We have all been told not to use table sugar as a starter medium. Well, continuous propagation using molasses as the carbon source is like making a starter using table sugar on steroids. Molasses is a byproduct from refining table sugar. It's mostly sucrose. While sucrose and maltose share the same chemical formula, C12H22O11, maltose consists of two glucose molecules bound by a glycosidic bound whereas sucrose has one glucose and one fructose molecule bound by a glycosidic bound. Yeast cells cannot use maltose and sucrose directly; therefore, the glycosidic bonds have to be broken. Maltase is used to break the glycosidic bound that holds the two glucose molecules together in maltose whereas invertase is used to break the glycosidic bound that holds the glucose and fructose molecules together in sucrose.
Now, stay with me on this one because I have a hypothesis (more like a SWAG) as to why US-05 behaves differently in dry form than it does in liquid form. It has to do with US-05 being a BRY 96 descendent. As I mentioned earlier, BRY 96 is a diploid. I also mentioned that diploids are relatively rare in brewing because they tend to be more unstable than polyploids from a genetic point of view. Diploids are more common in vinting and baking strains of S. cerevisiae, and the reason for that difference is more than likely due to the fact that wine and bread yeast strains are usually not sent through the process, collected, and reused. Repitching puts selective pressure on a culture, often favoring mutations. Diploids are more mutation prone than polyploids because the only time that there is a duplicate copy of a gene is when a yeast cell is homozygous for a gene, that is, it inherits an identical copy of the gene from both parents. I believe that a selective mutation to a gene for which BRY 96 is heterozygous (a different copy from each parent) is occurring during aerobic propagation that results in US-05 creating increased levels of benzyl alcohol, which, when combined with acetic acid, forms benzyl acetate; otherwise, known as the peach ester.
Let's describe this phenomenon in human terms. Colorblindness is a genetic mutation (specifically, a single-nucleotide polymorphism, or SNP) that occurs on a gene in the X chromosome that is part of the sex chromosome pair; namely, pair number 23. The reason why colorblindness is more common in men is that men only have one X chromosome in pair number 23. The other chromosome is a Y. As colorblindness is passed on the X, a man inherits colorblindness from his mother. Women, on the other hand, receive an X from both parents. If both parents pass a defective X, a woman will be colorblind; otherwise, she will be a carrier who will pass the defective gene to 50% of her offspring via an X chromosome.
Red hair is also a genetic mutation. It is a melanocortin receptor 1 (MC1R) mutation. However, in this case, the mutation occurs on chromosome 16, which means that the mutation affects both sexes the same way. A person has to inherit this mutation from both parents (i.e., be homozygous) in order to have red hair. However, this mutation has a heterozygous (inherited from one parent) expression as well. It's easier to see in men than in women because men have facial hair (okay, some women have facial hair as well). Men who carry one copy of the mutation will have brown hair and a reddish brown to ginger colored beard. Their body hair will also tend be the same color as their facial hair. The MC1R mutation in both inheritance patterns tends to result in people having fair skin that burns quickly when exposed the strong sunlight. The UK has the largest percentage of MC1R mutation carriers in the world.
Getting back to US-05, I do not believe that the mutation is in the seed culture. I believe that the mutation is the result of being propagated for a large number of generations in a medium that is not wort while consuming the carbon source almost exclusively through the respirative metabolic pathway. This practice puts selective pressure on the cells. My experience with the culture leads me to believe that the peach ester problem is a true mutation and not an initial pitch deviation that is due to aerobic propagation in a bioreactor.