Beneficial mutations

One thing creationists like to harp about is the idea that mutations are always, inherently, bad. But, well, they’re not.

Mutations are, basically, copying errors in DNA. There are lots of different kinds, from effectively invisible ones that don’t actually change any proteins to losses or duplications of entire large chunks.

Now, it is true that, on average, more mutations are harmful than beneficial. If you randomly change something as complex as the DNA of an organism, you are more likely to “break” something than to make it better, if only because there are more possible ways for an organism to be constructed incorrectly than to be constructed correctly, just like if you took a page of text and randomly changed several letters, you would be more likely to make it make less sense than make it make more sense.

But that’s where reproduction and natural selection come in.

How natural selection works (highly simplified)

Imagine you have a population of 100 organisms. Each one has the potential to have up to 10 kids, but the environment can only support a total of 100 organisms, so on average each of them will have only one kid. Since we are talking about a fairly simplified system, let’s say that there are 3 possible outcomes: death (or, at least, no kids), a normal number of kids, or extra kids. Let’s call those last 2 outcomes “neutral” and “breeders”. Neutral organisms only have more than one kid if there isn’t a breeder taking up any extra slots. And if a breeder has no mutation or a neutral mutation, it will keep the breeder mutation.

The population starts out neutral. Now, let’s say that, in each generation, 60 organisms have either a neutral mutation (ie no real change) or no mutation, 39 have a lethal mutation, and 1 has a beneficial mutation. So, in the first new generation, there are 39 “spots” for an organism to have extra kids, to make up for the ones that got the lethal mutation. The breeder has 10 kids, and the other 29 “spots” are taken up by neutrals .

In the second generation, 6 of the breeder’s kids get to keep the breeder mutation, 54 organisms remain neutral, 39 of the entire population (likely including 4 of the breeder’s kids) get a bad mutation and die, and 1 random individual ends up as a breeder. So each of those 7 breeders will have, on average, 6 and a half kids (about), for a total of 46 kids between them–their own replacement kid, plus all of the extras.

In the third generation, you start with 46 breeder’s kids, about 28 of whom remain breeders, plus, again, a random extra breeder. So the fourth generation will start with 67 breeders. I trust you can see the progression from here. Pretty soon, no neutral organisms will be left, and the entire population will consist of breeders.

Now, this is obviously a pretty simplified situation, real life is a lot more complex. And maybe I was over-generous with the numbers, maybe “breeder” mutations would be rarer, and maybe they’d only result in, say, 3 extra offspring instead of up to 10. But, however you crunch the numbers, unless lethal mutations are so common that the population just can’t survive, beneficial mutations will just keep spreading as long as organisms with beneficial mutations have more kids than those without them.

But, of course, this only works if beneficial mutations *can* exist. So let’s see if we can find some.

Some actual examples of beneficial mutations

Let’s start with nylonase. Well, more accurately, nylonases, as there’s more than one. Basically, a nylonase is an enzyme that can digest nylon. And scientists have *repeatedly* demonstrated that bacteria that did not previously have the ability to digest nylon can acquire the ability to do so, and bacteria that had minimal ability to digest nylon can get better at it. This is generally through changes in an existing enzyme, often (if I am understanding the article I linked correctly) one that was used to manipulate lysine, a common amino acid which the ends of nylon polymers often resemble. And I think it’s obvious that being able to eat something new is a beneficial mutation, if that new thing happens to be around.

Another major one is antibiotic resistance. While antibiotic resistance is pretty terrible for *us*, it’s *great* for the bacteria that develop it. And scientists have repeatedly found novel antibiotic resistance genes that did not (as far as they are aware) exist in previous generations of a particular bacterium. Thus, they were caused by beneficial (to the organism) mutations.

Some humans are genetically resistant to HIV infection, mostly due to mutatations in various genes that code for the proteins that the HIV virus uses to enter cells. Though at least one of these mutations is a good example of how a mutation may only be beneficial in a certain environmental context, but harmful in another, as it is also associated with a particular type of chronic liver disease.

Honestly, the same is true of many beneficial mutations. Most mechanisms of antibiotic resistance cause bacteria other problems (including increased susceptibility to other antibiotics). Something like nylonase is only useful if there is nylon present to eat. And so on.

But, well, that’s all it takes for a mutation to be beneficial. Organisms don’t have to be good at surviving in all possible environments and against all possible challenges, just the one(s) they happen to be dealing with. A clam would not do well on land, and a wolf would not do well in the ocean, but both are incredibly successful organisms *in the environments where they actually are*.