I wrote:

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.

My prediction was on target, hehehe!

Unwitting Pro-ID Peer-Reviewed Articles on the Increase . . .

"Front-loading is the idea that the designer made the first organisms with the future in mind, and that the original design influenced the course of evolution."

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?

What are the real or theoretical aspects of MET?

You've got me. I'm still trying to pin that down.

It's more about channeling and putting constraints on the Blind Watchmaker.

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.

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?

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?

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?

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

You might be interested in Stability of Large Segmental Duplications in the Yeast Genome .

From the paper:

We showed that a large variety of inter- and intrachromosomal segmental duplications appears spontaneously, at an estimated frequency of 10"“9/cell/division (revised from our initial estimate of 10"“10) and possibly through a new mechanism related to the replication process.

From the abstract:

The high level of gene redundancy that characterizes eukaryotic genomes results in part from segmental duplications. Spontaneous duplications of large chromosomal segments have been experimentally demonstrated in yeast. However, the dynamics of inheritance of such structures and their eventual fixation in populations remain largely unsolved. We analyzed the stability of a vast panel of large segmental duplications in Saccharomyces cerevisiae (from 41 kb for the smallest to 268 kb for the largest). We monitored the stability of three different types of interchromosomal duplications as well as that of three intrachromosomal direct tandem duplications. In the absence of any selective advantage associated with the presence of the duplication, we show that a duplicated segment internally translocated within a natural chromosome is stably inherited both mitotically and meiotically. By contrast, large duplications carried by a supernumerary chromosome are highly unstable. Duplications translocated into subtelomeric regions are lost at variable rates depending on the location of the insertion sites. Direct tandem duplications are lost by unequal crossing over, both mitotically and meiotically, at a frequency proportional to their sizes. These results show that most of the duplicated structures present an intrinsic level of instability. However, translocation within another chromosome significantly stabilizes a duplicated segment, increasing its chance to get fixed in a population even in the absence the duplicated genes.

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?

What about this one?

"This thread also doubles as an open thread. So talk about front-loading or something else."

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.

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

(art)[QUOTE] Plant viral vectors are not used for stable, "germline" or even somatic cell modification of the nuclear genomes of plants. For one very simple reason - virtually all plant viruses never, ever, ever see or use DNA as an intermediate in their life cycles, and none of the viruses that are used for GMO-related projects do. (I suspect that joy's misconception here comes from an undue focus, in most biology classes, on medicine-related systems. Much, much too little is spent on real RNA viruses - the ones that replicate without a DNA intermediate.) [/QUOTE]

(joy) Plant virus is used as a promoter. Are you attempting to assert that the CaMV 35S promoter (Cauliflower Mosaic Virus) is not a plant virus, or that it's "never, ever, ever" been used in the genetic engineering of plants? That's a heck of a brave and absolute assertion, Art. I just want to know if you mean it before I start supplying the FDA, USDA, EPA and Patent Office data (on all the current and in-process cultivars).

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.)