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
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