Friday quote: More wisdom from Kirschner & Gerhart
by KrauzeI've quoted from Kirschner's & Gerhart's The Plausibility of Life before, but here's another goodie, which could be adopted as the position statement of every front-loader:
"Much of the skepticism over the years about the capacity of random mutation or genetic reassortment to generate phenotypic change has arisen from the assumption that genetic change must create very specific, multiple, complex phenotypic changes. Our view is that specificity and complexity are already built into the conserved processes, as is the propensity for regulatory coupling. It is not necessary for genetic change to create those characteristics, though they are still needed for heritable change."
Marc W. Kirschner and John C. Gerhart, The Plausibility of Life: Resolving Darwin's Dilemma (Yale University Press, 2005), p. 142
This thread also doubles as an open thread. So talk about front-loading or something else. I'm like, whatever.
June 30th, 2006 at 1:21 pm
I'm reading through This book. I haven't gotten there yet, but what struck me is that they completely disowned non-random mutations in the beginning of the book. It seems to me that there is a whole group of biologists who have been asleep for the last 7 years while all of the evidence for directed mutation has come in.
Comment by johnnyb — June 30, 2006 @ 1:21 pm
July 1st, 2006 at 12:03 pm
Well, I have been wondering just what front-loading means.
What is it that was "front-loaded," the universe, the first life?
Is it mono-phyletic or poly-phyletic?
Is it deterministic?
Comment by Mung — July 1, 2006 @ 12:03 pm
July 1st, 2006 at 12:27 pm
Krauze and I hypothesize that the first life forms were front-loaded as a consequence of being designed.
That is something that can only be answer after the investigation. But I do propose that the original life forms were a consortium of cells, thus I favor a quasi-polypyhletic hypothesis.
No. It's more about channeling and putting constraints on the Blind Watchmaker. Like I noted before, FLE = RM & NS under control. My interest is in trying to decipher the nature, extent, and even objective of this control.
Some of this will be outlined in more detail in my books.
Comment by MikeGene — July 1, 2006 @ 12:27 pm
July 1st, 2006 at 5:13 pm
Interesting thoughts on front-loading… I'm inclined to think front-loading or directed mutagenesis sounds rather Lamarckian, but I'm interested in hearing what you have to say.
Please let me know when you'll have it outlined in more detail.
Thanks!
Comment by Daniel — July 1, 2006 @ 5:13 pm
July 2nd, 2006 at 9:33 am
It seems to me then, that front-loading would face many of the same objections as modern evolutionary theory.
Is there any aspect of MET, real or theoretical, that front-loading does not accept?
Are you guys ever going to front-load a forum for us to discuss front-loading on?
Comment by Mung — July 2, 2006 @ 9:33 am
July 2nd, 2006 at 10:05 am
Daniel,
"I'm inclined to think front-loading or directed mutagenesis sounds rather Lamarckian, but I'm interested in hearing what you have to say."
A good place to start reading about front-loading would be here.
Mung,
"Is there any aspect of MET, real or theoretical, that front-loading does not accept?"
That depends. What are the real or theoretical aspects of MET?
"Are you guys ever going to front-load a forum for us to discuss front-loading on? :)"
What about this one?
"This thread also doubles as an open thread. So talk about front-loading or something else."
Comment by Krauze — July 2, 2006 @ 10:05 am
July 2nd, 2006 at 4:34 pm
I gave Mike's book some free advertising over at the MacNeill's class. So do I get a discount? Seriously, can we expect to find some concrete proposals for research for FLE, or any other ID hypothesis, in the book?
Comment by Bilbo — July 2, 2006 @ 4:34 pm
July 2nd, 2006 at 7:11 pm
Mike, you blase' theist, you.
Comment by Bilbo — July 2, 2006 @ 7:11 pm
July 3rd, 2006 at 6:32 pm
Hi Bilbo,
Check this out to see if it helps.
Comment by MikeGene — July 3, 2006 @ 6:32 pm
July 3rd, 2006 at 7:29 pm
Mike,
Since this is an open thread, I was curious to learn more about the frequecy of lab-observed gene duplications and the needed regulatory apparatus to make the duplicate genes participate in redundancy.
This has teleological implications, obviously.
In reading the literature, they take duplicated genes as a given. But this seems rather odd, because why should genes duplicate with fidelity along with regulatory elements to help them form redundancy?
At the recommendation of Ricardo Azevedo, I'm studying Andreas Wagner's book on robustness. As I suspected, redundancy is weakly selectable, but it has obvious survival advantages. This is a rather odd fact that we have a funcitonal feature with weak selective advantage, but strong survival value. This has strong teleological implications.
Wagner (not so directly) points out that the redundancy has to originate based on somewhat fortuitous events because it's immediate selection value is low (redundant systems will help a creature survive with little, or no apparent loss of fitness!).
I'm not so convinced the events are that fortuitous, I am of the opinion the capacity to create redundancy is designed.
I was little frustrated because peer-reviewed literature was rife with circularly justified claims not being distinguished from empirical facts.
I know we have seen replication errors in the lab, but I'm extremely reluctant to say a gene duplication along with the necessary regulatory coupling is a complete error.
Do we see any evidence of complete, and clean duplications along with regulatory coupling directly in the lab?
Salvador
Comment by Salvador T. Cordova — July 3, 2006 @ 7:29 pm
July 3rd, 2006 at 7:55 pm
Its the closest open thread I can find, so…
Joy gets uncomfortable when others point out the, um, crankiness of her ideas.
Let's see how widely-shared they are on TT "¦..
Resolved "“ the TelicThoughts crew are on board with joy's assertion that the CaMV promoter is an infectious viral vector.
From this discussion
joy never, ever in the linked thread backed off from this ludicrous assertion, and she still clings to it, judging from another blog thread here.
So, what say ye, TTers? Is the 35S promoter a plant virus, or is it not?
And please, just for entertainment, give us more than a "yes" or "no". If yes, then explain, in some detail (names of the enzymatic and DNA players, etc.) how the promoter propagates as a virus. If no, then explain in terms joy might be able to grasp just how wrong she is.
(No answer will be interpreted as agreement with joy. I'm not into guessing games.)
Comment by Art — July 3, 2006 @ 7:55 pm
July 3rd, 2006 at 8:14 pm
Yeah! When is anyone going to comment on Paul Nelson's arguments re: ORFans. If his assertions are correct, then I'd have to say front-loading as a proposal for an evolutionary "mechanism" (I use the term very loosely) is DOA.
Comment by Art — July 3, 2006 @ 8:14 pm
July 3rd, 2006 at 9:23 pm
Since I'm setting off firecrackers here….
Over on Dembski's blog, a commenter remarked "There's simply too little information there to completely specify an organism ", talking in context of genome sizes, etc. DaveScot chimed in "I hear ya. There's less than a gigabyte of information in the ordering of 3 billion bases (approx. human genome)".
DaveScot didn't want the IDers on that blog to tackle a very simple question - I suspect because they would choke on it. Maybe the TT readers are better at this sort of thing.
Here's the puzzle - suppose that each and every of the 10^13 cells in a human body is specified by a completely different combination of regulatory factors. Thus, Cell 1 is specified by factor A, Cell 2 by Factor B, etc., etc. What is the smallest number of regulatory proteins that can accommodate the human body, given this simple model?
Bonus - how does this number compare with the number of protein-coding genes in the human genome? The number of regulatory genes?
Comment by Art — July 3, 2006 @ 9:23 pm
July 3rd, 2006 at 11:52 pm
Salvador,
You might be interested in Stability of Large Segmental Duplications in the Yeast Genome .
From the paper:
From the abstract:
Comment by MikeGene — July 3, 2006 @ 11:52 pm
July 4th, 2006 at 12:33 am
Mike,
Thank you very much. I'd be happy to hear your impressions about this or read it in your upcoming book (congrats and good luck, by the way)….
The mechanisms for this seem to be a deliberate part of the design to help the poplulation explore diversity and prepare the population for possible stresses. If this were a fluke, I'd imagine major damage would result,but since the damage appears largley absent, it seems like a normal function designed to help the populations evolve.
Salvador
Comment by Salvador T. Cordova — July 4, 2006 @ 12:33 am
July 4th, 2006 at 10:03 am
Seems like a simple exercise in combinatorics. Unfortunately I lack the training to carry it out myself. I'd imagine that it's not all that many. But is this really the correct question? How many cell types are there in the human body, and why not limit the exercise to cell types rather than implying that every cell is it's own type, which I would think we have no good reason to believe?
IOW, it's an interesting question, but the answer is likely to be misleading and irrelevant. We might think the answer is meaningful when it really isn't. So what actually is the point of the exercise? What is it meant to demonstrate?
Comment by Mung — July 4, 2006 @ 10:03 am
July 4th, 2006 at 10:06 am
re: gene duplication
Start with any known genome. Assume some minimal size for a gene. What is the maximum number of gene duplications that could have occurred in order to construct that genome? What does this simple model tell us, if anything?
Comment by Mung — July 4, 2006 @ 10:06 am
July 4th, 2006 at 10:12 am
You've got me. I'm still trying to pin that down.
Does this imply that blind watchmaker evolution is too unconstrained to account for present diversity and that unchanneled evoution is too chaotic to be an effective mechanism. You are likely to hear both that evolution is not constrained and that it is constrained from modern theorists.
Comment by Mung — July 4, 2006 @ 10:12 am
July 4th, 2006 at 2:31 pm
Hmm…
If the designer had the future in mind when he/she/it made the first organism, wouldn't it be more accurate to say that the course of evolution influenced the design of the first organism?
Comment by Mung — July 4, 2006 @ 2:31 pm
July 21st, 2006 at 11:28 pm
My prediction was on target, hehehe!
Unwitting Pro-ID Peer-Reviewed Articles on the Increase . . .
Comment by Salvador T. Cordova — July 21, 2006 @ 11:28 pm