The Origin of Biological Information, Part 3: CSI on Steroids

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April 7, 2011 Tags: Design

Today's entry was written by Dennis Venema. You can read more about what we believe here.

The Origin of Biological Information, Part 3: CSI on Steroids
If your heart is right, then every creature is a mirror of life to you and a book of holy learning, for there is no creature - no matter how tiny or how lowly - that does not reveal God’s goodness.

Thomas a Kempis - Of the Imitation of Christ (c.1420)

In part 2 of this series, we explored how the Long Term Evolution Experiment (LTEE) performed by the Lenski research group on E. Coli, demonstrates some key features of how biological “complex, specified information” (i.e. “CSI” as the ID movement terms it) arises through mutation and natural selection. To briefly recap, we noted that:

  1. CSI does not need to arise all at once, but can arise piecemeal through independent mutation events.

  2. Separate mutations that later combine to form CSI do not need to confer a specific advantage on their own. In other words, mutations that are “neutral” with respect to the survival of the organism can later be co-opted into CSI that does have a distinct survival advantage.

  3. Neutral mutations may open up new future paths. In the LTEE, the brand-new ability of one bacterial population to use citrate as a food source required that a neutral mutation appear several thousand generations before it combined with other mutations to provide the CSI for using citrate.

  4. When CSI arises, it can be pretty poor at the beginning. Nascent CSI, though poor, provides a survival advantage because it is the “best game in town” at that time. Further mutation in, and natural selection on, the offspring of the original CSI-holder quickly refine the nascent information into ever-more “specified” CSI.

And, as we noted at the close of the first post in this series, understanding how natural processes create information is in no way a threat to God’s ordaining and sustaining of creation. Rather, it is an opportunity to explore some of the mechanisms by which He does so.

With these important principles in mind, we are ready to examine a second fascinating case of a novel function arising through mutation and selection: the evolutionary history of steroid hormones and their protein receptors in vertebrates.

Experimental Evolution as Textual Criticism

The elegant work by the Lenski group has one very distinct advantage that other researchers surely envy: when new structures and functions arise in the experiment, a trip to the freezer is all that is needed to resurrect and examine the relevant ancestors. For researchers who study other organisms less amenable to laboratory experimentation, or for evolutionary transitions that happened deep in the past, other methods are needed. One approach to this type of problem is to “resurrect” ancient proteins in the lab in order to study their properties.

Bringing an ancient gene back to life starts with determining what its DNA sequence was, (and thereby determining the sequence of amino acids that made its functional protein product). While researchers don’t have direct access to ancient DNA, we have the next best thing: many modern examples of genes copied from the ancestral one.

For those who are familiar with textual criticism, the principles are very similar. Textual criticism is the process of recovering the words of an ancient manuscript by comparing several very similar, but still imperfect, copies. In general, as more copies agree on a certain wording, the more likely it is that the original had that wording. Also, the more widespread and older a certain wording is, the more likely it is original. Groups of manuscripts that have similar copying errors or other variations can be grouped together as more closely related, and so on. Given enough manuscripts, it is possible to recreate a copy of an ancient text with a very high degree of accuracy. As Christians, we benefit from this type of analysis daily when we read the Bible: though no two Greek manuscripts of the New Testament are exactly alike, scholars have used these methods to recover the original text with a very high degree of confidence.

And so too, for ancient gene sequences. Consider a hypothetical amino acid sequence in six modern organisms:

Though none of the modern sequences are identical, it is easy to see that there is a “consensus” at each of the 12 amino acid positions. This consensus sequence is very likely to be the ancestral sequence: explaining the pattern in any other way requires many more changes, with many changes occurring in parallel after species separate.

Once the researchers determine the correct ancestral amino acid sequence, it’s a relatively small matter to engineer a DNA sequence that encodes it and give it to cells to make into protein. This protein can then be tested to see how it functions compared to the modern sequence.

What makes this type of analysis even more interesting is that sometimes related genes acquire new functions. In cases like these, bringing the ancestral gene back to life in the lab allows researchers to not only test its properties, but to test hypotheses about what the specific amino acid changes were that changed the protein’s function over time:

The laboratory of Joseph Thornton at the University of Oregon has used this method (with great success) to determine how certain hormone / protein receptor complexes arose during vertebrate evolution. Hormones are small molecules that act as signals by binding to a protein target, called a receptor. The receptor / hormone pair then goes on to effect a change in the target cell by regulating other genes.

In vertebrates, two hormone – receptor pairs were of interest to the Thornton group: the mineralocorticoid receptor (MR), which binds a steroid hormone called aldosterone, and the glucocorticoid receptor (GR), which binds a second steroid hormone called cortisol (see diagram above). Cortisol can also activate MRs, but an enzyme that breaks down cortisol is present in tissues where MR is used so cortisol cannot accumulate. Aldosterone, on the other hand, cannot activate GR – it is specific to its binding partner MR. Even though these two hormone / receptor pairs regulate different processes in modern organisms, the two receptors are the result of an ancient gene duplication that occurred early in vertebrate evolution, around 450 MYA (million years ago). As time has gone by, the derivatives of the original gene have picked up distinct binding partners and physiological roles. Thornton and colleagues wanted to tease out the details of these important changes.

They started out by determining the ancestral sequence of the original receptor gene, prior to the duplication, and recreating it in the lab. When they tested this lab-designed protein, they found that it, like modern MRs, (but not GR’s)could bind either cortisol or aldosterone indicating that the ancestral protein must have been able to bind both. This result suggested that somewhere along the line the GR lost its ability to bind aldosterone and became specific to cortisol. This is interesting, because at the time the ancestral receptor was present, aldosterone didn’t exist. Aldosterone is a relative newcomer on the scene: it is present only in four-limbed vertebrates (tetrapods), which arose around 390 MYA. So, the ancestral receptor present prior to 450 MYA already had the ability to bind a hormone that wouldn’t evolve for tens of millions of years. Of course, the ancestral receptor “didn’t mind” – it had its own binding partner - a steroid hormone closely related to cortisol and aldosterone. It wasn’t sitting around doing nothing in the meantime.

This finding strongly suggested that the reason aldosterone binds only to MRs is because modern GRs, in contrast to the ancestral protein, have lost the ability to bind it. By comparing the amino acid differences between MRs and GRs, the Thornton group was able to test different combinations to see what the key changes likely were. They also did the (difficult) work of determining the precise new shape of the receptor for each of the changes that had an effect. All in all, it is an impressive body of scientific work.

Through these techniques, the Thornton group demonstrated that the loss of aldosterone sensitivity in GR occurred in a series of mutational steps that progressively remodeled the portion of the GR that binds the hormone molecule:

  1. First, a mutation occurred that altered one of the amino acids near the hormone binding site. This change had no effect on its own (it was a neutral mutation).

  2. Second, a change in an amino acid outside the binding pocket bent one side of the binding site into a new shape. Now the amino acid from the first neutral mutation in step #1 was thrust up against the hormone binding site. This amino acid can interact appropriately with cortisol, but not very well with aldosterone. The receptor was now strongly biased towards cortisol.

  3. Later, several more mutations accrue that “tune” the receptor to its new specificity. Some of the mutations are neutral at first (like step #1) and then combine with later mutations to refine the receptor into its modern cortisol-specific role.

As the GR and MR lineages were becoming functionally distinct, other changes in other genes accumulated that refined their ability to regulate different processes (such as the enzyme that breaks down cortisol where MR is present, or the target genes that the two hormones regulate). While many of those details remain to be worked out, this work is an elegant demonstration of how a new function arose: gene duplication; sequence divergence with a neutral mutation that opened up a new possible trajectory; a second mutation that altered function in one of the gene copies; further mutations that refined this nascent difference; and the final result of new structures and functions that act as key regulators of important physiological processes in tetrapods, including humans.

In other words, new CSI.

Over and against these lines of evidence, however, the Intelligent Design Movement claims that such novelty is inaccessible to random mutation and natural selection. Rather, they claim that functional protein shapes are incredibly rare and therefore so isolated from each other that random mutation and natural selection cannot bridge the vast gulfs between them. Though Thornton’s work (and the work of Lenski that we examined previously) refutes this claim with detailed, concrete examples, new comparative genomics tools have addressed this issue with greater power and breadth than ever before. In the next post in this series, we’ll explore the question: are these examples rare, isolated cases, or indicative of a wider pattern?

Further reading:

Harms, M.J. and Thornton, J.W. (2010). Analyzing protein structure and function using ancestral gene reconstruction. Current Opinion in Structural Biology 20: 360-366.

Bridgham, J.T., Carrol, S.M., and Thornton, J.W. (2006). Evolution of hormone-receptor complexity by molecular exploitation. Science 312: 97-100.

Thornton, J.W. (2004). Resurrecting ancient genes: experimental analysis of extinct molecules. Nature Reviews Genetics 5: 366-375.


Dennis Venema is professor of biology at Trinity Western University in Langley, British Columbia. He holds a B.Sc. (with Honors) from the University of British Columbia (1996), and received his Ph.D. from the University of British Columbia in 2003. His research is focused on the genetics of pattern formation and signaling using the common fruit fly Drosophila melanogaster as a model organism. Dennis is a gifted thinker and writer on matters of science and faith, but also an award-winning biology teacher—he won the 2008 College Biology Teaching Award from the National Association of Biology Teachers. He and his family enjoy numerous outdoor activities that the Canadian Pacific coast region has to offer. Dennis writes regularly for the BioLogos Forum about the biological evidence for evolution.

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Bilbo - #58042

April 14th 2011

Alan: “But what do you mean by designed? And when you say “designed” there is
an implication of “design and build”. And the time line? I guess it
would be difficult to design something after their appearance. What does
“by nano-technology” mean?”

Designed:  Purposeful arrangement of parts.  Yes, design and build.  Time line:  Not enough evidence to determine.  Most likely at or before their appearance on earth, though if time travel is possible, that opens a whole other can of worms.  Nano-technology:  purposeful arrangement of parts at the molecular level.


Bilbo - #58043

April 14th 2011

Alan:  “Don’t wait to be asked. Jump right in. Please
define “front loading”. As a bonus, could you say if you believe there
is a consensus among “front loaders” as to definitions.”

Mike Gene’s front-loading:  Original cells were designed and pre-adapted, so that neo-Darwinian processes (natural selection acting upon random mutation) would have a more likely chance of producing metazoan life.  This does not mean that the genomes for specific animals already existed in the first cells.  It does mean that either the proteins and developmental “programs” that would be needed existed, or that they could be “reached” by random mutation more easily than a random assortment of proteins and developmental programs would be expected to allow.  

I don’t know how other front-loaders define it. 

By the way,  Alan, how the heck do you get quotes of other commenters to italicize?  It’s driving me crazy!


Alan Fox - #58056

April 15th 2011

Alan, how the heck do you get quotes of other commenters to italicize?


Use the buttons in the text box. But I just lost a post to you because it was way over the character limit, even when it wasn’t. More later.


Alan Fox - #58065

April 15th 2011

I am having difficulty seeing how a pre-adaptation could exist without being there in some form and what that form could be if not DNA. And if you are talking about first cells then I would have thought we would then be discussing theories of abiogenesis. If you are talking about proteins as precursors before being encoded in DNA, this is definitely in the sphere of abiogenesis. You also seem to be creating a problem for yourself as there is no reverse process where protein sequences can be dead back into DNA in vivo. Incidentally, what do you think of when you use the phrase “developmental program”?




Alan Fox - #58068

April 15th 2011

“dead back” should read as “read back…”


R Hampton - #58052

April 14th 2011

Bilbo,
Does the planet Earth exhibit a purposeful arrangement of parts?


Crude - #58055

April 15th 2011

But I don’t know what it means. I think it is wishful thinking but please correct my misapprehension. 


So, you don’t know what front-loading even means, but you think it’s wishful thinking?

The concept is not particularly hard to understand. 

Past states can influence or determine future states. 
A designer with sufficient knowledge can set up a past state to guarantee or make far more likely a particular future state.
Some results of evolution may have been determined or made more likely by one or several past states.
It’s possible in principle that this past state or past states may have been set up by a designer, so attempts to investigate this are made.

Honestly, if you’ve struggled for years to understand these concepts - concepts which are, at heart, second cousin to “cause and effect” or even “preadaptation”, the fault may not lie with Mike Gene. Maybe you’re just a little slow when it comes to this topic.

Alan Fox - #58057

April 15th 2011

Maybe you’re just a little slow when it comes to this topic.


Well, there’s no rush. Other than changing “the designer” to God, there’s nothing in your comment to disagree with, or that adds anything, so far. Perhaps it is a preamble.

Crude - #58058

April 15th 2011

Yeah, nothing that adds anything. I just explained in baby steps the basic concept of what front-loading is as you’ve requested, while you’ve been saying that both A) You don’t know what front-loading is, and B) you’re sure it’s wishful thinking. You’re struggling with the concept and don’t understand it despite monumental effort - but you know you reject it.


Again: Have you considered the possibility that - with regards to this topic - you’re actually pretty slow and are having trouble with what’s easy for most people to grasp? That this very basic idea is very easy to get, and that the fact that you’ve apparently been struggling for years with the concept that past states can determine or influence future states may not be someone else’s fault?

I mean, it’s either that or willful misrepresentation, combined with disingenuously blaming others for your “confusion” when this is called out. But let’s go with the generous interpretation: Maybe you’re just rather slow.

Alan Fox - #58066

April 15th 2011

Crude:


I just explained in baby steps the basic concept of what front-loading is…

I think we must differ on our understanding of the concept “explain”.

Incidentally, take you take a correspondence course with  the Joseph Gallien School of Charm and Charisma?

Alan Fox - #58067

April 15th 2011

Did you take etc


John - #58076

April 15th 2011

Crude:

“So, you don’t know what front-loading even means, but you think it’s wishful thinking? The concept is not particularly hard to understand.”

Why is the concept apparently impossible for its advocates to put into practice if they understand it so well?

“Past states can influence or determine future states. A designer with sufficient knowledge can set up a past state to guarantee or make far more likely a particular future state.”

And hypotheses about the timing of such setups are empirically testable, but no ID proponent wants to test them.

“Some results of evolution may have been determined or made more likely by one or several past states.It’s possible in principle that this past state or past states may have been set up by a designer, so attempts to investigate this are made.”

Why the passive voice? 

And how do you define “investigate” in this context? Surely not the empirical testing of hypotheses!

Gregory - #58097

April 15th 2011

“A designer with sufficient knowledge can set up a past state to guarantee or make far more likely a particular future state.”

Made me wonder whether or not ‘decider’ might be a suitable substitute for ‘designer’. That would lead us to discuss ‘intelligent decisions’ instead of ‘intelligent designs,’ the latter which were also presumably based on ‘decisions.

One of the glaring faults of ‘intelligent design’ is what it declares is outside of its research province up-front: *No* discussion of ‘who, when or where’ wrt ‘how’ the process of designing (or deciding) is/was happening. To pretend ‘intelligent design’ has much ‘scientific explanatory power’ without those things is of course a stretch.

The ‘arguments for/to design’ by religious folks have been around for years and years. ‘Arguments for/to decision,’ now there’s an idea that if followed would give intelligent decisionists something to investigate!

Such a topic, however, is not predominantly in the natural-physical sciences; those are not the ‘scientific fields’ in which ‘decision’ & ‘choice’ are paramount (& most often non-existent). What we therefore require is to dislocate or relocate the naturalistic dialogue away from its comfortable zones, to highlight for days and days, uncomfortable things for ‘naturalism,’ i.e. ‘real, historical’ supra-natural-physical things, like Sophia.

She won’t decide for you or anyone here, crude - but we would be wiser for the seeking.


Ashe - #58087

April 15th 2011

John wrote: 

nor is it required for epilthelial formation. 

Actually, beta-cateinin in Dicty is required for epithelial formation. Also, Aardvark has an alpha-catenin binding site, but fungal Arm repeat proteins like yeast Vac8 do not.   I think the presence of this site is diagnostic of a “true” beta-catenin, at least from the point of view of its role in epithelial structure.  


Ashe - #58090

April 15th 2011

Actually, it appears that it was more wishful thinking than careful analysis, if you had bothered to read what I cited. Wishful thinking is a very strong drug, and careful scientists do things like double-blinding before analysis.”

Huh? You said Aardvark isn’t required for epthelial formation, the actual data and the paper state the exact opposite:

“Although D. discoideum lacks a cadherin homolog, we identify an α-catenin ortholog that binds a β-catenin–related protein. Both proteins are essential for formation of the epithelium, polarized protein secretion, and proper multicellular morphogenesis. ”

“both Ddα-catenin and Aardvark are required to organize and polarize the tip epithelium during culmination.”

“Yes, but it lacks the signalling features of beta-catenin”

Which signaling features? 

“More importantly, it’s an outlier in the nested hierarchy to the group of beta-catenins plus plenty of non-beta-catenins.”

What do you mean by that exactly? 

 


Bilbo - #58111

April 16th 2011

Alan:  “I am having difficulty seeing how a pre-adaptation could exist
without being there in some form and what that form could be if not DNA.”

Sounds good to me. 

” And if you are talking about first cells then I would have thought we
would then be discussing theories of abiogenesis.”

Why?

 “If you are talking
about proteins as precursors before being encoded in DNA, this is
definitely in the sphere of abiogenesis.”

Why?

 “You also seem to be creating a
problem for yourself as there is no reverse process where protein
sequences can be dead back into DNA in vivo.”

If I were starting with proteins, yes.  I’m not and I don’t think Mike is either.

“Incidentally, what
do you think of when you use the phrase “developmental program”?”

DNA sequences that help cells develop certain features as they grow.

And I still can’t get the italicize thingy to work.  I must certainly be slow.



Bilbo - #58112

April 16th 2011

RH:  “Does the planet Earth exhibit a purposeful arrangement of parts?”

Maybe, but that it isn’t a part of Mike’s hypothesis.

Yeay!!! I got the italicize thingy to work!


Jon Garvey - #58114

April 16th 2011

“Yeay!!! I got the italicize thingy to work!”

Just goes to show - keep changing things at random and eventually things are bound to improve…


Alan Fox - #58139

April 17th 2011

Why? (to first cells.)


Because evolutionary theory does not attempt to explain the origin of pre-cellular life, if there was such a thing. It picks up at the point when the first self-replicating organism arrives on Earth.

Alan Fox - #58140

April 17th 2011

If I were starting with proteins, yes.  I’m not and I don’t think Mike is either.


So… What are you starting with?

Me:

Incidentally, what do you think of when you use the phrase “developmental program”?

Bilbo:

DNA sequences that help cells develop certain features as they grow.

But that is the role of all DNA that contributes to the growth and development of an organism. It’s a very vague statement. 

Bilbo - #58145

April 17th 2011

Alan:  “Because evolutionary theory does not attempt to explain the origin of
pre-cellular life, if there was such a thing. It picks up at the point
when the first self-replicating organism arrives on Earth.”

Agreed,  But why is that relevant to Mike’s hypothesis?

“So… What are you starting with?”

Mike’s hypothesis is that the first cells were designed.  By “cells” he includes what we normally find in bacteria:  DNA, RNA, proteins.

“But that is the role of all DNA that contributes to the growth and development of an organism. It’s a very vague statement.

True.  The point is that front-loading would either include that DNA, or would make it easier to evolve that DNA.


Bilbo - #58146

April 17th 2011

BTW, that italicize thingy is very finicky.


Bilbo - #58150

April 17th 2011

Also, though Axe doesn’t refer to Dennis’s presentation, it does seem to be relevant to it:

http://biologicinstitute.org/2011/04/16/when-theory-and-experiment-collide/


John - #58155

April 17th 2011

I don’t see how it’s relevant, Bilbo. Can you spot the big difference?


John - #58157

April 18th 2011

John:

“Anyone else notice the extra word that Mike slipped in to construct his straw man? I wrote “a beta-catenin,” and Mike claims I wrote “a beta-catenin homolog.”“

Mike:
“Okay, let’s deal with the semantics, as I was not trying to construct any straw man by slipping in any word.”

Then why did you slip in a word and misrepresent me?

“You are the one who framed your claim as a choice between beta catenin and “just” an “Arm repeat-containing protein.”  In reality, there is middle ground between the two, middle ground that would be occupied by transitional states.”

But those transitional states are not beta-catenins.

Let’s make it more clear, Mike. Take the following two statements:
1) Alpha-catenin is a beta-catenin homolog.
2) Alpha-catenin is a beta-catenin.
Now even most laypeople could guess from the terms that the 1 is true and 2 is not only false, but stupid. 

So, are Aardvark and the Volvox protein closer to beta-catenin than alpha-catenin is to beta-catenin?

“The question that interests me is whether this middle ground was already being traversed prior to the emergence of metazoa.”

Why the emergence of metazoa? Why not the emergence of multicellularity?

“In other words, were preadaptations in play helping to facilitate the emergence of metazoa?”

Your word games say yes, while the data say no.

“The alternative would have the initiation of these transitions occur concurrently with the evolution of metazoa as part of a vast co-evolutionary network under some broad selection pressure for the metazoan state.”

Except that there’s no such thing as “the metazoan state,” Mike. Multicellularity is a state, but since Dictyostelium can exist in that state, you’re fudging because the evidence shows that initiation of those transitions did occur under selection pressure for multicellularity.

“For a few years now, my front-loading perspective has led me to expect the former and I am thus encouraged to see the recent Science paper conclude:…”

Ah, quote mining. Precisely what my hypothesis predicts from you!

“Not exactly conclusions that should discourage me from viewing through the prism of front-loading.”

But the data should, so you quote conclusions instead. Do you think the authors have any enthusiasm for front-loading?

John - #58159

April 18th 2011

Mike:“Look, we’re both supposed to be Christians, right?”


Right.

“Instead of pointing fingers, making accusations, and trying score points, let’s agree that we have a classic example of miscommunication here.  For it seems to me that you are under the mistaken impression that I am proposing the human beta catenin protein is floating about in the cytoplasm of Volvox.”

And there you go, pointing fingers and making false accusations to score points! Are you saying that you’re not a Christian?

“For that is the claim that your 5 minute BLAST test would refute.  It’s not a test that falsifies a homologous relationship, as I showed with Aardvark. What I have been proposing is that this Volvox protein is a beta-catenin-like protein.”

No, Mike. You claimed that it was a beta-catenin. Full stop. Who’s making a mistake here?

“The beta-catenins are found in green algae (Volvox), indicting that they existed in the last common ancestor of green algae/plants and animals.”

That’s from your blog post before you corrected it, you sneaky debbil.

“It’s a hypothesis - the middle ground of transitional states toward beta-catenins was already under way  before the emergence of metazoa.”

That’s not a hypothesis that makes empirical predictions. It’s a cheater’s hypothesis-like proposal.

Fortunately, you did include a testable hypothesis in your post that you forgot to delete, falsely presented as fact:

“Beta-catenin is a protein with two different crucial roles to play in metazoan existence: it is a key component of the adherens junction, thus epithelial tissue, and it is part of a key circuit that regulates gene expression needed for growth and development. In essence, beta-catenin integrates information from multiple sources: the genome, the cytoskeleton, the membrane, and the environment.
“As you can now see, this integrator existed prior to the existence of metazoan life, where it plays same basic functions in an organism that exists most of the time in a single-celled state.”

But since the Dickinson et al. paper shows that Aardvark does not regulate gene expression, your unintentional hypothesis has been falsified.

What would a Christian do? 

I suspect that while when you wished for it to be true, gene expression was incredibly important, but now that you know that the transcriptional regulation functions aren’t there, it will magically become unimportant.

What did Jesus Christ say about hypocrisy? Here’s another question: is beta-catenin important primarily for evolutionary or for clinical reasons?

Bilbo - #58172

April 18th 2011

Hi John,

I think you are replying to Mike in the wrong thread, though I’m not sure what the right thread is.  And you’re right, on second reading, Axe’s comments aren’t that relevant to Dennis’s point.


Mike Gene - #58183

April 18th 2011

John: And there you go, pointing fingers and making false accusations to score points! Are you saying that you’re not a Christian?

We really can’t communicate here.  I simply point out that we are miscommunicating and note that your impression about my position is mistaken, and you exclaim you are being attacked.  Sorry John, I am not making any false accusations against you to score points.  I am pointing out that your understanding of my position is mistaken. 

No, Mike. You claimed that it was a beta-catenin. Full stop. Who’s making a mistake here?

You are.  Let me show you.  You support your accusation by quoting from my blog as follows:

“The beta-catenins are found in green algae (Volvox), indicting that they existed in the last common ancestor of green algae/plants and animals.”

So rather than acknowledge we have been talking past each other, you insist on sticking with your mistaken impression by supporting it with a quote mine that relies on a very uncharitable interpretation.  

First, you ignore the context of the whole blog post.  There are many more places where I describe the Volvox protein as a homolog of beta catenin and not beta catenin itself.  For example, two sentences after that quote, I also wrote, “The bottom line here is that homologs for all components of the adherins junction existed long before the simplest of metazoans came into existence (even though no single celled organism in particular contains all components).”   And “I began to suspect a homologous relationship between the alpha importins and beta catenin from sequence comparison between a Volvox protein that I previous scored as a beta catenin-like protein and human beta catenin.” There’s more, but that should be enough to show the selective nature of your quoting.

Second, and even more importantly, you ignore the context of our discussion we had back in early December  2010 here at BioLogos.  Here is how I introduced it:

One such example of a “different angle” is looking at evolution through the “conception” of design.  For example, what if epithelial, nervous, connective, and muscle tissue have had been in the cards long before they came into existence?  What if it was just a matter of time before such tissues would appear?  This perspective allowed me uncover what clearly appears to be a homolog of the beta-catenin gene in Volvox, a species of green algae.

You’ll note I clearly described it as a homolog of the beta-catenin gene.  I never claimed it was human beta catenin.  I thought you understood this because your original reply was to challenge the homology inference.  You wrote, “What’s clearly homologous about mid-20s percent Identity?” So I replied, “It’s a 27% identity over the entire 525 amino acids of the Volvox protein with an E value of 1e-25.  Also, the Conserved Domain Database representation predicts almost an identical domain arrangement of the two proteins (although beta catenin has an extra 100 amino acids on both ends).”

It’s then that you proposed your 5 minute BLAST test.  I did that, and more, and concluded our exchange as follows:

However, I do think your concern is indeed legitimate, as you may be right.  But I would maintain the Volvox protein can be scored as putative homolog of beta-catenin (more than “just a protein with Arm repeats”) and this scoring is supported by some circumstantial evidence.

I clearly described it as a putative homolog of beta-catenin (more than “just a protein with Arm repeats”). 

The bottom line here is that, once you understand my position correctly, contrary to your accusations on the first page, that 5 min BLAST test you proposed failed to show my hypothesis was wrong. 

What your full-stop shows me is that you have ignored the context of the blog entry and our previous discussion from four months ago and chose to quote mine one particular instance where I was a little sloppy in my wording so that you can score points.  

That’s from your blog post before you corrected it, you sneaky debbil.

Yes, after my last reply to you here, the source of confusion had finally become clear to me so I took a few minutes to tidy up the blog entry to prevent future needless confusion.   There is nothing sneaky about it, especially given that the argument of the entire post does not change and the originals are still posted on my blog (the link Ashe provided you a few days back is an entry that combines those posts and links to them).  Besides, if you had bothered to show up here over the weekend, I might have informed you of the changes.


Mike Gene - #58184

April 18th 2011


What would a Christian do?

With you, John, I must practice turning the other cheek. I’ll turn to scripture:

You,
my brothers and sisters, were called to be free. But do not use your
freedom to indulge the flesh; rather, serve one another humbly in love.
For the entire law is fulfilled in keeping this one command: “Love your
neighbor as yourself.” If you bite and devour each other, watch out or
you will be destroyed by each other.

Galatians 5:13-15

But
the fruit of the Spirit is love, joy, peace, forbearance, kindness,
goodness, faithfulness, gentleness and self-control. Against such things
there is no law.

Galatians 5:22-23


John - #58207

April 19th 2011

Mike Gene:

“We really can’t communicate here.  I simply point out that we are miscommunicating and note that your impression about my position is mistaken,…”

But you misrepresented my impression.

“You support your accusation by quoting from my blog as follows: “The beta-catenins are found in green algae (Volvox), indicting that they existed in the last common ancestor of green algae/plants and animals.” “
“There are many more places where I describe the Volvox protein as a homolog of beta catenin and not beta catenin itself.”

Mike, I described your false claim as portraying it as “a beta-catenin.” I have never included the word “itself,” and I have pointed out that you are dancing around the term “ortholog.” You portrayed it as an ortholog. All orthologs are homologs, but most homologs are not orthologs.

“You’ll note I clearly described it as a homolog of the beta-catenin gene.  I never claimed it was human beta catenin.”

I never used the adjective “human” in describing your misrepresentation of Aardvark as an ortholog (a beta-catenin), so you are falsely attributing a position to me. 

Me: “That’s from your blog post before you corrected it, you sneaky debit.”


“Yes, after my last reply to you here, the source of confusion had finally become clear to me so I took a few minutes to tidy up the blog entry to prevent future needless confusion.   There is nothing sneaky about it,…

“There is everything sneaky about it, Mike, given that you had retained the false statements:

“This entry combines all the front-loading beta-catenin posts into one without any editing.”

”...it is a key component of the adherens junction, thus epithelial tissue, and it is part of a key circuit that regulates gene expression needed for growth and development. In essence, beta-catenin integrates information from multiple sources: the genome, the cytoskeleton, the membrane, and the environment.
“As you can now see, this integrator existed prior to the existence of metazoan life, where it plays same basic functions in an organism that exists most of the time in a single-celled state.”

tinyurl.com/3mmqpgx

Aardvark doesn’t have the same basic function in regulating gene expression. 

“Besides, if you had bothered to show up here over the weekend, I might have informed you of the changes.”

This is more about what other people will be fooled into believing, not me.


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