In HbS the approach was: we had something to start with, it has changed.

In flagellum the approach was: we had nothing, what are the odds for flagellum in such and such a number of building blocks to appear.

In first example, you use evolutionary approach, in the second you don't. In second, you assume what you are trying to prove - that there was nothing evolution could work on to finish with flagellum.

Agreed.


No, with flagellum we had something to start with too.  We had bacteria with 500 proteins of which contained all the proteins required to construct flagellum.  Each of these proteins was involved in some other functional system.  Then by the only process I can think of (as a combitorial object) an evolutionary change occured to cause the flagellum to be constructed by this change.   I am willing to entertain any evolutionary pathway you can conceive of to cause the appropriate events to occur.  Please suggest an alternative.  This is where I puased previously because I suspected that this is where we will have difficulty in coming to terms with my calculation methods.  At the time you did not object but now you do, and that is ok.  So please suggest an alternative.


I disagree.  In both cases I use the same approach.  In the first case of HbS the pathway selected is simple base pair substitution.  In the second case we have no actual or verified pathway so I stipulated one, namely an all in one combinatorial mechanism.  I stipulated this because I cannot conceive of any other way this system could be constructed stepwise because the components as configured don't have function apart from each other.

Again I ask you to propose an alternate pathway and we can put the numbers to it.  Realize that as we become more precise about a pathway we also should revise the stipulations I used to simplify the math.

This is an elimiative filter.  It argues nothing from ignorance it does eliminate chance and necessity as possible explanations for events.  With those modes eliminated the only one left is design unless you can posit an additional mode.

Correct that we don't insert God.  We can infer design but we cannot infer who or what the designer was.


That is a question for another thread.  This one is on specification and complexity.

I have already stipulated that the components all exist with probability of 1.0.  If I understand correctly gene duplication and horizontal gene transfers are mechanisms that deal with origination.  Any relaxation from 1.0 reduces the odds for material mechanisms.


Since by this mode the odds for chance and necessity are dramatically reduced, and we could do the calculations, but the simpler mechanaismpreviously suggested is the favored chance mechanism for HbS.   In a sense this suggestion looks at origination of Hb(X) from non-Hb


Yes, and this hypothesis adds boundary conditions to the localization and configuration permutations.  It will improve the odds.  However evolutionary theory requires function for each component.  The motor has function on its own as a proton pump (I doubt it would make a for a protein pump given the configuration).  The protein injector that delivers proteins for filament construction also has clear alternate function.  I can think of no function for the shaft, the universal joint or the fillament.    You suggested one for the filament but didn't follow it. Once we have subdivided the system into these alternate systems and have identified a use for each we can rework the numbers.  I don't think the results will change much relative to the 10^150 universal limit.

I mean the process by which the required proteins came to exist.


I think I understand.


A single selectable substitution should occur in very little time. In less than a day.


Each of the steps in the pathway must be functional and selectable or the mutations will not be retained.  Given  that experimental and theoretical protein analysis indicates that fewer than 1 in 10^55 roughly 400-500 base pair protein configurations are functional (Axe, 2003) I would predict that 50% drift could never occur.  We can go through the math if you like but it appears from Axe's analysis that functional proteins may differ each other by an average of 6-20 base pairs depending on the lengths considered.


It is the upper bound of all the macro-events that could ever have occured in this universe.  It is the number of atoms in the universe times the number of atomic collisions per second times the number of seconds this universe is old.  It places a reasonable upper bound on what chance can explain.

Of benign or mostly benign alterations including for example base pair substitutions that give redundant coding etc.  These changes also don't contribute to new forms and funtion.  If I am wrong on this point, please correct me.  I would be very interested in a detailed explanation of how genetic drift accomplishes this.  Then if you would offer an example of an actual pathway to new protein function by genetic drift it would help me to understand what you are talking about and it would help us decide if this pathway can be considered actual.


I don't think my statement about function and selction disregards this reality.  It was a high level statement.  Your elaboration adds clairity.  Once mutation disables a metabolic pathway, the dysfunctional proteins are subject to gentic drift by random mutations.  Any single mutation of a nonfunctional gene won't generally be retained it is subject to further drift since it contributes no function.


Given that evolutionary processes are proficient at breaking function and in bacteria, gene transfer can move funtional systems, it makes sense that multiple metabolic pathways exist and that several are disabled.

In any case the primary focus of this portion of the discussion deals with propsing an evolutionary pathway other than by combitorial objects.  We can quibble about what is and what isn't theoretically in play but we need a stepwise complete hypothetical pathway in order to test for Specified Complexity.  Can we derive such a pathway by genetic drift.



I don't think I make this assumption.  Again the focus here is to identify a plausible pathway.



Given that a 150 aa sequence has 20^150 or 1.4*10^195 permutations, by Axe's analysis we still have well over 10^100 functional combinations so it should not be a surprise that you observe alternate alignments that are functional.  The issue is whether or not there are functional pathways from one to the other observed proteins.  The data indicate there are not.  If there is no functional pathway, the other possibility is drift.  the problem with drift (the way I understand it ) is that without selection pressure conservation of the binding sites and fold areas is not guarenteed and the odds of randomly hitting a functional protein becomes insurmountable for strings longer than about 50 amino acids in the time frames we have to work with.


It was selected to be conservative and to avoid needless argument over probability opportunities. No, it is not just a guess.  It represents the theoretical largest total number of probalistic resources available in the entire universe.

Exactly. When you have that you can attribute it to evolutionary processes. Everything else without a complete pathway, hypothetical or otherwise, defaults to design. What's the point?

I offered a hypothetical pathway for flagellum so I don't understand your objection.

I am asking for any hypothetical evolutionary explanation.  One that honors the narrative and is specific.  It needs to be specific so we can be objective about the permutations and probability landscape.  I have proposed a hypothetical pathway for HbS from Hb and chance easily explains HbS.  I also proposed one for flagellum from a hypothetical bacteria that lacked the structure but had access to all the materials.  In this case chance could not explain flagellum.  If you propose other mechanisms we can put those to the test too.