUSSION:
Ethanol stimulates acinetobacters to grow to higher cell density, as measured both by optical density and by counting the number of CFU. Since ethanol is consumed by these bacteria (unpublished observation), it is likely utilized as a carbon source (albeit a poor one, since it is present at low levels). However, the benefit of ethanol to acinetobacters extends beyond increasing cell number. Ethanol stimulates salt tolerance but not thermotolerance or resistance to oxidative damage in acinetobacters. Ethanol-fed acinetobacters can also kill a natural predator more efficiently than bacteria fed other carbon sources. These data indicate that ethanol also induces signaling pathways required for specific stress tolerance and virulence.
Although our studies were confined to the laboratory, we expect them to be pertinent to nature, as they involve organisms that we predict to interact in nature.
It is possible that the relationship between the two microbes is proto-commensalistic. That is, in certain environments the bacteria benefit, while in others the yeast benefit. The preferred carbon source for the yeast Saccharomyces is sugar, as its name indicates. Yeast typically ferment sugar into ethanol and carbon dioxide, even in the presence of oxygen,
Thus, many acinetobacters would be dependent on yeast to convert a plentiful sugar source into a more readily catabolized one, namely ethanol. The reciprocal situation may also exist, in which acinetobacters metabolize compounds that yeast cannot and provide yeast with a more suitable metabolite.
hope this was helpful in a little way!!!
