Since I have a particular interest with acid production of yeast, mainly acetate, I take to opportunity to submit a follow up question specific on trying to make sure I understand the regulation of acetate production.
I've read a few articles on the topic and from what I think I understand, during anaerobic fermentations it's a cytosolic aldehyde dehydrogenase (ALD3) that seems responsible for acetate production, via NAD+ regeneration? For some reason I did not find this in the S.C Genome Database?
Is it newly discovered, or why?
I've read a few articles on the topic and from what I think I understand, during anaerobic fermentations it's a cytosolic aldehyde dehydrogenase (ALD3) that seems responsible for acetate production, via NAD+ regeneration?
For some reason I did not find this in the S.C Genome Database?
Is it newly discovered, or why?
Believe me the ALD3 gene is there in the SGD database, I have come across it before. If it is not giving you the gene try using ALD only as the query and it should return the list for the whole ALD family. ALD3 will be there. Otherwise try the CYGD at MIPS ( Munich Information Centre for Protein Sequences ) .
So it seems that acetate production has to do with the NAD+/NADH level in the cytosol as well as perhaps the cytosolic acetaldehyde stress?
Since acetaldehyde is supposedly a highly stressful and toxic compound I assume that unless it's promptly converted into ethanol maybe because of too high NAD+/NADH level (due to for example glycerol production?) or because of elevated acetaldehyde pools due to glycolysis overflow, the yeast has no choice but to dispose the acetaldehyde as acetate(??), even at the cost of being counterproducing regarding cytosolic pH, this conversion should also help restore the redox balance i the event that it was skewed.
The only "sense" I can see in the acetate production atm, is that it is:
1) either a way to get rid of the (even more) toxic acetaldehyde, when that starts to pool for some reason,
2) or a way to generate NADH when called for.
Then if you on top of this relate to nutrition and limited growth. Would it be decent enough to say that a reduced growth *might* in some cases lead to increased acetate because a declined demand for acetyl-CoA and thus less consumption of NAD+? So making some acetate make up for that? Or is the mechanism another one?
Of the genes in the ALD family only one is constantly being expressed and this is almost certainly to prevent the build up of acetaldehyde while producing acetate, which is one of the more central building blocks in yeast. The other enzymes are generally repressed by glucose and so are not an issue in this context. The enzyme that is constantly expressed does not use NAD+, but rather NADP+. So it is not entirely clear.
Also, since I've seen reports with correlations on elevated glycerol (HOG response) and elevated acetate as a means to restore the skewed redox balance caused by glycerol production? I've seen the HOG response would induce ALD3, and the cytosolic enzyme making acetate.
Can you briefly comment on this? Do you think it is anywhere near the truth or I am missing some other keys?
Once you start involving the HOG response you will be in an even worse situation,( can the HOG response over-ride the effect of Glucose repression?). Another thing to remember is that the HOG response will vary from strain to strain and it may even vary depending on the background of each particular propagation. Same yeast strain from different propagations may perform, principally, in the same manner, sugar to alcohol etc but there secondary, behaviors may very quite considerably.
Is there any chance that simple sugars, may induce a moderate HOG response? Now sucrose may be different as I still don't know the rate of inversion on the bulk sugar, but 1P glucose or fructose would initially have the osmotic influence as 2P maltose? Any chance the simple sugar - HOG response - acetate, can be a factor?
So far I made most of my sugarbrew tests with sucrose, could sucrose and the surface bound invertase enzymes somehow cause a HOG responses by messing with local sugar gradients around the cell wall and cell membrane cause an apparent higher osmotic stress somehow?
With the HOG response you may need more of one sugar than that of another. Plus if the yeast was to come from an environment where the HOG response had recently been elicited then it will probably take a bigger sugar concentration to elicit the response than before. I think this unlikely.
For the invertase to be present and active (in-between the cell wall and membrane) then there should a HOG response according to the level of sucrose. I do not believe the release of glucose and fructose would add to any HOG response. They will be transported quite rapidly and used by the yeast. The bigger risk with invertase may be that it's activity produces significant glucose levels to initiate the "Crabtree effect" and if this were to occur then the yeast would lose the invertase activity. However, I believe that this is unlikely in healthy yeast.
Typical industrial samples of invertase normally have rates of around 40 Units per mg........this means that in one minute 1mg of enzyme will convert 43 micromoles of Sucrose into invert sugars(at a given temp and pH) I have read reports of quite a varied level of activity for the enzyme in different yeasts, both Saccharomyces and non-Saccharomyces.