I study wheat genetics, which aren’t quite like the pea plant pedigrees you may have learned about in high school biology. Whereas peas (and humans) inherit one copy of each gene from each parent (meaning everyone has two copies of each gene and is called “diploid”), wheat inherits three copies of each gene from each parent (so wheat has six copies of each gene and is called “hexaploid”). As you can imagine, this makes our Punnett squares quite a bit more complicated. Because “gluten” is really a word for many different types of wheat proteins, we have many different genes that encode “gluten.” Take these many different genes and multiply them by their six copies, and we are dealing with around a hundred different genes in one wheat variety (and there are many wheat varieties).
Mendel’s head would be spinning.
The human genetics of CeD aren’t so simple, either. We know some of the genes that predispose someone to get celiac disease, but we don’t completely understand why some people get it and some people don’t, or why their reactions are so different.
Taking all this together, we have a lot of different people and a lot of different gluten proteins that interact in a lot of different ways. While engineering a celiac-safe wheat variety is a great goal to shoot for, it will take a lot of time and effort- and the finished product will be a gluten-free cereal that lacks the structural integrity we value wheat for.
What can we do in the meantime? There is much to learn about the roles of different gluten proteins. Which are the worst triggers for CeD? Which are the most important for flour quality? By examining subsets of gluten proteins, we can get a better understanding of intermediate steps we can take within the larger objective of engineering celiac-safe wheat. For example, we recently found that knocking out a certain group of proteins, called the alpha-gliadins, can be beneficial both in terms of CeD reactivity and breadmaking quality. A win-win!