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:
1) environmental factors cause genomic (heritable) changes
2) the induced changes (mutations) are targeted to a specific gene(s)
3) the induced changes provide adaptation to the original causative factor
—Koonin and Wolf
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:
Perhaps, the most straightforward and familiar case in point is evolution of antibiotic resistance. When a sensitive prokaryote enters an environment where an antibiotic is present, the only chance for the newcomer to survive is to acquire a resistance gene(s) by HGT, typically, via a plasmid. This common (and, of course, extremely practically important) phenomenon seems to be a clear case of Lamarckian inheritance. Indeed, a trait, in this case, the activity of the transferred gene that mediates antibiotic resistance, is acquired under a direct influence of the environment and is clearly advantageous, even essential in this particular niche.
—Koonin and Wolf
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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