In this case, APOB is still functioning as a cholesterol transport molecule to get cholesterol into the bloodstream. This isn’t a loss in function. This is a fine-tuning of activity.
Let’s say the opposite happened. Let’s say that a mutation in polar bear APOB, which changed it to the same amino acid sequence as that found in brown bears, increased transport function by 50% resulting in atherosclerosis and early death in polar bears. Would this be a damaging mutation in polar bear APOB?
Exactly. It’s what he did with malaria, too.
The NCBI entry is what I am using as the reference for all of this.
As far as slogging through the data, it is actually eye-opening, and giving me new understanding and appreciation of the issues attendant with genome sequence assembly.
If you get sick of read mapping, I can probably help out. Let me know. The struggles of variant calling in non-model systems are something I’ve had to deal a lot with in my research.
It’s fun debating the impact of the APOB variants in polar bears because Behe used it as an example but it almost certainly is not loss of function. Regardless, at the end of the day, we know evolution sometimes occurs through “degradation” of some gene function as Behe likes to argue, but these examples are special cases where activity is being tuned for a specific environment. This type of evolution exists independent of adaptive evolution. Red apples exist, but the existence of red apples doesn’t affect the existence of green apples. The evolution of new traits is obvious and we know the mechanisms. For example, Lenski’s long term evolution experiment indicates, unpredictable genetic changes lead to new improved phenotypes. Behe’s argument is not a challenge to evolution at all.
A return to the allele found in brown bears would be a damaging mutation for the polar bear but arguably a constructive mutation at the biochemical level. If loss or reduction of function can be adaptive, then a gain or increase of fonction can likewise be maladaptive.
Then Behe’s thesis makes no sense. When you divorce function from fitness it loses all meaning.
I think his thesis still makes sense. Evolution can only (or almost only) destroy complex structures, not build them. If destruction happens to be beneficial, it will be positively selected for. Regardless, evolution still lacks the ability to create much in the way of complexity.
Hi Steve,
What are your thoughts on constructive neutral evolution? That seems to provide an evolutionary pathway to build complex structures, if I am understanding it correctly. (I may not be.)
Thanks,
Chris
Oh sure, there are no doubt non-adaptive contributions to complexity. I was just trying to sketch out Behe’s argument, not trying to evaluate it. How the different processes play out is likely to be difficult to sort out – which is why I haven’t really paid a lot of attention to Behe’s claim.
How does it lose all meaning?
I don’t see how this makes sense in the case of APOB. The protein is still transporting cholesterol from the gut into the bloodstream (or lymph). The same function is there, and complexity has still the same. The change that Behe and others are suggesting is a change in the rate of transport.
No biologist would denied that a loss of function can be adaptive in a given environment. There are many examples of this. If you don’t like the APOB example, you can look at the LYST example also in polar bear instead. And if the loss of a given function can be adaptive in a given environment, it follows that the restoration of that fonction in the same environment would be maladaptive. So divorcing function from fitness makes perfect sense IMO.
APOB hasn’t lost its function. It is still transporting cholesterol.
This goes back to Venema’s critique:
You can cite all of the damaging mutations you want. That doesn’t prove that constructive mutations don’t exist.
ID proponents don’t deny the existence of constructive mutations. But the point is precisely that I can cite all the damaging mutations I want, which you’d have a hard time doing for constructive ones because the former are immeasurably more numerous than the later. Hardly a good configuration for constructive evolution! But rather a good one for devolution.
Where has the number of constructive and damaging mutations ever been measured in real species?
Well, this just seems wrong. Let’s consider color of polar bears for example. Everything living that has no color (i.e white) can easily be argued to be the result of devolution, but everything that contains a different combination of primary color pigments must would be credited as the result of constructive evolution. Can you list more non-colored than colored animals or plants?
A good counter example is the increase in melanin producing in rock pocket mice that allowed them to camouflage themselves in black basalt rocks.
For a bit of fun, I took the mutations in pocket mouse mc1r (see above) and plugged them into PolyPhen-2. According to the paper, at least one of the mutations is responsible for the darkening of fur color and is considered a gain in function mutation.
Sequence (light colored mice):
10 20 30 40 50
MPMQEPQRRL LGPFNSTRTG VPHLELSANQ TGPWCLHVSI PDGLFLSLGL
60 70 80 90 100
VSLVENVLVV ISIAKNQNLH SPMYYFICCL ALSDLLVSVS IVLETTLILV
110 120 130 140 150
LEAGALATRV TVVQQLDNVI DVLICGSMVS SLCFLGAIAV DRYISIFYAL
160 170 180 190 200
RYHSIVTLPR TRWAIVAIWV ASISSSTLFV AYYNHTAVLL CLVTFFLATL
210 220 230 240 250
ALMVVLYVHM LARAHQHAQA IAQLHKRQHL VHQGFRLKGA ATLTILLGIF
260 270 280 290 300
FLCWGPFFLY LTLIVLCPKH PTCGCFFKNL NLFLALIIFN SIVDPLIYAF
310
RSQELRMTLK EVLLCSWPolyPhen-2
Mutation (HumDiv) (HumVar)
R18C 0.034 0.018
R109W 0.005 0.005
R160W 0.539 0.246
Q233H 0.185 0.168
Only one of the mutations was described as being possibly damaging (R160W, HumDiv). However, one of those mutations is responsible for the gain of function in mc1r. Perhaps the benign mutations in polar bear APOB are constructive mutations that overcome any damage caused by the other mutations.
So, I think Betteridge’s Law of Headlines holds true yet again… 