The article has a few problems with regards to the assumptions it makes.
For instance:
> often caused by random mutation, preferentially selecting the most fit organisms to propagate their genes into the future
So, mutations are not entirely random; transposons, for instance, have preferential hotspots, same with individual nucleotide positions. But by and large there is a lot of randomness, so this is not necessarily the main problem with the statement. However had, it is then stated that there is a preference towards selection ("most fit organism") as well as a "propagating their genes into the future". I am quite certain that the assumption made here is largely by e. g. Richard Dawkins babbling about the selfish gene.
The thing is that evolution as-is, operates primarily over the phenotype as such. If you have, let's assume, mutations in genes that yield some benefit, in certain ecological environments, you may be "more fit" in the environment, assuming you can reproduce (as an organism). Still the selection step happens on the phenotype level though; you could have "negative" genes too that may offset that advantage. So the assumption of "most fit" in and by itself is already a tautology, even more as the concept of the gene itself is poorly definable - see books explaining this, such as "The Gene: From Genetics to Postgenomics".
Of course one can say that for some entities, the genome is the selection step, e. g. for organisms that may integrate into a given genome and then be propagated as part of that genome. But even then the phenotype is the important part; you need to see the DNA replicated, and if, for instance, the bacterium dies, the DNA is often degraded, so if you were some entity here that integrated (transpoon, viruses etc...) and the DNA is degraded, that is the game over step for you already. So you absolutely need the phenotype and this is the real level of selection. All the information prior to that, e. g. the genome sequence (aka many "genes", but again, the concept of the term gene is not well describable; after all RNA matters a lot as well but are all RNA-yielding sequences automatically "genes"?), has to pass that gauntlet.
Or this:
> By leveraging modularity at the genetic level, populations of organisms can increase the rate that useful genetic variants spread through the population, effectively increasing their rate of information acquisition. Sexual reproduction, along with other ways of sharing genetic material like horizontal gene transfer, is essentially a mechanism for doing this.
I understand what he refers to and while it is not incorrect, you also have constraints such as the fact that meioses requires double-strand breaks in order to resolve the Holliday junction. That's simply how crossing-over works. Yes, you can say that more variation is the net outcome of this, that is true, but without that resolution and the double-strand break, you can not do the later step of pulling the sister chromatids onto opposite poles of the cell. That's a cell biology constraint, not a genetic one at its core. Resolution is also not totally random either, as chromosomes have some kind of position regularly (Rabl orientation); see hotspots that exist (biological transposons naturally don't have this constraint anywhere near as much, but even transposons show preferential integration sites, which makes all variation not 100% random per se, in addition to other constraints such as the fact that organisms have to be viable, so not all random integration is possible to begin with).
The article has a few problems with regards to the assumptions it makes.
For instance:
> often caused by random mutation, preferentially selecting the most fit organisms to propagate their genes into the future
So, mutations are not entirely random; transposons, for instance, have preferential hotspots, same with individual nucleotide positions. But by and large there is a lot of randomness, so this is not necessarily the main problem with the statement. However had, it is then stated that there is a preference towards selection ("most fit organism") as well as a "propagating their genes into the future". I am quite certain that the assumption made here is largely by e. g. Richard Dawkins babbling about the selfish gene.
The thing is that evolution as-is, operates primarily over the phenotype as such. If you have, let's assume, mutations in genes that yield some benefit, in certain ecological environments, you may be "more fit" in the environment, assuming you can reproduce (as an organism). Still the selection step happens on the phenotype level though; you could have "negative" genes too that may offset that advantage. So the assumption of "most fit" in and by itself is already a tautology, even more as the concept of the gene itself is poorly definable - see books explaining this, such as "The Gene: From Genetics to Postgenomics".
Of course one can say that for some entities, the genome is the selection step, e. g. for organisms that may integrate into a given genome and then be propagated as part of that genome. But even then the phenotype is the important part; you need to see the DNA replicated, and if, for instance, the bacterium dies, the DNA is often degraded, so if you were some entity here that integrated (transpoon, viruses etc...) and the DNA is degraded, that is the game over step for you already. So you absolutely need the phenotype and this is the real level of selection. All the information prior to that, e. g. the genome sequence (aka many "genes", but again, the concept of the term gene is not well describable; after all RNA matters a lot as well but are all RNA-yielding sequences automatically "genes"?), has to pass that gauntlet.
Or this:
> By leveraging modularity at the genetic level, populations of organisms can increase the rate that useful genetic variants spread through the population, effectively increasing their rate of information acquisition. Sexual reproduction, along with other ways of sharing genetic material like horizontal gene transfer, is essentially a mechanism for doing this.
I understand what he refers to and while it is not incorrect, you also have constraints such as the fact that meioses requires double-strand breaks in order to resolve the Holliday junction. That's simply how crossing-over works. Yes, you can say that more variation is the net outcome of this, that is true, but without that resolution and the double-strand break, you can not do the later step of pulling the sister chromatids onto opposite poles of the cell. That's a cell biology constraint, not a genetic one at its core. Resolution is also not totally random either, as chromosomes have some kind of position regularly (Rabl orientation); see hotspots that exist (biological transposons naturally don't have this constraint anywhere near as much, but even transposons show preferential integration sites, which makes all variation not 100% random per se, in addition to other constraints such as the fact that organisms have to be viable, so not all random integration is possible to begin with).
Breaking knowledge down into combinable modules is a great insight; ultimately, I think that’s the idea behind Zettlekasten.