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Author | Topic: About New Lamarckian Synthesis Theory | |||||||||||||||||||||||||||||||||||||||||||
Dr Jack Member Posts: 3514 From: Immigrant in the land of Deutsch Joined: Member Rating: 8.4 |
Epigenetics is not Lamarckian. It shares some small piece in common but it does not allow Lamarck's method of change. There are two fundamental reasons for this:
1. Epigenetic change is not accretional. Epigenetic switches are there or not based on genetic sequences, changing epigenetic state does not create new opportunities for new epigenetic changes. This means that epigenetic change can only alter an organism's phenotype within finite limits. 2. There's a major part of Lamarck's ideas that tends to be forgotten. Lamarck believed in a kind of "chain of being" where new organisms rose up the chain in a largely linear fashion, so that "primitive" organisms such as, say, a leech were not evolved for a niche but simply less advanced along a chain of being that we had long since crossed. Obviously, epigenetics provides no support for this notion.
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Dr Jack Member Posts: 3514 From: Immigrant in the land of Deutsch Joined: Member Rating: 8.4 |
Epigenetic changes pave the way to relevant epig. changes. In an entirely limited fashion. Epigenetic changes cannot build on each other. The primary form of epigenetics is methylation. A CpG island is either methylated or it is not. That's it. That's all it can do. Chromatin modifications have more scope and, in a very limited sense, one modification can enable another, but it cannot build new functionality or enable new modifications in the way DNA can. Remember that the very most epigenetic modification can do is enable or disable existing genetic components, or vary their levels of expression. I don't want to diminish the importance of these features - expression regulation is extremely important - but they don't compare to the ability of genetic change to form entirely new proteins, duplicate proteins, form hybrid proteins, and so on.
That is why i am talking about the NEW SYNTHESIS OF LAMARCKISM Sure, I just wanted to emphasise that epigenetics is not Lamarckism.
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Dr Jack Member Posts: 3514 From: Immigrant in the land of Deutsch Joined: Member Rating: 8.4 |
Perhaps you'd like to define what you mean by epigenetics, because what I mean by epigenetics is what biologists mean by epigenetics and they do not alter DNA sequences. It seems you want to go beyond anything we actually know or have evidence before.
Tell me, Zi ko, in your own words, what is epigenetic modification and how does it - at the molecular level - operate?
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Dr Jack Member Posts: 3514 From: Immigrant in the land of Deutsch Joined: Member Rating: 8.4 |
Both PTSD and depression are known to trigger increased methylation in the brain. However, these changes have AFAIK only been observed in somatic tissue not the gametes.
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Dr Jack Member Posts: 3514 From: Immigrant in the land of Deutsch Joined: Member Rating: 8.4 |
Firstly, Giraffe's have exactly the same number of vertebrae has other mammals. They're lengthened to produced the longer neck, not multiplied.
Secondly, classical theory does not suggest that giraffes first acquired a long neck, then long legs, then lost corns, etc. It suggests that these different features evolved alongside each other, stepwise genetic changes altering one increased selective pressures for the other features alongside the existing environmental pressures.
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Dr Jack Member Posts: 3514 From: Immigrant in the land of Deutsch Joined: Member Rating: 8.4 |
Epigenetic changes do not change into DNA changes.
There is utterly no doubt that you simply could not alter an Okapi (the Giraffe's closest relative) into a Giraffe by epigenetic change alone; you need DNA changes.
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Dr Jack Member Posts: 3514 From: Immigrant in the land of Deutsch Joined: Member Rating: 8.4 |
I do indeed mean sequence change, my bad.
None of that changes my point: there is no mechanism for the transfer of epigenetic changes to sequence changes, and no reason to think epigenetics played any major role in giraffe evolution.
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Dr Jack Member Posts: 3514 From: Immigrant in the land of Deutsch Joined: Member Rating: 8.4 |
I don't say so. What i am saying is that epigenetic changes pave the way( so guide) DNA sequence change. And how does it do that? What reason is there to think it does? You're making really quite an outlandish claim here. Epigenetics is not a wonder solution capable of all kinds of wonders; although it's true that epigenetics is still a field in its infancy we already have a decent idea about the generalities.
It is your belief. No, it's my informed opinion. Should you be able to provide evidence why I should change that opinion I will.
You don't answer my question. Which question in particular do you think I haven't answered? Do you mean this?
My question is:Are giraffe's neck and front legs elongation etc epigenetic in nature, or due to DNA sequenc change? And at which point of evoljtion the inevtable initial epigenetic effect was zeroed and was replaced by the DNA sequence change? Perhaps I wasn't clear. The elongation of a giraffe's neck are primarily due to DNA sequence changes* and there's no real reason to think epigenetics has any real role to play at all. This means your second question is essential moot. * - By the way, this contrast between DNA sequence change and epigenetics is kinda wrong-headed. Epigenetic capacity for change depends on the underlying DNA sequence. For example effective methylation requires CpG dinucleotide pairings at the very least, and appears only truly effective with CpG islands.
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Dr Jack Member Posts: 3514 From: Immigrant in the land of Deutsch Joined: Member Rating: 8.4 |
Nothing in that paper supports your assertions or contradicts anything I wrote.
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Dr Jack Member Posts: 3514 From: Immigrant in the land of Deutsch Joined: Member Rating: 8.4 |
What does any of that have to do with giraffe's necks? If you want to concede on megafauna and move on to discussing prokaryotes we can do that? Otherwise you will need to post something relevant to our long necked friends.
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Dr Jack Member Posts: 3514 From: Immigrant in the land of Deutsch Joined: Member Rating: 8.4 |
Taq is quite capable of reading, Zi Ko, as am I. We're asking you to make your own argument and present the relevant points you wish to discuss. Simply linking to the Koonin and Wolf paper again doesn't do that.
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Dr Jack Member Posts: 3514 From: Immigrant in the land of Deutsch Joined: Member Rating: 8.4
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In their paper (Is Evolution Darwinian or/and Lamarckian), Koonin and Wolf argue that recently discovered mechanism of change constitute Lamarckian mechanisms for evolutionary change. Let's go through the paper and see what their arguments are.
The paper begins with a historical perspective on Lamarck's ideas. There's nothing here we need to discuss, I'll just note that they draw particular attention to the point made by Lamarckists that his scheme suggests the inheritance of adaptive features only not any and all acquired traits and insist that Lamarckism needs to be more than mere "inheritance of acquired characteristics". Following the introduction we get to a section where Koonin and Wolf attempt to recast the Lamarckian hypothesis into genetic terms so that it can be assessed in a modern light. They summarise Lamarck's hypothesis as "Lamarck's idea of heridity is based on a threefold causal chain: environment-habit-form". That is, the environment alters the organism through the alteration of behaviour and that behaviour alters form in a heritable fashion. Koonin and Wolf then reformulate that idea as:
quote: This isn't a direct reinterpretation of Lamarck's ideas but I think we can see that it entails a modern reinterpretation of a similar scheme. Since Science regularly recasts ideas as we develop greater knowledge I think this is perfectly allowable. However, if it is to retain the essence of Lamarck's idea and remain a coherent and useful framework we need to be very careful in how we allow the key concepts to be understood. As we shall see, Koonin and Wolf fail to do this throughout the rest of the paper, and their failure renders their reformulation so broad as to be meaningless. Note also that Koonin and Wolf's "Lamarckian" makes no claims about change over time. Whereas Lamarck proposed a mechanism for explaining the diversity of life, Koonin and Wolf are not even requiring that it take even a supporting role. Having established what "Lamarckian" means to them, the authors then move on to present the examples they believe constitute Lamarckian processes. The first of these is the CRISPR-Cas system and it is probably their strongest example but, as we shall see, even it is only questionable Lamarckian and utterly limited in its scope. Before we move on to the problems with their interpretation I should probably explain what the CRISPR-Cas system is. CRISPR is a system present in prokaryotes that functions as an adaptive protection system that limits attack by phages and the acquisition of unwanted plasmids. In a manner analogous to RNAi in eukaryotes, the CRISPR systems produces short RNA sections (crRNAs) which are complementary to the target DNA sequences and allow the cells attack mechanisms to disrupt the target DNA. Cleverly, rather than relying on random mutation to develop the sequences from which these crRNAs are transcribed the CRISPR system instead works by directly incorporating fragments of the foreign DNA into specific sites in their core DNA. (See Marraffini and Sontheimer (2010) CRISPR interference: RNA-directed adaptive immunity in bacteria and archaea, Nature Review Genetics 11:181-190 for a fuller review) Thus the CRISPR system is a mechanism for producing inheritable change based on environmental factors (phage and plasmid encounters). The authors would have you believe that this meets their criteria for Lamarckism; I disagree. A key feature of the Lamarckian schema is the three fold process environment-habit-form but CRISPR is not environment-habit-form it is environment-form; it's not induced change in response to the environment; it's actively incorporating some part of the environment into the genome. This, it seems to me, is a key difference. However, even if we are to accept CRISPR as Lamarckian then it stands not as a mechanism for generating iterative change (and thus a mechanism that could explain diversity) but rather a highly controlled and specialised mechanism with tightly defined limits. Following on from CRISPR they briefly discuss similar mechanisms in other organisms, there's not much meat here and little new so I'll skip straight over it and move on to the most bizarre and false of their claims: that horizontal gene transfer is Lamarckian. I'll quote at length here:
quote: Oh dear. This is, at best, poorly phrased and on the face of it simply wrong. One interpretation is that the environment referred to here is the plasmid itself but if we're to allow such an understanding there's no reason not to go further and argue that sexual partners are part of the environment and thus all sexual reproduction in Lamarckian - clearly rendering the concept meaningless. It seems they instead are suggesting that the environment (antibiotic) causes the uptake of the correct plasmid to resist the antibiotic but this is not the case. Plasmid uptake is not triggered by the antibiotic and is not selective. It is a random, Darwinian, process. Plasmid uptake occurs at all times at random; the retention of the plasmid is then maintained in the presence of the antibiotic by selection. Cells that lose the plasmid die; cells that retain it do not. Simple, Darwinian, selection. The source of variation is now not sex or mutation but transformation but the process remains essentially Darwinian. Next up, they move on to what they call "quasi-Lamarckian" processes and begin by bumbling a description of stress-induced mutagenesis. I'll leave as moot the question of whether stress-induced mutagenesis is actually adaptive or whether it is a simple consequence of stress limiting the ability of an organism to suppress mutation. So, a quick recap: stress-induced mutagenesis occurs when an organism (prokaryotes are the main group known to undergo this process but there is emerging evidence in other organisms) is placed under stress conditions and results in an increased mutation rate. This can be adaptive if the high mutation rate produces beneficial mutation(s). Koonin and Wolf themselves admit "(a)daptive evolution resulting from stress-induced mutagenesis is not exactly Lamarckian because the stress does not cause mutations directly and specifically in genes conferring stress resistance." I'd go further: it's not Lamarckian at all. It does not meet their criteria. There is a response to the environment, yes, but the heritable change is strictly random and Darwinian; it's mutation followed by selection. There is no targeting (it does not meet their criteria 2). If we're to consider this "quasi-Lamarckian" then it is not clear that any mutation is not "quasi-Lamarckian" since nearly all mutation are induced by the environment - whether by radiation, free radicals or carcinogenic compounds. Thus allowing stress-induced mutation as Lamarckian renders the concept meaningless. Having presented their examples - each of which we have already seen to be flawed in interpretation - they go on to try and bring their ideas together. I'll not go over what they write here in detail, it seems pointless with their examples so obviously flawed that their conclusions have no foundation, but I'd like to draw particular attention to the laughable Figure 3 in which they absurdly claim that the "Lamarckian modality" takes over from the "Darwinian modality" under conditions of increasing stress. But, as we've seen, stress-induced mutagenesis is a strictly Darwinian process! The mechanism relies on basic Darwinian principles of mutation and selection. tl;dr: The papers examples are balls, and thus their conclusions are meaningless.
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Dr Jack Member Posts: 3514 From: Immigrant in the land of Deutsch Joined: Member Rating: 8.4 |
I am more than willing to classify the CRISPR system as a Lamarckian system with guided mutations. It is exactly what I have in mind when I think of such a system. I'm not so convinced. It's not clear to me that it's anything more than a specialised form of HGT. Importantly, it's missing any kind of middle step; it's environment->adaptation not environment->habit->form. Instead what we see is a random acquisition of phage fragments followed by maintenance of those fragments only in the presence of selection. The process is unusual and targeted but I think calling it Lamarckian is pushing it.
Yes and no. Phage induction can occur with LexA dependent SOS type mechanisms. These phage can carry antibiotic resistance genes as well as toxins (the Panton-Valentine leukocidin in S. aureus being a good example). I wouldn't be surprised if sex pilli were upregulated in harsh conditions. There is some merit in the claim that cellular damage can trigger mechanisms that increase HGT. Yes, you're correct. I'm afraid I didn't phrase that very well. HGT is increased by stress conditions (hell, the standard lab procedure for transformation uses chemical conditioning and heat shock) however it (a) occurs anyway and (b) isn't targeted. The bacteria aren't responding to antibiotic presence by searching for antibiotic resistance they're still adopting a process of random uptake (variation) and selection.
Most importantly, the authors focus on prokaryotes while zi ko is focusing on eukaryotes, so I am not sure why zi ko is going with this paper. Indeed.
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Dr Jack Member Posts: 3514 From: Immigrant in the land of Deutsch Joined: Member Rating: 8.4
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Why did not a single plant dsevelop this property? Because, I think, they did not need it. Precisely. Natural selection in plants did not reward the steps towards developing a nervous system so not such system developed.
Why did random mutation did not create a nervous system in even a single plant? Because a nervous system is not created by a random mutation; it's formed over millions of years by iterative positive mutations building it up in small steps.
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