Fragmentary thoughts

Why hasn’t (Darwinian) evolution evolved the building blocks of Lamarkian evolution?

Well it has once – with us – but why hasn’t it done so at the biological rather than the cultural level?

Perhaps smuggled into Lamarkianism is the idea of telos, which can exist within consciousness, but not at the biological level.

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Mike Pepperday
Mike Pepperday
9 years ago

For children to be born already circumcised (say) there would have to be a feedback to the gametes. But that would mean that someone who accidentally lost a finger would bear children without that finger. That’s not a goer so it would have to be so arranged that the feedback only kicks in after, say, a hundred generations of circumcision, or maybe a thousand. Successive generations—or a high percentage of successive generations—so that the lost finger count did not accumulate over a long period. It is hard to see how any such complex program could evolve through natural selection.

I am wondering if the question makes sense. There’d have to be a mechanism in the genome to allow the genome to be changed by the environment—and then it wouldn’t be the same genome.

Organisms die and species die but genes live forever. If they allowed themselves to change with environmental influence then by definition, that is not living forever. Genes must “strive” to stay the same, to reproduce exactly.

Any that allow themselves to be changed cease to exist. In fact they do get changed (by cosmic rays for instance) and in their mutated form they probably overwhelmingly perish because the organism they next contribute to is defective. For the rare mutation that is beneficial, the benefit has nothing to do with the cosmic rays—it’s just some unrelated, accidental feature that is not selected out and goes on to spread in the gene pool.

It looks as if Lamarckism is logically absurd.

john r walker
john r walker(@annesanders)
9 years ago
Reply to  Mike Pepperday

Yes !

Pedro
Pedro
9 years ago

plus, the genes that have to change are the ones in your nads or the eggs in your ovaries. I think it was a very fragmentary thought.

Tel
Tel
9 years ago

If you suppose there was some mechanism that might evolve where an injury to the parent (e.g. remove a finger or foreskin) is passed on to children, I would expect strong natural selection against such a mechanism. Given that humans live an injury-prone lifestyle, the fact that these injuries are not passed to children should be a great boon to survival of those children.

On the other hand, a useful discovery by the parent would be an excellent thing to pass on to children. There’s plenty of evidence of parents teaching survival skills to their offspring in the animal world, so selecting for the ability to learn makes a lot of sense. Not that I’m into Internet squee or anything, but there was a video of a mother otter dunking her baby in the creek, the links are just about everywhere.

I remember some research on Holocaust survivors that showed their grandchildren somehow inherited a significantly changed metabolism, I can’t find a link to it. Mitochondrial DNA operates independently to human DNA, and the mitochondria are our primary metabolic engines. Not outside the realms of possibility that we have a mechanism to adjust rapidly to environmental shifts such as the availability of food. Feasts and famine are common features of history.

john r walker
john r walker(@annesanders)
9 years ago

Since their discovery in the 1960s, the class of misfolded proteins known as prions has posed a fundamental challenge to the foundation of molecular biology: the idea that heritable information flows from DNA and RNA to protein, but never from protein to any other molecule. Contrary to this rule, prions are able to transmit information from one molecule to another through the transmission of their misfolded shape, with devastating consequences in diseases such as mad cow disease and Creutzfeldt-Jakob disease. The broader implications of this unusual transmission mechanism, however, are not well understood.

Among these implications, research on yeast prions has suggested that beyond their well-known role in diseases, some prions may confer survival advantages by helping organisms respond to environmental stress.

The idea is that in environmental stress situations prions increase the rate of mutations and thus increase the chance of producing some new yeast cells that are not as stressed as their parents .

john r walker
john r walker(@annesanders)
9 years ago
Reply to  Nicholas Gruen

Prions have been a puzzle for a long time. They are ‘inert’ strings of protein they are not DNA RNA … , They make the simplest virus look like a large project, yet they seem to be able to re-produce replicas of themselves. and have tha ability to ‘infect’ hosts.

The thought is that the prions that produce mad cow disease are sort of harmful mutations of prions that normally serve some useful (or harmless) purpose.

Did you get my email? Godel Escher Bach Chapter XVI Self-Rep and Self-Ref is a pretty good intro into the complexity of the intertwined braid of genotype/phenotype

john r walker
john r walker(@annesanders)
9 years ago
Reply to  john r walker

“mad cow disease was Creutzfeldt-Jakob disease.” I don’t think so , as best as I know mad cow came from scrapie a similar disease of sheep .
Mad cow started when the processing of dead livestock into cattle feed supplements was changed , from memory ,temperatures were dropped to about 200C and less acid was used . Understandably nobody realised that this was not sufficient to destroy a prion!

Sancho
Sancho
9 years ago
Reply to  john r walker

Prions are nucleants. Like other proteins, they’re twisted into a complex shape, but when they meet normal proteins, they cause them to take the same shape as the prion.

Because the shape of proteins act like the cut of a key in metabolic processes, the now-prion-shaped proteins no longer function as they should.

Eventually the rogue proteins convert too many of the normal ones for the physiological stuff to happen properly.

john r walker
john r walker(@annesanders)
9 years ago

Sancho

when they meet normal proteins, they cause them to take the same shape as the prion.
How do they do this?

Sancho
Sancho
9 years ago
Reply to  john r walker

The Wikipaedia section on the subject explains in detail the ways that nobody’s quite sure how it works.

john r walker
john r walker(@annesanders)
9 years ago
Reply to  Sancho

Thanks.

Jason Collins
9 years ago

The question is not so much why there are no Lamarckian evolution – as horizontal gene transfer between bacteria and epigenetics are, in a sense, Lamarckian – but why is it so rare?

One proposal I have seen in the literature is that Lamarckian evolution is a much more complex engineering problem. How do you reverse engineer an acquired (likely adaptive) characteristic back into the genome? Tinkering with mutations at the single nucleotide level and seeing what happens is very different from trying to determine what changes are required in the genotype to phenotypically express a characteristic in the next generation.

Sancho
Sancho
9 years ago
Reply to  Jason Collins

It could happen if a remarkable range of mutations occurred in a few short generations, allowing some Lamarckian features to emerge. But that would just be Darwinian evolution in a beret.

john r walker
john r walker(@annesanders)
9 years ago
Reply to  Jason Collins

Agree . Evolution does not have (or need) intention

The Genome is code, code needs an interpreter to become ‘something’. Small changes to the settings of the control knobs (of the code) for the interpreter is almost certainly more likely than rewriting the large slabs of code involved in building a leg ,fin or wing. A lot of evolution involves changes to the way and rate that the code is expressed or suppressed by the interpreter .

Sancho
Sancho
9 years ago
Reply to  john r walker

I don’t know enough about the topic to say whether introns provide more mutations than actual changes to DNA sequence, but the idea that we’re all supra-beings in our junk DNA seems like the sort of thing the Intelligent Design crusaders just love.

john r walker
john r walker(@annesanders)
9 years ago
Reply to  Sancho

Susan Lindquist’s idea has taken about ten years to be accepted, it does upset some of the more rigid dualists about phenotype and genotype . (When Darkins talks about genotype/phenotype it often sounds like a extreme version of the old soul/ body dualism.)

Would be surprised if what works fine for a single cell fungi would work in a large multi-cellular mammal …. rapid division/mutation is OK for yeast, it is cancer for us.

Was thinking of neoteny type changes.

john r walker
john r walker(@annesanders)
9 years ago

sorry should have said Dawkins

john r walker
john r walker(@annesanders)
9 years ago

Speculation but it looks plausible that somehow turning on a similar (to the yeast cell prion) mechanism in some cells in a large creature could result in cancer like growth, maybe?