A Tenet Of Evolutionary Biology May Be Completely Wrong
Delving into the depths of newly published science in the field of biotechnology, welcome to Bioscription.
Not every tenet of science is set in stone. That’s often been seen in fields like physics and astronomy over the past few decades, where huge innovations and discoveries have been made.
But biology isn’t isolated from these sorts of findings. Today’s topic of discussion is new research that calls one of the tenets of evolutionary biology into question.
More Is Better
It has long been believed in the field of evolutionary biology that the reason why polyploidy, the duplication of genes and even entire genomes, occurs so frequently in organisms and especially in plastic plant genomes is that having duplicates offers more protection against negative mutations.
In addition, more copies of genes allows more experimentation with changing genes into new forms, without those changes harming or even killing the organisms. To put it another way, more copies of genes were thought to make the core genome more rigid and resilient to mutational forces that could otherwise harm them.
More Is Dangerous
But this might not be the case at all. New research from Laval University in Canada suggests that having this sort of duplicated redundancy effect can actually make the genome more fragile and likely to be damaged from mutational forces.
Well, the researchers were looking into bread yeast (Saccharomyces cerevisiae), an example of an organism fond of duplicating genes and a model organism in microbiology, and its 56 different copied genes. They then took those genes and measured their protein output and the activity of those proteins.
Afterwards, they ran the measurements against variants of the yeast that had slightly modified copies of the genes. They did this process thousands of times, compiling tens of thousands of data points.
What they found is that for 22 of the pairs of duplicates, they worked as expected. When one of them is mutated, the other takes over the original function. This is how it protects the core genome from being changed.
However, for 22 of the rest of the pairs, this didn’t happen. When one of the duplicated pair was mutated or removed, its protein copy did not take up the function as it should. They seemed to have formed a co-dependence that required both pairs to be functioning in order for cellular activity to be maintained.
This means that the genome actually had more targets for damaging mutations. Since, if either of the pair is mutated, it knocks out the entire functionality of the set.
How Can We Use This?
This cooperativity may explain certain disorders in humans that occur from mutations, even when there is still an intact gene copy. For example, the ability to distinguish certain colors and smells is due to duplications in the human genome. What this may mean is that certain forms of color blindness and lack of scent sensors may be due to mutations causing this double knockout effect.
Overall, a more in-depth understanding of the connection between gene function, protein activity, and expressed phenotype will help push forward scientific knowledge, both in the human medical field and in general.
Photo CCs: Scanning electron micrograph of phagocytosis of a dead yeast particle from Wikimedia Commons