While heterozygous sickle cell confers a beneficial resistance to malaria, it’s kind of hard to argue that that makes homozygous sickle cell not a disease. And I was also thinking of hemochromatosis when I wrote that, though you’re right that it probably would be neutral or beneficial in a situation where humanity was somehow nearly wiped out.
Still, a gene need not be prevalent in the general population to cause problems with inbreeding. It’s my understanding (though I may of course be wrong, and welcome correction) that most humans carry unpaired genes for several different serious genetic diseases (different ones for each person, of course), but that they usually go unnoticed because they’re so rare in the general population that they almost never get matched up. In a heavily-inbred population, though, such genes will fairly quickly become apparent.
That’s true, but even in 50% crosses it occurs less than one in a thousand. What that effectively means is that it’s not going to affect the first generation at all. And after that it’s not such a big issue provided the population is growing fast. Under the ideal conditions we’re discussing here we’d expect the population to be increasing at least four-fold every generation. That means that so long as the trait affects less than 50% of all individuals the population’s going to be fine. As soon as an individual becomes homozygous they are culled and the gene frequency actually diminishes.
That’s why the rate of reproduction is the real key here. If the population stabilize at low levels you can’t afford to lose members. If it’s increasing fast then the losses from inbreeding are insignificant and non-carrier lines will rapidly dominate.
Aren’t there animals whose eggs can be fertilized by non-living substances? I thought I read somewhere about a bird whose eggs can be fertilized with a pin prick? Or am I misremembering?
They’re not being fertilised, it’s just another example of parthenogensis. In some organisms zygote development starts within a set time period after the membrane of the ovum is broken. Normally it would only be broken by the entry of the sperm, but if it is carefully ruptured by a needle devlopment still occurs.
They have not been fertilised however and the offspring contain the same genetic material as the mother. In species where sex is determined by the male ( as in most mammals) the offspring are universally female.
As I understand it, it DOES; the low endurance of cheetahs is due to a genetic defect that became universal after the population bottleneck.
Unlikely, for a long time; they are nearly a species of twins. So close that you can perform tissue transplants between any two random cheetahs successfully. Evolution needs variation to work with, and cheetahs have almost none.
It has to do with inbreeding because outbreeding isn’t an option for cheetahs. What you are looking at is a species that has lost it’s genetic diversity, between the population bottleneck and then the inbreeding homogenizing what was left.
That doesn’t work when ALL the animals have the recessive trait. And there really isn’t any such thing an outbreeding for cheetahs.
Which is why negative recessive genes are a problem; with such low variability, they will or almost always will manifest themselves, because all individuals have them.
It’s believed that many island species got their start in just this way. A pregnant female ends up washed out to sea and lands on a new island, thus beginning a new isolated population. So it’s not just a theoretical question.
I’ll believe it when I see a reference. Until then it’s like claiming that the low sprinting ability of sloths is due to a genetic bottleneck. No cats have high endurance. Cheetahs are even more highly adapted to sprinting than other cats and based on fossil skeletons they always have been. As such it will require some pretty convincing evidence to support your claim that before the bottelneck some cheetahs could run a marathon.
Once again, I will believe I see a reference. And I mean a reference for your claim that there is less genetic variation in endurance between cheetahs than there is between sloths or alligators or kangaroos.
And once again I will believe it when you provide refercnes for your twin claims that:
A) There is less genetic variation in endurance between cheetahs than between any other mammals.
and
B) That lack of variation in speed did not exist before the bottleneck.
Until then what I said stands: It has nothing whatsoever to do with inbreeding and is no different to that seen in any other population.
And once again I will believe this when you provide a reference.
So now that is three references:
A) There is less genetic variation in endurance between cheetahs than between any other mammals
and
B) That lack of variation in speed did not exist before the bottleneck.
and
C) All cheetahs exhibit the same detrimental recessive trait.
And once again I will believe this when you provide a reference that all cheetahs exhibit the same detrimental recessive trait.
Seriously Der Trihs, these claims seem to be extraordinary. Do you have any evidence for any of them?
It’s believed that some species of Muridae (rats and mice) arrived in Australia that way, since the only placental mammals in Australia are those that could cross the sea, i.e., Chiroptera (bats) and Cetacea (whales and dolphins), and the species introduced by Homo sapiens, starting with Canis lupus dingo (the dingo). A single pregnant mouse or rat carried on a piece of driftwood could have carried her species to Australia millions of years ago.
I generally agree with Blake, but I’d say it slightly differently:
It’s hardly controversial to say that there’s a lack of genetic variability in endurance among the current cheetah population, because there’s such a lack of genetic variability in general in the current cheetah population, compared to other mammals. So I’ll take that as a given.
But that’s only a problem for cheetahs if the endurance in the current population is sub-optimal. If genetically increasing endurance in cheetahs results in decreasing speed, increasing energy requirements, or some other drawback, then endurance is right where it should be, from a fitness point of view. Since cheetahs make their living by short-distance speed, I tend to believe that endurance isn’t that important to them. They’re dragsters, not long-distance racers, so having a small gas tank is OK. In fact, a large gas tank on a dragster is just more dead weight.
In other words, it’s fine if everybody’s the same color/shape/size/whatever as long as they’re the right color/shape/size/whatever. The major exception, as Blake has said, is disease resistance, where everybody being the same can be devastating.
My population genetics classes were (mumble) years ago, and I can’t find that textbook. But I clearly remember the professor making the point that IF the heterozygous form of a negative allele has NO ill effects on the individual, then its frequency in a population will NOT be reduced over time.
In very small populations, chance has more effect on what happens. The frequency of a ‘bad’ allele can decrease, stay the same, or actually increase. There’s some genetic defect that became quite prevalent on Pitcairn’s Island, but I forget what it was.
[Damn! Did you know if you try to edit your post, and take too long doing it, they throw out the original post? Grrr]
My population genetics classes were (mumble) years ago, and I can’t find that textbook. But I clearly remember the professor saying that if a negative allele has no ill effects on the individual then its frequency in a population will not decrease.
As for tiny populations, chance plays the major role in what happens. See “island effect” and “Founder’s Effect”. The frequency of any given ‘bad’ allele can go down, stay the same, or actually increase. It depends on which individuals happen not to reproduce for whatever chance reason and/or which indivuals happen to leave larger than average numbers of offspring, again for whatever chance reason.
This wikipedia page Founder effect - Wikipedia does a good overview. Especially note the paragraphs near the bottom about an island in Micronesia where colorblindness is at 5% (vs .0003% in the United States) and an additional 30% of the population are carriers.
Wouldn’t two non-related couples be enough, as long as they each had at least a male and a female child? The children would form two couples who could breed and group A & B could breed so on down the line.
To look at an overly-simplified example: Let’s suppose that the heterozygous form of a gene has no effect whatsover, but the homozygous form is instantly fatal. And let’s start with the gene having a frequency of 50%, to make the numbers easier: That is to say, everyone’s a carrier. If we label the defective “die instantly” gene by d and the normal “don’t die instantly” gene by D, then everyone in the population has Dd.
Now, everyone in the population pairs off, and each couple has an average of 2.6 children. The Punnet square gives us four possibilities for each child: DD, Dd, dD (which is the same as Dd), or dd, so on average, each couple is going to have an average of 0.6 dd children (who all die instantly), 1.3 Dd children (all of whom are carriers, but survive), and 0.6 DD children (who don’t have the defective gene at all). Each couple has an average of 2 children who survive, so the population stays steady, but the incidence of the gene in the second generation is only 1 in 3, down from the 1 in 2 in the parent generation. So yes, the incidence of the gene will decrease, even if the the heterozygous case is harmless.
There’s another case that sometimes comes up, though, where the homozygous case is bad, but where the heterozygous case is actually good. In this case, there will be some equilibrium level for the gene where the good effects of being heterozygous balance out the bad effects of being homozygous. Sickle cell is a famous example of this. In this case, if the incidence of the gene is already at equilibrium, it won’t decrease any further.
You’d have no incest in the first or second generations, but everyone in the third generation would be double first cousins, about as closely related as half-siblings, and it’d just get worse from there. You’d never need to have actual siblings mating, but you would eventually have folks who were genetically as close as siblings mating.
