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| ▲ | skissane 8 hours ago | parent | next [-] |
| I wonder how that works? Speculation: there is some kind of genetic/epigenetic signalling which modulates DNA repair mechanisms, such that certain DNA regions can be marked as more mutation-prone than others. And there may be selective pressure to make genes associated with disease-resistance more mutation-prone, because that’s a gene whose mutation is more likely to be beneficial (compensating mutations for evolution in existing diseases or to respond to new diseases), less likely to be harmful (most of the time, most likely outcome of the “wrong” mutation would be less resistance to diseases, but it probably wouldn’t otherwise be lethal or cause serious disability). But if that is what is actually going on here, is there any actual challenge to Darwin’s views? He didn’t know about DNA; I don’t think he ever claimed all mutations were equally likely (why would he when he had no idea what the actual mechanisms behind them were) |
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| ▲ | rolph 5 hours ago | parent [-] | | darwin had the idea that many individuals with variation were culled according to relative fitness. mendel later demonstrated that this variation was passed fractionally, to decendants. this was a conserved probability of fixed combinations
[consult "mendels peas" ] the two taken together resulted in neo-darwinist mechanisms.
darwin was not wrong, mendel was less wrong, contemporarily we are still scratching the surface of getting it right, primarily what rules apply to what groups, what mechanisms are conserved, what combinations of functions are served by a particular structure, departing from the one gene one function hypothesis. |
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| ▲ | fooker 6 hours ago | parent | prev | next [-] |
| It's clear that purely random mutations don't work in the sense that an infinite number of monkeys won't produce Shakespeare even if you kill of the monkeys that fail. |
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| ▲ | foxglacier 5 hours ago | parent [-] | | The monkeys would write Shakespeare if you tested their output character by character instead of waiting till the end. That's how evolution works too - in tiny cumulative achievable steps. |
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| ▲ | ch4s3 12 hours ago | parent | prev | next [-] |
| I don’t really see that as anti-Darwinian. Those genes successfully attach themselves to a new organism and provide advantages such that they are selected for in the population. |
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| ▲ | macleginn 11 hours ago | parent [-] | | The selection is classical, but the mutations are supposed to be random, not skewed towards more useful genetic variants. One can speculate that a purely random (and otherwise neutral, say) prior mutation led to this directionality, but the actual resulting mechanism is AFAIK still unknown. | | |
| ▲ | ch4s3 6 hours ago | parent | next [-] | | Natural selection has nothing to do with randomness per se, it’s merely differential selection based on environmental fitness. The fitness function of a given environment can even narrow a range of existing genes without any mutation occurring during the period where the new fitness function is applied. The classic example of this is peppered moths shifting toward the darker range of their preexisting color range during the Industrial Revolution. Horizontal gene transfer is another way organisms can acquire new traits. | |
| ▲ | rolph 9 hours ago | parent | prev [-] | | plasmids https://en.wikipedia.org/wiki/Plasmid |
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| ▲ | RobotToaster 6 hours ago | parent | prev [-] |
| Lysenko wasn't entirely wrong then, crazy. |
