First you must define information. Really for your argument to mean anything at all you must do this; otherwise you're just playing humpty-dumpty. For the recognised definitions of Information used in Infromation Theory, it is relatively trivial to show mutations can increase information. So what do you mean? Be specific.
The occasional point mutation can be "seen" by natural selection, but these generally switch an existing gene on or off, so they don't constitute additional information.
That's nice. What about the ones that aren't "generally"? Like the mutation that produced chloroquine resistance in Plasmodium (the malaria parasite).
So what is the absolute minimum novel genetic structure required to be "seen" by natural selection and added as new information to the genome?
I don't understand what you mean here? Could you elaborate?
DNA that has, or contributes to, an effect on phenotypic form or function.
So, you're saying that a section of DNA contains information if and only if it has an effect on phenotypic form or function. Okay. How is that to be quantified? Do we simply count genes that have "an effect"? Or is there a more subtle measure here? One, that would, for example, take notice of a change to DNA that improves or changes it's function?
Are you suggesting that it is this form of mutation that has caused the functional, non-redundant genome to grow 7.8 fold every billion years?
With other forms of mutational events, yes, it accounts for all increase in gene function, however meaningfully measured
The supposedly observed increase in the size of the genome requires the addition of new information. That new information must be created from non-functional DNA (otherwise it is simply modifying existing information). What is the minimal genetic structure that can be randomly assembled from non-functioning DNA that will be visible to natural selection?
According to you, if a gene is copied, and the one of those copies mutates adopting a new function is that an increase in information?
The vast majority in increase in gene function is produced by gene copying followed by modification of one of those copies or the resplicing of exons from one or more genes. We know this because of the patterns formed by similarities in the genes of living organisms.
Now then, these "patterns formed by similarities in the genes", can you give me a reference to that?
Gosh, there's so many of them. I'd expect any decent general undergraduate textbook on Biology to cover it at least in passing; a book on genetics or evolution should cover it too. Unfortunately the best reference I have for it is drawn from Open University course materials and they are not accessible to you.
It is irrelevant because DNA does not need to function to be "seen" by natural selection. For instance, junk DNA can act as a buffer to protect functional DNA from damage, and it would confer an evolutionary advantage.
And conversely all non-coding DNA applies a cost everytime it's copied. Probably not a relevant factor in Eukaryotes; but it probably accounts for some of why bacterial and viral genomes are so much more densely packed with protein coding regions (Viruses often even overlap genes).
The problem with gene duplication as a path to increased genomic complexity is that in some ways the phenomenum is its own worst enemy. When a gene duplicates its susceptibility to natural selection is (roughly) halved. A deleterious mutation to one copy is compensated for by the other copy, rather than being selected out. This results in rapid "subfunctionalisation", with two damaged genes doing the work of the undamaged original.
This means that the two subfunctionalised copies are actually constrained to their tasks (assuming the original gene was a vital one) and neither of them actually have the luxury of evolving into something novel.
Firstly, so what? What differences does it make if some gene duplication and modification doesn't add "information"? Secondly, most multi-part proteins where the parts are from different families are better at their function than their single part equivalents - does being better as something constitute a change in information by your standard?
quote:How does an entirely new function originate after gene duplication? More detailed molecular studies of model gene families are needed to look into the emergence of novel gene function.
I think your "probably" is almost entirely errant; certainly no such inference is drawn by Zhang himself. And can we be quite clear than Zhang does not question that it does happen, but merely recognises the limits in our knowledge of this area, please?
Anyway, let's look at an examples.
Lactation. Lactose is synthesized in placental mammals by an enzyme called Lactose synthase. This enzyme is composed of two proteins: galactosyltransferase and α-lactalbumin.
Galactosyltransferase on its own will form lactose from UDP-galactose and glucose but only at glucose concentration levels far about those found in vivo, it's primary purpose on it's own is the transfer of galactose units from UDP-galactose to N-acetylglucosamine linked to proteins.
α-lactalbumin binds to galactosyltransferase to form lactase synthase by modifying the shape of galactosyltransferase slightly so it now readily catalyses the combination of UDP-galactose and glucose to form lactose.
Now, the α-lactalbumin gene has substantial sequence similarity to a gene family that code for lysozymes (specifically to Ca2+ binding c-lysozymes). Lysozymes are enzymes that form part of the innate immune response by attacking molecules called peptidoglycans found only in bacterial cell walls. More intriguingly still, monotremes do not synthesize (much) lactose in their milk but they do include a large quantity of lysozyme with it (presumably, to help protect the offspring from bacterial infection) - the particular kind of lysozyme that α-lactalbumin is most similar too - and this lysozyme has a very weak lactose catalysis effect when combined with galactosyltransferase.
150 years of science in found something out shocker
Still reading up on lysozymes, and fascinating stuff it is. Came across this pearler and thought I'd share it with youo:
I know, amazing isn't? A biologist speculating 150 years ago got some sutff wrong. Wow. A man who didn't know about genes, didn't know about the molecular basis for tissue differentiation, didn't know about the existence of control genes, or how they work, didn't know about the chemicals involved in lactation - and so ad nauseum - didn't get his ideas about the details right? I'm staggered.
While you're at it why don't you have a quick crow about how his ideas on sexual reproduction were so wonderfully, absurdly incorrect? I'm sure a good laugh will do you good.
What I don't understand is why you'd think it'd make any difference to me? Or any modern scientist?
Hardly "substantial" when you consider human and mouse DNA is 92% similar.
Gene similarity is a concept that has many different ways of being understood. When scientists talk about similarity between individual genes they are usually talking about aligned sequence similarity - that is you place the two genomes and look for the base pairs that are identical and occur in the same order and count matches. Figures such as the 92% mouse DNA figure come from a completely different method which simply involves dropping DNA from both into solution and measuring temperature changes. These methods give completely different numbers.
Then there's the relatedness figures given for siblings - 50% of your DNA with your brother, etc. - these are looking only at genes that vary between individuals in one of the possible populations. Different numbers again.
It's not that Darwin got it wrong. It's that this scientist decided to make an editorial point about the theory and used, as it turned out, a very poor example to do so.
Do you read many scientific papers, Kaichos Man? What you've identified as "an editorial point" is actually the part of the paper that might be characterised as the "literature review". It's normal practice in these to discuss the historical context of the research into which the paper fits. This often, maybe even usually, includes a quick overview of once popular ideas that turned out to be false.
Your lack of scientific background is showing, Kaichos. Find some scientific papers on something you haven't discarded without knowing about, and have a read. The style you're bizarrely mocking is standard scientific style.