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Author Topic:   Are human tails an example of macroevolution?
Brad McFall
Member (Idle past 5032 days)
Posts: 3428
From: Ithaca,NY, USA
Joined: 12-20-2001


Message 46 of 61 (355753)
10-10-2006 7:48 PM
Reply to: Message 44 by bernd
10-10-2006 3:23 PM


Re: A radiograph of a human tail
Here is short way through a thought process whereby "human tails" may be functionally-structural only and NOT an aspect of history. This is an overview of the reasoning. There is no reason that data can not falsify the claim. Thanks for being patient. I dont want to wait and have a misplaced hype for a response.
Gould argued twice in "Structure of Evolutionary Theory" that Dobshansky misrevealed the nature of Wright's adaptive landscape by trying to attach ideas of "ecological topography" at the species level which Gould sustained were wholly due to history. This is comparable (so it seems to me but redirect me if you disagree)to your query as to how it could be claimed that the tail phenotype in humans is NOT due history.
Thinking like Dobshansky and not like Gould, I would suggest that creationists attempt to interpret the notion of harmony (peaks)and disharmony (pits) in Wright's ideas (between gene combinations in individuals subject to being the grave or vehicle phenotype of cell death continuity which can be structural as to gene frequecies in populations). Thus the species of apes are on peaks that only the grave of cell death crosses doing so by "datamining" disharmonious concatenations and thus abberant formal (form)spaces. The gene combinations of cell death vehicles survive this transit but these being in terms of cell lineages do not constitute history (deme vs species)but only the ordered topology of embryogeny and thus subject to the neurulation idea and the sum of graves WITHIN the apes.
I can add the quotes from Gould and Wright and Dobshansky and Ameisen if these would be helpful. I am thinking that the "harmony" of multiple leveled peaks to "mountain" ranges depend on canalization while the depth of the disharmony, disturbed by disequilibria contrarily have no bottom diagrametically. Here actual cell death histories compete with molecular manifestations. It seems that it is failure to notice that there is an "upper bound" to the peak but no "lower bound" to the valley that had continued to frustrate interpreations of the "adaptive landscape" as Wright intended the "phenotype." Cell death certainly populates the "deserted and empty" valleys of Dobshansy's Wright but harmony is only subject to equilibria not non-linearlity and non-equilibria (except by pure natural selection and we had moved from that point in the conversation). I think that cell death speculations tend to make this interpretation easier even though Amiesen's best ideas are interms of geneic selectionism only (toxic vs nontoxic bacteria).
The result will be that the peak range of Apes is one without tails but that the pits never result in "underground" connections to a different set of peaks with tails (as in monkeys) but only that chance expressions and surviving cell death graves can get to a "caudal appendage." This would overdetermine a possible "kind" in baraminology as well I would guess. Cell death vehicles do not travel in this space even if they do for other mammal clades that contain tailed and nontailed grades.
This is the general idea. I looked quickly at your links about cell death and the vertebrate tail. I do not think there will be any ideas in these papers that can not be contained by the above analysis. If you think there are please let me know.
This idea would be wrong if the regulatory genes for tail expression was found conserved as in hox genes for general segmentation. It is also possible that some aspect of hoxology may disrupt my structural prescription for which I was trying to take more time to figure out. I wanted to get the general stages in the argument out however even if I am completely off base here. So that others can do some of of the surfing as well.
Edited by Brad McFall, : No reason given.

This message is a reply to:
 Message 44 by bernd, posted 10-10-2006 3:23 PM bernd has replied

Replies to this message:
 Message 48 by bernd, posted 10-14-2006 1:17 PM Brad McFall has replied

  
Brad McFall
Member (Idle past 5032 days)
Posts: 3428
From: Ithaca,NY, USA
Joined: 12-20-2001


Message 47 of 61 (356487)
10-14-2006 12:38 PM
Reply to: Message 26 by ReverendDG
10-06-2006 4:48 AM


Re:focusing on legs when it is really the tail.
It seems to me that the entire issue of to detail or not to tail, has to
do with this picture below:
quote:

Gould wrote (SETH p 1030)about it in terms of cats and dogs but he went to flying zebras(as I shewed earlier in this thread)
instead of working out an angle of allometry that appears from symmetry in clades expressed in a prior time of biological study phyletically as:
as snout/lower jaw shortening in bears vs. longer nose/heads of haeyneas.
quote:

Gould wrote it that way because of how Collin Tudge
covered "carnivores"(notice placement of "tails" in the clade diagrams).
quote:
other non-quoted clade diagrams from Tudge
But from the pictures alone one can observe that there are only words making the differences. Premeditation about flying zebras or gate differences when other allometrics might be causal seems gratuitous to me.
I still retain the ability to write of top to bottom mammal allometry(effective in issues of locomotion) but I take a different view of "punctuation" or "catastrophe" or saltus"" than Gould. Working in the issue of cell death makes this a much more complicated undertaking.
quote:
Structure of Evolutionary Theory by SJ GOULD page 922 with my own supplement
Edited by Brad McFall, : spelling and grammar
Edited by Brad McFall, : restoring last comment deleted during edit

This message is a reply to:
 Message 26 by ReverendDG, posted 10-06-2006 4:48 AM ReverendDG has not replied

  
bernd
Member (Idle past 3980 days)
Posts: 95
From: Munich,Germany
Joined: 07-10-2005


Message 48 of 61 (356495)
10-14-2006 1:17 PM
Reply to: Message 46 by Brad McFall
10-10-2006 7:48 PM


Re: A radiograph of a human tail
Hello Brad,
You mentioned a potential falsification of your approach:
This idea would be wrong if the regulatory genes for tail expression was found conserved as in hox genes for general segmentation. It is also possible that some aspect of hoxology may disrupt my structural prescription for which I was trying to take more time to figure out. I wanted to get the general stages in the argument out however even if I am completely off base here. So that others can do some of of the surfing as well
I take this to mean that if we find the same regulatory genes that control the tail phenotype lets say in mice also in humans, we would have to assume that “evolutionary history” is a good explanation of the rare occurrence of this phenotype in men.
So let’s start with a hox gene. Hoxb-13 has been found in both human and mice
(see:
Hoxb-13: a new Hox gene in a distant region of the HOXB cluster maintains)
Colinearity
The function for tail development in mice has been detailed here:
To address the expression and function of Hoxb13, the 5_ most Hox gene in the HoxB cluster, we have generated mice with loss-of-function and _-galactosidase reporter insertion alleles of this gene. Mice homozygous for Hoxb13 loss-of-function mutations show overgrowth in all major structures derived from the tail bud, including the developing secondary neural tube (SNT), the caudal spinal ganglia, and the caudal vertebrae. Using the _-galactosidase reporter allele of Hoxb13, also a loss-of-function allele, we found that the expression patterns of Hoxb13 in the developing spinal cord and caudal mesoderm are closely associated with overgrowth phenotypes in the tails of homozygous mutant animals. These phenotypes can be explained by the observed increased cell proliferation and decreased levels of apoptosis within the tail of homozygous mutant mice. This analysis of Hoxb13 function suggests that this 5_ Hox gene may act as an inhibitor of neuronal cell proliferation, an activator of apoptotic pathways in the SNT, and as a general repressor of growth in the caudal vertebrae.
from
Hoxb13 mutations cause overgrowth of caudal spinal cord
and tail vertebrae
Considering the role of Hox genes in pattering the anterior posterior axis in all mamals, I think it’s probable that the gene has had a similar functions in the ancestor of humans and great apes.
Another confirmation of a shared genetic base for tail development can be found when looking at Wnt3-a, a regulatory gene found in all vertebrates. In mice it plays an important role in tail development. When its expression is downregulated, for example by treating diabetic mice with retinoic acid, the the probability of a caudal regression is significantly increased.
Similar defects under equal circumstances - diabetes in interaction with RA - are observed in humans:
Maternal diabetes increases the risk of congenital malformations in the offspring of affected pregnancies. This increase arises from the teratogenic effect of the maternal diabetic milieu on the developing embryo, although the mechanism of this action is poorly understood. In the present study, we examined whether the vitamin A metabolite retinoic acid (RA), a common drug with well-known teratogenic properties, may interact with maternal diabetes to alter the incidence of congenital malformations in mice. Our results show that when treated with RA, embryos of diabetic mice are significantly more prone than embryos of nondiabetic mice to develop caudal regression, a defect that is highly associated with diabetic pregnancy in humans. By studying the vestigial tail (Wnt-3a(vt)) mutant, we provide evidence that Wnt-3a, a gene that controls the development of the caudal region, is directly involved in the pathogenic pathway of RA-induced caudal regression. We further show that the molecular basis of the increased susceptibility of embryos of diabetic mice to RA involves enhanced downregulation of Wnt-3a expression. This positive interaction between RA and maternal diabetes may have implications for humans in suggesting increased susceptibility to environmental teratogens during diabetic pregnancy
from Maternal diabetes increases the risk of caudal regression caused by retinoic acid
Besides, in this article you’ll find an overview about segmentation in vertebrates and the role of Wnt3-a in this process. Have a look at figure 2 in the chapter “Gradient and clock are joined through Wnt3a”
Finally, a request for clarification. Could you please explain in greater detail what exactly is a "grave of a cell death"? The other point would be to explain why you think that there is no lower bound to a valley of an adaptive landscape. Quotes would be appreciated.
-Bernd

This message is a reply to:
 Message 46 by Brad McFall, posted 10-10-2006 7:48 PM Brad McFall has replied

Replies to this message:
 Message 49 by Brad McFall, posted 10-14-2006 6:23 PM bernd has replied

  
Brad McFall
Member (Idle past 5032 days)
Posts: 3428
From: Ithaca,NY, USA
Joined: 12-20-2001


Message 49 of 61 (356528)
10-14-2006 6:23 PM
Reply to: Message 48 by bernd
10-14-2006 1:17 PM


Re:falsification of non-historical interpretation
Ok, let's see...
Is colinearity to be thought equivalent in insects/arthropods as in vertebrates?
Gould was conscious enough to notice that it might not be the case that the simple use of fly probes to find frog hoxes was more than a hoax (SETH page1102
quote:
The initial discovery of homology in genetic structure of arthoropd and vertebrate Hox did not seal the case for evolutionary meaning, since no one yet knew how vertebrate Hox genes operated.
Only one sentence later Gould said,
quote:
Evidence for similarity of action soon followed, thus securing the argument for...
What "action" was secured?
quote:
The established rules of "hoxology"* vindicated the central principles of morphogenesis in Lewis's model.SETH page 1099
This principally was:
quote:
Lewis's model neatly explained the most famous and puzzling homeotic transformations, both based on loss-of-function mutations. Bithorax., the celebrated four-winged fly, does not represent an atavistic reversion to the ancestral state, but arose by a weaking of the gradient that caused the third thoracic segment...
Gould (SETH 1099)quoted,
quote:
As Warren et. al. (1994, p.461) write: Hoxgenes "provided a pre-existing groundplan upon which insect segmental diversity evolved."
Gould concluded (SETH 1100)
quote:
The perfect colinearity of spatial order along the chromosome with the sequence of morphological differentiation along the developing animal's antero-posterior axis summarizes the most stunning conclusion of this research, and also generates most other hoxological regularites
Gould went so far as to say (SETH 1100 ),
quote:
The ultimate loss, a fly developing with noHox gene function at all, leads to lethality, with the dead embryo as a grim and facinating manifestation of expected rules: a misfit bearing antennae on each of its segments (Shubin et al., 1997, p644).
Do we see vertebrates with gain-of-function mutations having tails in the place of analogous arms and legs?
Could it not be that the is NO "colinearity" in the sense pre-existing but only a discrete "vectors" between ordinally different topographies from chromosomes not a morphogenetic gradient?
Gould's presentation of Hoxd-13 praises the author "Dolle'et al.s'" "conscious linkage to classical data on heterochrony (SETH p 1103) but via a conscious reciprocation to gain-of-function mutations there are no "tails" extending from vertebrae but only ribs and lateral projections from segements more anterior than tails.
quote:
"Structure characteristic of more posterior vertebrae", "pair of ribs..."
I can tell you quite confidently, but it would take some time for me to document it that the word "anlage" is ambiguous in the technical literature of squamate morphogenesis. So the phrase "elongating" 'anlage' in you review article CONTINUES to raise some mental concern on my part, ie when one is only observing ecotypic expressions in misplaced somites. The word "vector" rather than "gradient" seems more consciously appropriate here, where, one does not deal with the the discontinuity between linear order on a chromosome and spatialization FROM that linear order(you could note that in a short page of text Gould uncharacteristically moves from the word "read" to "write"(Seth page 1099 (dealing with ?wolpert's notion of positional information)). It is not clear to me that the so-called 'segmentation' is not really a scalar magnitude only.
Thus if the reading of hoxology requires a vetor field rather that an gradient IDENTICAL to 3'-5' transcription direction we have only a co-ordinate system or inertial frame of reference at best to extend the somite variation developed into the clades of monkeys vs apes. I am not sure this is enough data to gain the function of a tail historically homogenously throughout the primates. Notice also how with respect to insects Gould displaced the historical explanation FOR THE MATHEMATICAL (but not physical) configuration of a gradient (a line). He went on to sustain this based only on "geometric duplication" when discussing from the old Lewis model to actual hoxology(SETH 1096-1098).
I am guessing, and this can be a good test, that reading through in detail on Wnt3-a substituting the word "vector field" for "gradient" will not disturb the experimental predications and results.
Do you work with Wnt3-a?
I will add the quotes for a prior post and more about my own position in a next post as well as working up how I guess now, BOTH clock and gradient need not necessarily be an issue for chromosome linearity where an inertial system rather than a simple chemical gradient theorizes the formations format. Sorry I still have not downloaded an uptodate PDF reader.

This message is a reply to:
 Message 48 by bernd, posted 10-14-2006 1:17 PM bernd has replied

Replies to this message:
 Message 50 by bernd, posted 10-16-2006 1:58 PM Brad McFall has replied

  
bernd
Member (Idle past 3980 days)
Posts: 95
From: Munich,Germany
Joined: 07-10-2005


Message 50 of 61 (356876)
10-16-2006 1:58 PM
Reply to: Message 49 by Brad McFall
10-14-2006 6:23 PM


Re: Re:falsification of non-historical interpretation
Hello Brad,
Brad writes:
Is colinearity to be thought equivalent in insects/arthropods as in vertebrates
That depends on what type of colinearity you are talking about - spatial, temporal or quantitative. While in Drosophila only spatial colinearity of hox genes has been described, in mammals we find also temporal and quantitative colinearity
Hox genes were initially identified in Drosophila as grouped regulatory genes, known as homeotic genes. They encode positional information during development following the colinearity rule, that is, their physical location in the cluster parallels the physical order of their expression along the anterior to posterior (AP) axis of the developing embryo (Lewis, 1978). Some years later, their molecular characterisation in both Drosophila and vertebrates proved that they code for proteins that bind DNA through the homeodomain, a domain of 60 highly evolutionarily conserved amino acids. Furthermore, mammals have the same clustered chromosomal organisation, where four copies of the Hox cluster, homologous to that of Drosophila, were found. Transcriptional analyses performed on sectioned and whole-mount embryos subsequently demonstrated the conservation of the colinearity rule (McGinnis and Krumlauf, 1992). So it seemed that Hox genes might provide a common molecular representation of the body plan at an early stage of the development of all animals. This is referred to as the phylotypic stage, during which embryos from distinct species tend to resemble to each other (Slack et al, 1993). Consequently, it was expected that the Hox gene cluster might have had this crucial developmental role even in the common ancestor of all bilaterally symmetrical animals.
However, in vertebrates, the spatial colinearity rule turned out to be only part of the story. In mammals, it was shown that the temporal order of activation of the Hox genes during development also corresponds to the order that these genes are arrayed in the genomic cluster (Kmita and Duboule, 2003). This temporal regulation is not observed in Drosophila embryos, where Hox genes are split into two half-clusters and are activated simultaneously. Genetic manipulations in mice show that the clustered organisation of Hox genes is required to implement such a tight temporal control. In contrast, Hox clustering is not necessary to achieve a proper spatial expression in other numerous cases (see in Kmita and Duboule, 2003).
from Evo-devo: Relaxed constraints on Hox gene clustering during evolution
After quoting Gould about hox genes and their colinearity and as it seems disagreeing with his remarks, you ask:
Brad writes:
Do we see vertebrates with gain-of-function mutations having tails in the place of analogous arms and legs
No, we don’t, at least not in mammals. And why should we expect this? I have already posted a link to an article which explains the development of the mammalian tail. I quote the relevant part:
The mammalian tailbud, like that of zebrafish, exhibits developmental features congruent with both Holmdahl's and Vogt's ideas. The bud consists of a ball of histologically homogeneous tail bud mesenchyme overlain by a ventral ectodermal ridge (VER) at the caudal tip continuous with a more transient ectodermal groove rostrally (Grneberg, 1956; Gajovic & Kostovic-Knezevic, 1995). Grneberg (1956) was the first to point out the histological similarity between the tailbud and embryonic limb bud, and, by extension, the possibility that secondary inductive events (as seen in the limb; reviewed in Capdevila & Izpisua Belmonte, 2001) were involved in tail formation.
There is growing evidence to suggest that this is indeed the case. Grneberg & des Wickramaratne (1974) described a mouse mutant (vestigial tail) bearing an undeveloped tailbud with only traces of an ectodermal ridge. This phenotype is copied by mutants for the genes T (Herrmann et al. 1990) and Wnt3a (Takada et al. 1994; Greco et al. 1996). More recently, Hall (2000) and Goldman et al. (2000) showed that ablating the VER results in tailbud regression and prevents somitogenesis and chondrogenesis in the tail.
The VER is also a genetically discrete structure, expressing specifically Msx1, Wnt5a, BMP2 and FGF17 (Lyons et al. 1992; Gofflot et al. 1997, 1998; Goldman et al. 2000). Although inductive functions have yet to be determined for each of these genes, their localized expression suggests that the VER, like the AER, is a source of molecular signals that regulate underlying bud mesenchyme. The VER, however, does not appear to employ extensive FGF signalling (as seen in the AER) and, accordingly, cannot regulate development when grafted onto limb bud explants (Goldman et al. 2000).
It is unlikely, however, that secondary development is the sole mechanism of tail formation in mammals. Several mapping studies have demonstrated that tailbud materials originate from the primitive streak and Hensen's node, suggesting that rostral developmental mechanisms may continue into the caudal portion of the embryo (Tam & Tan, 1992; Wilson & Beddington, 1996). Gofflot et al. (1997) provided more convincing evidence of this. They followed the expression of several gastrulation marker genes (Wnt5a, T, Hoxb1 and others) from the primitive streak and Hensen's node into distinct regions of the tailbud.
What we observe is, that a mution in Hoxb-13 results in an overgrowth of the tail, in other words most probably the function of this gene is to stop tail development.
Brad writes:
Could it not be that the is NO "colinearity" in the sense pre-existing but only a discrete "vectors" between ordinally different topographies from chromosomes not a morphogenetic gradient?
With regard to colinearity see above. Morphogenetic gradients have been described in great detail, have a look at the references in the chapters about Wnt and FGF8 gradient, described here or alternatively read this article
You continue with:
Brad writes:
Gould's presentation of Hoxd-13 praises the author "Dolle'et al.s'" "conscious linkage to classical data on heterochrony (SETH p 1103) but via a conscious reciprocation to gain-of-function mutations there are no "tails" extending from vertebrae but only ribs and lateral projections from segements more anterior than tails.
quote:
"Structure characteristic of more posterior vertebrae", "pair of ribs..."
Interesting, but I don’t see the connection to my argument. I have discussed the function of Hoxb-13 not Hoxd-13. (With regard to the function of the Hoxd cluster, see above under quantitative colinearity)
Brad writes:
I can tell you quite confidently, but it would take some time for me to document it that the word "anlage" is ambiguous in the technical literature of squamate morphogenesis. So the phrase "elongating" 'anlage' in you review article CONTINUES to raise some mental concern on my part, ie when one is only observing ecotypic expressions in misplaced somites.
There is no need to document this ambiguity in the literature about squamate morphogenesis. Relevant in the context of our discussion is the article I quoted. In which way is here the usage of “anlage” ambiguous?
Brad writes:
The word "vector" rather than "gradient" seems more consciously appropriate here, where, one does not deal with the the discontinuity between linear order on a chromosome and spatialization FROM that linear order(you could note that in a short page of text Gould uncharacteristically moves from the word "read" to "write"(Seth page 1099 (dealing with ?wolpert's notion of positional information)). It is not clear to me that the so-called 'segmentation' is not really a scalar magnitude only.
Could you please explain why you think that “vector” is more appropiate than “gradient”? And why do you think that segmentation is only a scalar magnitude? The hox genes in Drosophila specify the characteristic structure of each segment.
Do you work with Wnt3-a?
No, I’m not a biologist.
-Bernd
Edited by bernd, : spelling, inserted "not Hoxd-13" after "(..)function of Hoxb-13"
Edited by bernd, : inserted missing quote

This message is a reply to:
 Message 49 by Brad McFall, posted 10-14-2006 6:23 PM Brad McFall has replied

Replies to this message:
 Message 51 by Brad McFall, posted 10-17-2006 5:45 PM bernd has replied
 Message 52 by Brad McFall, posted 10-19-2006 8:06 PM bernd has replied

  
Brad McFall
Member (Idle past 5032 days)
Posts: 3428
From: Ithaca,NY, USA
Joined: 12-20-2001


Message 51 of 61 (357118)
10-17-2006 5:45 PM
Reply to: Message 50 by bernd
10-16-2006 1:58 PM


Re: Re:falsification of non-historical interpretation
I would be contending that the "phylotypic stage" does not homogenously exist across the psm. I would revert to the Elder Darwinian, Erasmus instead who used the word PLAN(in the section quoted in Carter I displayed interthreadalia), which now would mean(for me at least) the split(left and right)-somite-formation, whether clocked or not, rather than the current version that the adjective("polytypic") derives as to a "body" plan which is Logically referable to Woodger's use on any dissection I should think( unless I am mistaken in this attribution). I do not see how short of prejudice one is out of the woods on bilaterally symmetric animals here, SINCE the somites themselves divide among left&right.
I can see how a reductionist would try to read the parallel signaling paths as a means to remove this ambiguity but that does not seem to mean that it MUST be extended to the "tail bud." There just is not as much information on the tail bud as there seems to be speculation about recruitment INTO the PSM.
I say all of that without thinking about cell death in this context.
You said,
quote:
What we observe is, that a mution in Hoxb-13 results in an overgrowth of the tail, in other words most probably the function of this gene is to stop tail development.
but even if the VER looked like a limb bud, where is the evidence sans speculation and hope for future research information that, "it appears" that Hoxb-13b stops tail development when the creature has a bud but nothing tail wiser.
In other words how can be certain that if Hoxb-13 does not stop "overgrowth" (even though it appears to in tailed creatures) that it is not neutral or functions differently in a differently familiar situation where the development does not normally yield a "tail"? I have not looked THIS up, but on reading that the PSM can be inverted without directional periodicity being upset could not the Hoxb13 effect affect at this "stage" rather than the difference of anterior and posterior PSM which have different signaling relations anyway??
You seem to supporting the contention that the tail embryogeny must be historical by anatomical divisions which I do not see supported by data as it exists. I do not deny that the literature seems to be written with this idea, as a goal or target but I can sense how the information portrayed in the actual literature is nothing other than a feeling for belief in evolution rather than discrimination within evolutionary thought that challenges if the data really supports an historical contingency rather than a formal configuration both of which may or may not remain purely "evolutionary" when retained in sustained thought.
I am happy to see that readers of EvC might be beginning to notice a tangible difference between yours and my views and do not be discouraged or fell timid about asking to me answer other questions you have already asked. We have covered a lot a ground and I am more than happy to revisit older posts and other places I said I would update. I just do not have a lot of time as we all do not so I felt posting something was better than little to an avalanche later style.
You are correct I misread "d" and "b", my bad. That post however was a general romp though "hoxology" but I am going to try to let Gould go if I consciously can and just talk to you from me. I will refer back to his schism between positivity and negativity if I need it but as you have done a great job pointing me to sufficient sources to carry out this dialogue I pray they were so indeed. I do see that there is some theoretical "tension" between multiple signaling pathways in the caudal end and the space and time correlations FROM homeodomains so perhaps I am premature here@Best, Brad.
Edited by Brad McFall, : spelling

This message is a reply to:
 Message 50 by bernd, posted 10-16-2006 1:58 PM bernd has replied

Replies to this message:
 Message 53 by bernd, posted 10-20-2006 11:34 AM Brad McFall has replied

  
Brad McFall
Member (Idle past 5032 days)
Posts: 3428
From: Ithaca,NY, USA
Joined: 12-20-2001


Message 52 of 61 (357576)
10-19-2006 8:06 PM
Reply to: Message 50 by bernd
10-16-2006 1:58 PM


Response to falsification of non-historical interpretation
quote:

The idea (“core effector mechanism”) upstream and the view that genetic programs allowing regulated cell suicides in single-celled organisms (also discussed by Amesien) extends the whole matrix of the “quirky functional shift” (when applied to an ”organ’ rather than a ”social organism body’) into a nexus of thought where it is far from clear whether one is able to get on the side of the altruist or selfishist.
Thus when I challenge that the embyrogenic facts bear more on recruitment OF cell lineages INTO the area of the PSM than of the tail bud lineages cellwise one has a hard time sustaining a thought linked to Amesien’s dissection of various levels (cell vs individual organism) in an evolutionary perspective of cell death no matter how the bacteria competed or not.
Thus without that, it seems to me that cell death in whatever way it might be retained genetically could be providing simply a space or rather lack of cell area to morphogenetics rather than being a positive construcutor IN THE TAIL (the end) even though this would not necessarily simply be such a bound and is rather constitutive for other areas of a developing body. I have read somewhat of the cell death in the tails of frog tadpoles and in reading that literature I have only been lead to think that cell death “destroys” a morphology in order to provide another (stronger back legs than front legs (to the gills)) (altruistically) and not that it regulates a part (tail bud) for the function of the tail itself(which seems to be necessary if the human tail is to be explained by the same history that gave up the frog’s lack). This thought gives a purely structuralist explanation for cell death in the tail of a vertebrate and removes even the functionalist one.
Here is how I thought of the idea of cell death in plants. It could be related to that in animals via the right angles in the plant if the nodes intercalate(interfinger) the spatialization of molecular reaction pathways in the animals.
I have added a page TheTrainer's pregram which contains comments that fully spatialize cell death as I understand it and explains a bit why this idea has not been developed as of yet. If hoxologos is the correct arrow for this quiver in this particular threads case, I will have to adjust that page at least.
Edited by Brad McFall, : subtitle changed for information
Edited by Brad McFall, : plant idea added
Edited by Brad McFall, : with link to external ideas on how cell death relates to any soma

This message is a reply to:
 Message 50 by bernd, posted 10-16-2006 1:58 PM bernd has replied

Replies to this message:
 Message 56 by bernd, posted 10-27-2006 10:24 AM Brad McFall has replied

  
bernd
Member (Idle past 3980 days)
Posts: 95
From: Munich,Germany
Joined: 07-10-2005


Message 53 of 61 (357707)
10-20-2006 11:34 AM
Reply to: Message 51 by Brad McFall
10-17-2006 5:45 PM


Re: Re:falsification of non-historical interpretation
Hallo Brad,
Brad writes:
I would be contending that the "phylotypic stage" does not homogenously exist across the psm
In vertebrates the pharyngula stage is normaly described as phylotypic, so why do you associate phylotypic stage with presomitic mesoderm?
Brad writes:
I would revert to the Elder Darwinian, Erasmus instead who used the word PLAN(in the section quoted in Carter I displayed interthreadalia), which now would mean(for me at least) the split(left and right)-somite-formation, whether clocked or not, rather than the current version that the adjective("polytypic") derives as to a "body" plan which is Logically referable to Woodger's use on any dissection I should think( unless I am mistaken in this attribution)
In Erasmus Darwins text which may be downloaded from here the word “PLAN” doesn’t appear, he uses the term “structure” instead. But how can structure (or “PLAN”) mean “the split (left and right)-somite-formation”? Please back up this claim with a quote from E. Darwin.
Brad writes:
I do not see how short of prejudice one is out of the woods on bilaterally symmetric animals here, SINCE the somites themselves divide among left&right
Somites don’t divide themselves among left and right. The presomitic mesoderm is organized “as two rods of mesenchymal tissue, forming the presomitic mesoderm” (see The International Journal of Developmental Biology )
And what do you mean with “bilaterally symmetric animals”?
Brad writes:
I can see how a reductionist would try to read the parallel signaling paths as a means to remove this ambiguity but that does not seem to mean that it MUST be extended to the "tail bud
Which ambiguity? What “Must” be extended to the tail bud?
Brad writes:
There just is not as much information on the tail bud as there seems to be speculation about recruitment INTO the PSM.
Please have a look at figure 2 of the above linked article. As you can see tail somites are formed from psm.
Brad writes:
(..) but even if the VER looked like a limb bud, where is the evidence sans speculation and hope for future research information that, "it appears" that Hoxb-13b stops tail development when the creature has a bud but nothing tail wiser.
Humans have an embryonic tail. It is described here:
The development and disappearance of the human tail between stages 14 and 22 were studied using scanning and transmission electron microscopy, supravital staining and light microscopy. The tail is a prominent feature of the human embryo during stage 14 and is composed of paired somites, mesenchyme and extensions of the neural tube, notochord and gut. The tail grows with the embryo through early stage 17 when it extends more than a millimeter from the trunk. Overgrowth by the trunk at the base of the tail may account for the loss of part of its length during late stage 17 and stage 18. However, during stage 17 cells begin to die in all structures throughout the tail. Cell death continues in the succeeding stages reaching massive numbers by stages 18 and 19, and the tail becomes less and less prominent with developmental time. Most of the dead cells are phagocytosed. The debris-laden macrophages appear to migrate from the tail to the body. By late stage 21 or early stage 22 there is no free tail. We conclude that cell death has a major role in the destruction of tail structures and the concurrent loss of the human tail.
From Evidence of a role for cell death in the disappearance of the embryonic human tail.
Brad writes:
In other words how can be certain that if Hoxb-13 does not stop "overgrowth" (even though it appears to in tailed creatures) that it is not neutral or functions differently in a differently familiar situation where the development does not normally yield a "tail"?
How does this address the argument I formulated in messsage 76? Let’s assume for a moment, that Hoxb-13 functions differently in humans. But in mice it is expressed acccording to its chromosomal position in the tip of the tail and its function is most probable to stop tail development. All mammals have 4 hox clusters. We find the gene in mice and men at the same relative position of the hoxb cluster. With regard to homo sapiens this is easily explained by descent from a common ancestor with tail. How can this be somehow due to a structural constraint of development?
Besides, do you plan to comment on the second example I described in msg 76?
-Bernd
Edited by bernd, : clarification, spelling.

This message is a reply to:
 Message 51 by Brad McFall, posted 10-17-2006 5:45 PM Brad McFall has replied

Replies to this message:
 Message 54 by Brad McFall, posted 10-20-2006 3:53 PM bernd has replied

  
Brad McFall
Member (Idle past 5032 days)
Posts: 3428
From: Ithaca,NY, USA
Joined: 12-20-2001


Message 54 of 61 (357798)
10-20-2006 3:53 PM
Reply to: Message 53 by bernd
10-20-2006 11:34 AM


Re: Re:falsification of non-historical interpretation
There are some difficulties of language going on here. When I quoted Carter on Darwin I had in mind his anglo-expressions. I had hoped that by moving THROUGH Gould's lingo we would have exhausted our likely different linguisitic backgrounds. That does not seem to be the case given you response.
I was reading "stage" in an general evolutionary sense. The general point is that I can not see how the topography of embyryogeny presents a topology that *must* be historical. Your reply in this post NOW is about me simply reading text(s) you provided. The questions are not of the same quality as before. The internet might have others thinking differently and mistakenly thus.
Yes tail somites ARE formed from the psm, as I read, but the "bud" exists as labeled beyond and BEFORE the somite pair appears as it appeared in the figure one, I think.
Am I seeing things wrong? Are not the two "rods" of tissue not each on a side off the a drawable midline??
In frogs the macophages also destroy the tail but I do not see how the tail exisiting outside the psm in humans indicates a "lower" stage evolutionarily, necessarily. The tail is simply tissue at the end of the creature. If there was some archetypical difference between radially symmetric and bilateral organisms as some creationists may wish to claim, then there might be reason to argue immediately from the last place in the tissue as due to constituitive form-making. The psm marks the place between this edge and "interior" tissue.
As for what "may" (MUST(sic!)) be extended, they are(were) the signalling pathways however interpreted. If you can show me that hox molecular biology(relations of hox cluster physcial chemistry as promixate cause of all allomteric regularities) regulatory for the tail bud tissue itself then yes, I might be inclined to accept an historical interpreation for the functioning of the this "organ" or "tissue area" and would.
Perhaps I have misread the hypotheticals with regard to the pathways but If one intends on also involving the evolutionary notion of cell death rather than a simple list of genes involved in cell death itself it seems that anatomy will be even more difficultly supporting the historical falsification of my view or one similiar.
It was not necessary therefore that I thought the somites "divided" left and right but only that there was (INTERNAL TISSUE) between the period when a new somite "pair" develops even if there were some asyhchornicity. The issue of how the EDGE gets divided from the zygote is a real one. I notice the topological issue is probably at the blastula to gastrula stages, saying it plurivocally.
Maybe I missed it, I am not trying to be obtuse, but I do not see how the existence of HOX cluster implies that the the terminal segement area must be non-scalar with respect to the magnitdue of a matrix metric that links(Correlates) the parts UP TO the END (of the creature). This would not apply to the internal structures logically however.
Sorry about msg 76 I will back over to that if I knew which thread it was in?? this number is 54
I take it your position is that if it was not for cell deaths which destroy the end/free embryonic tail no matter how much was overgrown by the trunk that, humans would posses in sexual maturity, a tail, as sometimes has been clinically recorded in a some hundreds at most individuals and because there are some deeply conserved issues of segementation between the vertebrates and invertebrates the end member of a serial division of the anatomy from head to end necesarily implies that the region between the free end the "trunk" must be explained as simply a matter of historical continuity from a heritable program saved over the generations?
Do notice that there is "gut" tissue in this end region. When thinking about tadpole tails I was able to think about ecological uses of the tail itself. Are we certain that there is not some gestational use for a free tail in fetuses? Could the few cases of adult human tails not be due rather than one associated with hoxology to one of overexpresion of genes possibly associated with a behavorial cause of embryonic free tails (assistance in untangling the umbilical?)?
quote:
The Umbilical Cord

Edited by Brad McFall, : msg number issue
Edited by Brad McFall, : small words
Edited by Brad McFall, : generalization
Edited by Brad McFall, : umbilical link

This message is a reply to:
 Message 53 by bernd, posted 10-20-2006 11:34 AM bernd has replied

Replies to this message:
 Message 55 by bernd, posted 10-27-2006 9:21 AM Brad McFall has replied

  
bernd
Member (Idle past 3980 days)
Posts: 95
From: Munich,Germany
Joined: 07-10-2005


Message 55 of 61 (359278)
10-27-2006 9:21 AM
Reply to: Message 54 by Brad McFall
10-20-2006 3:53 PM


Re: Re:falsification of non-historical interpretation
Hello Brad,
Brad writes:
There are some difficulties of language going on here. When I quoted Carter on Darwin I had in mind his anglo-expressions. I had hoped that by moving THROUGH Gould's lingo we would have exhausted our likely different linguisitic backgrounds. That does not seem to be the case given you response.
I was reading "stage" in an general evolutionary sense.
There are indeed “some difficulties of language going on here”. When you try to “read” stage in a general evolutionary sense then it is quite misleading to combine it with the word “phylotypic” - you’ll find the term “phylotypic stage” in the meaning “stage which typifies a phylum” probably in all text books about developmental biology. And when you claim that in E. Darwin's usage “PLAN” means “the split(left and right)-somite-formation” you should not be surprised when asked to back this up.
Another example of the same problem:
Brad writes:
Maybe I missed it, I am not trying to be obtuse, but I do not see how the existence of HOX cluster implies that the the terminal segement area must be non-scalar with respect to the magnitdue of a matrix metric that links(Correlates) the parts UP TO the END (of the creature). This would not apply to the internal structures logically however.
When you use concepts of linear algebra to model the expression of a hox cluster you should define your terms. So let’s have a look at the standard meaning of matrix and metric.
(In the following R denotes the set of the real numbers)
Each matrix can be expressed as a linear transformation. A transformation F: V->W between the vector spaces V and W (about R) is called linear, when the following conditions hold:
1. F(v+w) = F(v) + F(w)
2. F(λ*v) = λ*F(v)
With v, w ∈ V, λ ∈ R
A metric is defined as a function d: M × M -> R which meets the following conditions:
1. d(x, y) = 0 ⇔ x = y
2. d(x, y) = d(y,x)
3. d(x,z) ≤ d/x,y) + d(y,z)
With x,y,z ∈ M.
So when you talk about the “magnitude of a matrix metric” please define V, W and show that F is a linear transformation. Then define M and d and demonstrate that d meets the requirements for a metric. Done this you may tell me again what you tried to express with your sentence, specifically why you think that the “terminal segment must be non scalar”.
The following statements are probably due to another problem
Brad writes:
In frogs the macophages also destroy the tail but I do not see how the tail exisiting outside the psm in humans indicates a "lower" stage evolutionarily, necessarily. The tail is simply tissue at the end of the creature
Brad writes:
The psm marks the place between this edge and "interior" tissue
Brad writes:
The issue of how the EDGE gets divided from the zygote is a real one
I suspect these quotes reflect some misunderstandings about somitogenesis. Have a look at this:
During somitogenesis, at the body level, the paraxial mesoderm consists of the somitic region anteriorly and of the unsegmented PSM posteriorly. Because new somites are constantly added during somitogenesis, the ratio of segmented mesoderm over unsegmented mesoderm increases over time. While somite formation periodically removes unsegmented material from the PSM anteriorly, new mesodermal cells are added at the posterior extremity of the unsegmented tissue by the ongoing gastrulation process taking place in the primitive streak and later on in the tailbud. However, the net balance between the removal and addition of unsegmented tissue is not null and the length of the PSM varies during development. In mouse and chick embryos, PSM formation starts soon after the beginning of primitive streak regression. Its length progressively increases and peaks 1 day later, when it contains 12-14 presumptive somites in the chick embryo and around six somites in the mouse embryo (Packard and Meier, 1983 ; Tam and Beddington, 1986 ). The PSM length then gradually decreases until almost no unsegmented material remains, which coincides with the end of axis elongation
The “edge” - which I read as the tail bud - creates all tissue contributing to the lumbar, sacral and caudal regions. The tail bud itself is described as:
The tailbud is a small mass of highly packed undifferentiated cells, which undergo complex stereotyped movements similar to gastrulation before contributing to the definitive layers. These features suggest that the tailbud corresponds to a functional remnant of the blastopore or of the primitive streak (Cambray and Wilson, 2002 ; Catala et al., 1995 ; Gont et al., 1993 ; Kanki and Ho, 1997 ; Knezevic et al., 1998 ).
In other words, the “edge” gets divided from the “zygote” by producing new psm, while in the anterior part psm is constantly transformed into somites. When the last somites are formed - that are the somites of the tail - axis elongation stops.
For a detailed account compare the quoted article.
With regard to bilateral symmetry, you wrote:
Brad writes:
Yes tail somites ARE formed from the psm, as I read, but the "bud" exists as labeled beyond and BEFORE the somite pair appears as it appeared in the figure one, I think.
Am I seeing things wrong? Are not the two "rods" of tissue not each on a side off the a drawable midline??
I don’t dispute that the two rods of the psm are bilateral symmetric. But you seem to generalize this observation beyond the vertebrates. Obviously there are animals which are bilateral symmetric but don’t pass through an embryonic stage with somites. (If I didn’t understand your idea, please reformulate it.)
Brad writes:
If you can show me that hox molecular biology(relations of hox cluster physcial chemistry as promixate cause of all allomteric regularities) regulatory for the tail bud tissue itself then yes, I might be inclined to accept an historical interpreation for the functioning of the this "organ" or "tissue area" and would.
There are at least two genes which are regulatory for the tail bud:
Wnt-3a and Hoxb-13. Without Wnt-3a the tail bud does not form:
Amphibian studies have implicated Wnt signaling in the regulation of mesoderm formation, although direct evidence is lacking. We have characterized the expression of 12 mammalian Wnt-genes, identifying three that are expressed during gastrulation. Only one of these, Wnt- 3a, is expressed extensively in cells fated to give rise to embryonic mesoderm, at egg cylinder stages. A likely null allele of Wnt-3a was generated by gene targeting. All Wnt-3a-/Wnt-3a- embryos lack caudal somites, have a disrupted notochord, and fail to form a tailbud. Thus, Wnt-3a may regulate dorsal (somitic) mesoderm fate and is required, by late primitive steak stages, for generation of all new embryonic mesoderm. Wnt-3a is also expressed in the dorsal CNS. Mutant embryos show CNS dysmorphology and ectopic expression of a dorsal CNS marker. We suggest that dysmorphology is secondary to the mesodermal and axial defects and that dorsal patterning of the CNS may be regulated by inductive signals arising from surface ectoderm.
As already discussed Hoxb-13 probably regulates the apoptosis of the tail bud mesenchyme, stopping thereby tail and axis elongation.
Brad writes:
I take it your position is that if it was not for cell deaths which destroy the end/free embryonic tail no matter how much was overgrown by the trunk that, humans would posses in sexual maturity, a tail, as sometimes has been clinically recorded in a some hundreds at most individuals and because there are some deeply conserved issues of segementation between the vertebrates and invertebrates the end member of a serial division of the anatomy from head to end necesarily implies that the region between the free end the "trunk" must be explained as simply a matter of historical continuity from a heritable program saved over the generations?
My position is not topic of this thread. (But to give you an answer: no, that’s not my position, some of the reasons you may deduce from the above quotes about somitogenesis)
Brad writes:
Do notice that there is "gut" tissue in this end region. When thinking about tadpole tails I was able to think about ecological uses of the tail itself. Are we certain that there is not some gestational use for a free tail in fetuses? Could the few cases of adult human tails not be due rather than one associated with hoxology to one of overexpresion of genes possibly associated with a behavorial cause of embryonic free tails (assistance in untangling the umbilical?)?
Do you have you any evidence for the assumed function of the embryonic free tail? Besides that, doesn’t your idea imply that humans have a developmental pathway to develop a tail?
-Bernd

This message is a reply to:
 Message 54 by Brad McFall, posted 10-20-2006 3:53 PM Brad McFall has replied

Replies to this message:
 Message 59 by Brad McFall, posted 11-04-2006 5:59 PM bernd has replied

  
bernd
Member (Idle past 3980 days)
Posts: 95
From: Munich,Germany
Joined: 07-10-2005


Message 56 of 61 (359288)
10-27-2006 10:24 AM
Reply to: Message 52 by Brad McFall
10-19-2006 8:06 PM


Re: Response to falsification of non-historical interpretation
Hello Brad,
according to your source programmed cell death is regulated upstream by the same signals that control cell proliferation and differentiation. When we compare this with the end of somitogenesis in mice we find:
Somitogenesis normally ceases at ~E13.25 in the mouse,
when the TBM regresses by apoptosis. However, when ~E13
TBM cells are grafted into the primitive streak of the ~E8.5
embryo, they survive and make significant contributions to
paraxial mesoderm of the trunk (Tam and Tan, 1992). This
observation suggests that TBM survival and perhaps other
processes such as cell proliferation, fate determination and/or
differentiation are influenced by extrinsic signals.
The TBM (tail bud mesenchyme) is the source for all of the paraxial mesoderm in the caudal, lumbar and sacral region of the embryo and in consequence of all somites that form in these regions of the embryo.
Combine this with the observation that hoxb-13 in mice is expressed spatially in the tail tip and chronologically at the end of axis elongation, further that its function seems to be to stop tail growth. We can hopefully agree then that your idea about cell death simply providing “a space or rather a lack of cell area to morphogenetics rather than being a constructive constructor IN THE TAIL” is mistaken.
You seem to base your conclusion on your readings about frog tadpoles:
Brad writes:
I have read somewhat of the cell death in the tails of frog tadpoles and in reading that literature I have only been lead to think that cell death “destroys” a morphology in order to provide another (stronger back legs than front legs (to the gills)) (altruistically) and not that it regulates a part (tail bud) for the function of the tail itself(which seems to be necessary if the human tail is to be explained by the same history that gave up the frog’s lack).
A counter example to your claim that cell death “destroys a morphology in order to provide another”, is the role of apoptosis in vertebrate limb development. Developmental processes that include programmed cell deaths are for example:
” Elimination of transitory organs and tissues. Examples include phylogenetic vestiges (pronephros and mesonephros in higher vertebrates), anuran tails and gills and larval organs of holometabolous insects.
” Tissue remodeling. Vertebrate limb bud development (Fig. 11.42, Saunders, 1982; Fig. 1, Saunders, 1966) is an example. If PCD fails, in formation of the digits, digits remain joined by soft tissue. Compare, for example, the situation in the chick and duck hind limbs. If chick limb mesoderm is combined with duck ectoderm, PCD fails and the digits remain joined (Saunders, 1966). This observation implicates the ectoderm in providing the signal to trigger PCD. Another example is formation of heart loops during vertebrate development. Depletion of cells in spinal ganglia occurs during development of the chick embryo. As shown in Table 11.1 (Saunders, 1982), there is precise chronological and spatial control over this process. Interestingly, injections of nerve growth factor reduce the frequency of cell death in the spinal ganglia. This observation provides a link between growth control and PCD.
Brad writes:
This thought gives a purely structuralist explanation for cell death in the tail of a vertebrate and removes even the functionalist one.
Given that the tail of the tadpole is not replaced by “stronger legs” I see no explanation at all here.
-Bernd
Edited by bernd, : No reason given.

This message is a reply to:
 Message 52 by Brad McFall, posted 10-19-2006 8:06 PM Brad McFall has replied

Replies to this message:
 Message 58 by Brad McFall, posted 11-04-2006 5:35 PM bernd has not replied

  
Brad McFall
Member (Idle past 5032 days)
Posts: 3428
From: Ithaca,NY, USA
Joined: 12-20-2001


Message 57 of 61 (359929)
10-30-2006 4:41 PM
Reply to: Message 3 by Dr Adequate
09-29-2006 12:54 PM


wending the winding way or will the umbilical not be cut
According to the E. Darwin info I used in message 9
EvC Forum: Are human tails an example of macroevolution?
1st- metamorphosis
2nd- artifical selection or cultivation (in the garden)(Mendel distinguished this from cultivation in the country)
3rd - meteorologically torque affected biochange or nonadaptive trait procurement
- habit via employment (Marxist)
- hybrids and or subject of this thread
4th - WHEN WE OBSERVE(D) the essential unity of all plan of all warm-blooded animals
WHAT THE FILAMENT WAS as believed.
The FOUR that Bernd was want to express from E. Darwin was
quote:
Fourthly, when we revolve in our minds the great similarity of structure, which obtains in all the warm-blooded animals, as well quadrupeds, birds, and amphibious animals, as in mankind; from the mouse and bat to the elephant and whale; one is led to conclude, that they have alike been produced from a similar living filament
already had the triple 3rd above, which I asserted only makes sense ON ROTATION.
Bernd is challenging that my cross generational abduction (between points two(plants) and three(topic at hand)) is never physically rotated in the revolved thought of any stripe down the right and left at an terminal ordination of the datum. I think it is. There are horrendous difficulties in communicating in this thread. He now said that his own thoughts did not matter. He contends that this is a ready read thread or filament of ANATOMY not of phylogeny. I can only see this as possible if the connections of nonadaptive traits completed by seasonal and climate effects only dominate the "similarity of forms" and thus I find that this is actually an issue of translation between languages rather than a issue where one is trying to decide if the evidence pertains to a structural or an historical angle (or functional) in explanation of the clinical cases. He now redirects back to my own ideas. This is always easier to answer than to argue in general. I will. But you can see now as this thread has come and gone and goes some more that it is definitely NOT easier to sustain a creationist position vis a via a particular topic on EvC!!
The forum is with C. Darwin's not E. Darwin's view. Is the prosimian tail the Homo tail phylogenetically? C.Darwin indubitably took "similarity of form" as Bernd shortened it
quote:
He argues then that a process which transforms a simple filament into an organism, may also form the diversity of warm blooded animals, given that they share a similar structure (that's a simplification but it should do within the context of this thread)
http://EvC Forum: Are human tails an example of macroevolution? -->EvC Forum: Are human tails an example of macroevolution? and added the notion of
"history" precisely as Gould has narrated this past science somewhat but if one reads very very closely Charles Darwin's Power of Motion in Plants quote one can read that orthogonal directions decompose OUT the form of the seed. So if Mendelism changes C.Darwinism Within the third place (INTO the second) the "structure" that is the difference of the numerator and denominator can "constrain" the "Form" in the induction beyond E. Darwin IF the tail is read as the filament or flaccid rope (herein and of Galelio etc). Bernd continues to suspect that I am reading something into this that is not here. I will show him I am not. Bernd already agreed that he will take into consideration "heritability" on the "family" level.
Making this case out clearly is beyond the pale of what goes down at secular elite universities.

This message is a reply to:
 Message 3 by Dr Adequate, posted 09-29-2006 12:54 PM Dr Adequate has not replied

  
Brad McFall
Member (Idle past 5032 days)
Posts: 3428
From: Ithaca,NY, USA
Joined: 12-20-2001


Message 58 of 61 (361591)
11-04-2006 5:35 PM
Reply to: Message 56 by bernd
10-27-2006 10:24 AM


Re: Response to falsification of non-historical interpretation
Perhaps I was mislead a bit by the labeled picture of TBM in a link upthread.
I do not "visualize" evolutionarily that there was a larger "anatomical diversity" of life prior to the Permian as did Gould. Instead when we have to dicuss all of the creatures I have HAD this of "gestalt" in mind.
I probably constructed this template during my earlier years posting on EvC. It was probably NO COINCIDENcE that I cut out the tail end of the frog area TO BE ABLE TO ACTUALLY FIT IN the word "data."
Now if you feel I have still overridden the evidence from hoxology please let me know but under a term "transmorgification" I would still retain that cell death can possibly be theoretically capable of giving PHENOTYPES space. THE ACTUAL SPACE was triplicated by the brown /\'s in the following (notes on the relation between any given angle, behavior and canalization. I had thought that cell death is just a bunch of those symbols signified (but "programmed"). It may be possible that negative entropy is involved but after communicating with Gladyshev I am less prone to go there (source vs sink) as easily as I was when I first scrathed down the relations.
This was why I was saying that it might not matter to you but it does to me if the canalized pathway is wide or narrow. Obviously these are only my own marks.
By 'Stronger' legs I simply mean that frogs have back legs to jump with and the anatomy is proximate to the tail rather than the gills as to where the macrophages and destruction is going on.
I am not sure that "tissue remodeling" and "transmorgification" (as intended by Gould) are any different. I did find some of the herp papers on somites in lizards I had mentioned earlier.
You may note as to your other reply to me that I mention "vectorization" in the white picture above. I also say that this view of mine has not existed. Part of the interest in this relation of behavior to morphogenetics (across a mathmeatical construct of my own doing) was discussed with BEN (in part at least) when he first started posting on EVC. I can admit to this much.

This message is a reply to:
 Message 56 by bernd, posted 10-27-2006 10:24 AM bernd has not replied

  
Brad McFall
Member (Idle past 5032 days)
Posts: 3428
From: Ithaca,NY, USA
Joined: 12-20-2001


Message 59 of 61 (361604)
11-04-2006 5:59 PM
Reply to: Message 55 by bernd
10-27-2006 9:21 AM


Re: other post
The idea I got on reading some of the material you linked was:
There is always some part at the terminal "end" of the vertebrate embryo. I was trying to generalize beyond the vertebrates if and when I mention Agassiz. But so that we can maximally understand each other lets drop retrodictions to the very beggining of this thread unless it is the last position of discussion. I will assume we are only talking about vertebrates (not even echinoderms) and never about nodal space differences in plants that twist.
In the picture I was looking at there were no somites formed yet into the psm and the tail bud was labeled. I noticed that the the somites were also marked with with dots on each side of the axis of the back midline. In what I had thought was my last post in this series I suggested that BEHAVIORAL functionality may ADDITIONALLY format the embyronic functionality of this area and that instead of (as well as in addition to ) hoxology being the doxology of human "tails" rather there may be some deviant gene overexpression for this 'behavior' that extended beyond cell death protocols that would normally prevent the trait from appearing at birth.
Now there may be molecular evidence contrary to my own analysis and somewhat lame synthesis. But this property of the free tail may indicate a structural origin of the LACK of the great ape tail even while it faimiliar structure for the monkeys and other mammals as a whole. In this case I would have taken the destructive notion beyond the material destruction (as I have thought with frogs) and implicated gestational behavior as controlling genetic fate as well.
Look I dont deny that the tail might be historical as Gould is want to disclaim against Dobshanky's "topography" of lions and tigers, and wolves and jackals but I only wanted to make sure that there was not some other possibly wholy structural explanation that just might not have been recieved into the current literature.
I do not really feel we have made it to the place in the discussion to cause me to get even more rigorous with the "linear transformation" etc but I can go there if that is really what you are calling for.I thought the reference to "parallels" would suffice still for now. I, for my self, have a hard time trying to disuade myself that you are saying nothing more ( with great links to modern literature notwithstanding)than:
quote:
The Marvels and Mysteries of Science: An outline of scientific knowledge in astronomy, biology, chemistry, physics, geology, anthropology written in a popular style 1941 Wm H. Wise & CO., INC. NY
but look I have not tried to assimilate ALL of the hox literature. I am reading Gould rather deeply at this time and my confidence comes from mental sparring with his ideas on the subject more than what others may feel is possibly more representative of the current literature. I am not making apologies. I may be wrong.

This message is a reply to:
 Message 55 by bernd, posted 10-27-2006 9:21 AM bernd has replied

Replies to this message:
 Message 60 by bernd, posted 11-20-2006 3:15 PM Brad McFall has replied

  
bernd
Member (Idle past 3980 days)
Posts: 95
From: Munich,Germany
Joined: 07-10-2005


Message 60 of 61 (364938)
11-20-2006 3:15 PM
Reply to: Message 59 by Brad McFall
11-04-2006 5:59 PM


Re: other post
Hello Brad,
please excuse my late answer, but at the moment I am travelling with difficult access to internet and/or scientific literature. I am going to answer your posts in more detail in about 5 weeks.
Anyway it seems to me that the main difference relevant for this thread can be found here:
Brad writes:
In what I had thought was my last post in this series I suggested that BEHAVIORAL functionality may ADDITIONALLY format the embyronic functionality of this area and that instead of (as well as in addition to ) hoxology being the doxology of human "tails" rather there may be some deviant gene overexpression for this 'behavior' that extended beyond cell death protocols that would normally prevent the trait from appearing at birth.
The human embryonic tail reaches his maximum length at about the 5th week. In the following weeks its size decreases and at the end of the eight week it has nearly disappeared. Spontaneous movements of the embryo are not observed before the nineth or tenth week. In other words your behavioral explanation does not work for lack of behavior
Considering your remarks about a purely structural explanation of human tails, do you agree that up to now no supporting evidence was presented? And that on the other hand some observations in genetics seem to falsify your hypothesis?
-Bernd

This message is a reply to:
 Message 59 by Brad McFall, posted 11-04-2006 5:59 PM Brad McFall has replied

Replies to this message:
 Message 61 by Brad McFall, posted 11-20-2006 5:20 PM bernd has not replied

  
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