A commendable attitude I have to say. There’s absolutely nothing wrong with asking questions.
Yes this is a topic that sows an awful lot of confusion, among other things because scientists honestly aren’t being all that clear on this topic either.
I think you need to separate out these two questions:
- What is the selective effect of most mutations that occur and go to fixation across some organism’s genome, over generations?
- How does some specific, clearly adaptively beneficial organismal attribute, originate and subsequently evolve?
The idea is that a majority of mutations that go to fixation are selectively neutral, but there is still some small but significant portion that have selectively beneficial effects, and thus can contribute to optimizing some adaptation.
But you’re probably also thinking about two other things, which are rarely well articulated in these matters. You want to understand the relationship between evolutionary innovation, molecular complexity, and adaptation.
To what extend do mutations that occur and go to fixation constitute innovative mutations?(how often do mutations result in novel biological functions?).
To what extend do mutations that occur and go to fixation contribute to increases in molecular complexity? (like adding more functional genes to the genome, adding more proteins to some existing structure, and ultimately result in more complex multicellular organisms with multiple distinct organs and all that stuff)
To what extend do mutations that occur and go to fixation contribute to increases in reproductive success?
It’s important to understand that these three issues are not the same thing, and the relationship between them is complicated, depends on circumstance, and can be found anywhere from being correlated to anti-correlated.
-
Complexity can go up while fitness goes down, while number of total functions remains the same. Think of mere duplication resulting in multiple unnecessary gene-copies that negatively affects some organisms metabolic budget by the cost of expressing them, leading to a slight fitness decline. Genomic complexity has gone up as the number of functional genes and genome size has increased, but it has incurred a slight fitness loss. No new function was gained.
-
Complexity and fitness can remain the same while number of total functions goes up.
Think of point mutations that make some enzyme able to act on a novel substrate and break it down without altering it’s existing function, but the organism has no use for these novel break down products. Number of functions have gone up, but the organism is unaltered in terms of fitness or complexity. -
Fitness and functions can go up while complexity decreases.
An organism is suffering deletions in some gene, which makes the gene relocate to another part of the cell when expressed, which alters it’s morphology so it becomes better able to resist an antibiotic. It’s evolved a new function through a deletion(decreasing it’s genomic complexity), and this function happened to be beneficial.
And of course many other variations on those themes.
One can imagine, and find innumerable examples of mutations that have such effects. There IS NO easy or obvious relationship between fitness, innovation, or complexity. They can all go up or down independently of each other. Sad but true.
Evolution is not thought by any extant evolutionary biologist to constitute one long unobstructed gain in organismal complexity (or reproductive fitness) through the history of life. Lots of existing genes can be duplicated and degrade to mutations, and this can be beneficial, or it can be deleterious, or it can be neutral, and new functions can be found once in a while that might suddenly become beneficial and be super-optimized by positive selection.
That said, neutral processes can contribute to the evolution of both complexity and novel functions in something called constructive neutral evolution. Selection still plays a role in this process, but it’s mostly through so-called negative selection. Removing deleterious variants while merely retaining still functional ones.
It’s important to understand that complexity is not necessarily beneficial, nor necessarily deleterious. It is highly context-specific. Complexity can result in adaptations, but it can also be mal-adaptive. There is no simple relationship between fitness and complexity.
I’ve posted this figure before that is supposed to explain how even “devolution” (not a real term in biology, just borrowing it from Behe) can result in gains in functions and increases in genomic complexity, while being almost entirely driven by a combination of neutral changes and negative selection:
Squares represent genes, colors and intensity represent functions and their degrees(brighter color = higher degree of function). Red rectangles highlight what is being duplicated and passed on.
This is “adaptive devolution” of increased complexity, and new functions, by mostly “degrading” and mostly “breaking” genes. Because these extra genes are costly to express, their death is adaptive, and so is the eventual deletion of them. But because the still functional copies continue to accumulate deleterious mutations, as these are are more frequent than beneficial ones, their duplication is also some times adaptive(more expressed genes compensates for each individual gene being weaker).
Eventually over many generations a previously dead gene locus, a black square (effectively having become non-coding DNA) evolves into a de novo protein coding gene (purple square, Function B). This new functional gene suddenly comes under strong positive selection so is quickly improved over subsequent generations. So one new function is evolved and enhanced, while all the rest degrades and breaks. The net result is more complexity and more functions than there was to begin with. And it happened almost exclusively through neutral and adaptive degeneration. There was one innovative mutation among thousands of degenerative ones.