In a recent volume of the Vienna Series in a Theoretical Biology (2003), Gerd B. Muller and Stuart Newman argue that what they call the “origination of organismal form” remains an unsolved problem. In making this claim, Muller and Newman (2003:3-10) distinguish two distinct issues, namely, (1) the causes of form generation in the individual organism during embryological development and (2) the causes responsible for the production of novel organismal forms in the first place during the history of life. To distinguish the latter case (phylogeny) from the former (ontogeny), Muller and Newman use the term “origination” to designate the causal processes by which biological form first arose during the evolution of life. They insist that “the molecular mechanisms that bring about biological form in modern day embryos should not be confused” with the causes responsible for the origin (or “origination”) of novel biological forms during the history of life (p.3). They further argue that we know more about the causes of ontogenesis, due to advances in molecular biology, molecular genetics and developmental biology, than we do about the causes of phylogenesis--the ultimate origination of new biological forms during the remote past.
They are saying in essence we need to do more studies to determine the processes which created new morphologies.
In making this claim, Muller and Newman are careful to affirm that evolutionary biology has succeeded in explaining how preexisting forms diversify under the twin influences of natural selection and variation of genetic traits. Sophisticated mathematically-based models of population genetics have proven adequate for mapping and understanding quantitative variability and populational changes in organisms. Yet Muller and Newman insist that population genetics, and thus evolutionary biology, has not identified a specifically causal explanation for the origin of true morphological novelty during the history of life. Central to their concern is what they see as the inadequacy of the variation of genetic traits as a source of new form and structure. They note, following Darwin himself, that the sources of new form and structure must precede the action of natural selection (2003:3)--that selection must act on what already exists. Yet, in their view, the “genocentricity” and “incrementalism” of the neo-Darwinian mechanism has meant that an adequate source of new form and structure has yet to be identified by theoretical biologists. Instead, Muller and Newman see the need to identify epigenetic sources of morphological innovation during the evolution of life. In the meantime, however, they insist neo-Darwinism lacks any “theory of the generative” (p. 7).
What they are saying here is that Neo-Darwininism has succedded in explaining how preexisting forms have led to new forms such as deer from mice, But that current understanding of evolution and the emphasis on genetics may have us leading down the wrong path when trying to understand the origins of novel forms and structure like the eyes of an octopus.
As it happens, Muller and Newman are not alone in this judgment. In the last decade or so a host of scientific essays and books have questioned the efficacy of selection and mutation as a mechanism for generating morphological novelty, as even a brief literature survey will establish. Thomson (1992:107) expressed doubt that large-scale morphological changes could accumulate via minor phenotypic changes at the population genetic level. Miklos (1993:29) argued that neo-Darwinism fails to provide a mechanism that can produce large-scale innovations in form and complexity. Gilbert et al. (1996) attempted to develop a new theory of evolutionary mechanisms to supplement classical neo-Darwinism, which, they argued, could not adequately explain macroevolution. As they put it in a memorable summary of the situation: “starting in the 1970s, many biologists began questioning its (neo-Darwinism's) adequacy in explaining evolution. Genetics might be adequate for explaining microevolution, but microevolutionary changes in gene frequency were not seen as able to turn a reptile into a mammal or to convert a fish into an amphibian. Microevolution looks at adaptations that concern the survival of the fittest, not the arrival of the fittest. As Goodwin (1995) points out, 'the origin of species--Darwin's problem--remains unsolved'“ (p. 361). Though Gilbert et al. (1996) attempted to solve the problem of the origin of form by proposing a greater role for developmental genetics within an otherwise neo-Darwinian framework,1 numerous recent authors have continued to raise questions about the adequacy of that framework itself or about the problem of the origination of form generally (Webster & Goodwin 1996; Shubin & Marshall 2000; Erwin 2000; Conway Morris 2000, 2003b; Carroll 2000; Wagner 2001; Becker & Lonnig 2001; Stadler et al. 2001; Lonnig & Saedler 2002; Wagner & Stadler 2003; Valentine 2004:189-194).
This is debated, but the Theory is not being debated just the capacity of natural selection to produce truly novel forms. Although this is a minority view. Some beleive that there are other mechanisms at work within the framework of evolution which are waiting to be discovered.
What lies behind this skepticism? Is it warranted? Is a new and specifically causal theory needed to explain the origination of biological form?
Now this I am sure was added by whatever web page you got this from. The point I think this author is tryiong to make is that evolution is in shambles, which is simply not the case.
This review will address these questions. It will do so by analyzing the problem of the origination of organismal form (and the corresponding emergence of higher taxa) from a particular theoretical standpoint. Specifically, it will treat the problem of the origination of the higher taxonomic groups as a manifestation of a deeper problem, namely, the problem of the origin of the information (whether genetic or epigenetic) that, as it will be argued, is necessary to generate morphological novelty.
Again there is no problem with origin of information. The information lies in the genetic code.
In order to perform this analysis, and to make it relevant and tractable to systematists and paleontologists, this paper will examine a paradigmatic example of the origin of biological form and information during the history of life: the Cambrian explosion. During the Cambrian, many novel animal forms and body plans (representing new phyla, subphyla and classes) arose in a geologically brief period of time.
As I explained earlier if a classification was done during the cambrian explosion they would not be classified as separate phyla. Only in retrospect seeing the origins of todays forms in those primitive forms can we see this.
The following information-based analysis of the Cambrian explosion will support the claim of recent authors such as Muller and Newman that the mechanism of selection and genetic mutation does not constitute an adequate causal explanation of the origination of biological form in the higher taxonomic groups.
This seems to be a misinterpretation on the authors part.
It will also suggest the need to explore other possible causal factors for the origin of form and information during the evolution of life and will examine some other possibilities that have been proposed.
Novel Body Plans
The problems with the neo-Darwinian mechanism run deeper still. In order to explain the origin of the Cambrian animals, one must account not only for new proteins and cell types, but also for the origin of new body plans. Within the past decade, developmental biology has dramatically advanced our understanding of how body plans are built during ontogeny. In the process, it has also uncovered a profound difficulty for neo-Darwinism.
Significant morphological change in organisms requires attention to timing. Mutations in genes that are expressed late in the development of an organism will not affect the body plan. Mutations expressed early in development, however, could conceivably produce significant morphological change (Arthur 1997:21). Thus, events expressed early in the development of organisms have the only realistic chance of producing large-scale macroevolutionary change (Thomson 1992). As John and Miklos (1988:309) explain, macroevolutionary change requires alterations in the very early stages of ontogenesis.
Yet recent studies in developmental biology make clear that mutations expressed early in development typically have deleterious effects (Arthur 1997:21).
Typically but not always. Notice how this person is using selected quotes and articles out of context. This would mean sometimes morphological changes occur without deleterious effects, thus the poodle.
For example, when early-acting body plan molecules, or morphogens such as bicoid (which helps to set up the anterior-posterior head-to-tail axis in Drosophila), are perturbed, development shuts down (Nusslein-Volhard & Wieschaus 1980, Lawrence & Struhl 1996, Muller & Newman 2003).5 The resulting embryos die. Moreover, there is a good reason for this. If an engineer modifies the length of the piston rods in an internal combustion engine without modifying the crankshaft accordingly, the engine won't start. Similarly, processes of development are tightly integrated spatially and temporally such that changes early in development will require a host of other coordinated changes in separate but functionally interrelated developmental processes downstream.
What he doesn't point out or may not realize is that individual differences in development exist. Which means that the process is not as rigid as he proposes.
For this reason, mutations will be much more likely to be deadly if they disrupt a functionally deeply-embedded structure such as a spinal column than if they affect more isolated anatomical features such as fingers (Kauffman 1995:200).
This is true, however again notice more likely but this doesn't leave out the posibility.
This problem has led to what McDonald (1983) has called “a great Darwinian paradox” (p. 93). McDonald notes that genes that are observed to vary within natural populations do not lead to major adaptive changes, while genes that could cause major changes--the very stuff of macroevolution--apparently do not vary. In other words, mutations of the kind that macroevolution doesn't need (namely, viable genetic mutations in DNA expressed late in development) do occur, but those that it does need (namely, beneficial body plan mutations expressed early in development) apparently don't occur.
It's not that they don't occur, it's that changes to these areas of the genetic code are most likely to lead to failure.
6 According to Darwin (1859:108) natural selection cannot act until favorable variations arise in a population. Yet there is no evidence from developmental genetics that the kind of variations required by neo-Darwinism--namely, favorable body plan mutations--ever occur.
Just what types of morphological changes do you think this person is refering to?
Developmental biology has raised another formidable problem for the mutation/selection mechanism. Embryological evidence has long shown that DNA does not wholly determine morphological form (Goodwin 1985, Nijhout 1990, Sapp 1987, Muller & Newman 2003), suggesting that mutations in DNA alone cannot account for the morphological changes required to build a new body plan.
Thus the need to understand these factors and how they impact on possible changes to morphology they may cause.
DNA helps direct protein synthesis.7 It also helps to regulate the timing and expression of the synthesis of various proteins within cells. Yet, DNA alone does not determine how individual proteins assemble themselves into larger systems of proteins; still less does it solely determine how cell types, tissue types, and organs arrange themselves into body plans (Harold 1995:2774, Moss 2004). Instead, other factors--such as the three-dimensional structure and organization of the cell membrane and cytoskeleton and the spatial architecture of the fertilized egg--play important roles in determining body plan formation during embryogenesis.
These are inheritable traits as well. Also many of these structures are made of proteins which are encoded in the DNA.
Refer to the protein thread to see the relationship of DNA to proteins and the shape and functions that proteins take.
For example, the structure and location of the cytoskeleton influence the patterning of embryos. Arrays of microtubules help to distribute the essential proteins used during development to their correct locations in the cell. Of course, microtubules themselves are made of many protein subunits. Nevertheless, like bricks that can be used to assemble many different structures, the tubulin subunits in the cell's microtubules are identical to one another. Thus, neither the tubulin subunits nor the genes that produce them account for the different shape of microtubule arrays that distinguish different kinds of embryos and developmental pathways.
Not directly however the proteins are the shape they are because of the sequence of amino acids in them
the amino acids are in this order because of the sequence in the genetic code. Change the genetic code and the sequence of amino acids for the proteins making the tubules will change. And the way this protein folds will change because the amino acid sequence has changes. Now because the shape of the protein has changed its behaviour will change. See how it all boils down to genetic sequence?
Instead, the structure of the microtubule array itself is determined by the location and arrangement of its subunits, not the properties of the subunits themselves. For this reason, it is not possible to predict the structure of the cytoskeleton of the cell from the characteristics of the protein constituents that form that structure (Harold 2001:125).
Yes in this case the subunits bond onto existing subunits already in place. No cell is built from scratch, rather each time a new cell forms it is a result of cellular division.
Two analogies may help further clarify the point. At a building site, builders will make use of many materials: lumber, wires, nails, drywall, piping, and windows. Yet building materials do not determine the floor plan of the house, or the arrangement of houses in a neighborhood. Similarly, electronic circuits are composed of many components, such as resistors, capacitors, and transistors. But such lower-level components do not determine their own arrangement in an integrated circuit.
This analogy does not take into account the fact that chemicals do arrange themselves.
Biological symptoms also depend on hierarchical arrangements of parts. Genes and proteins are made from simple building blocks--nucleotide bases and amino acids--arranged in specific ways. Cell types are made of, among other things, systems of specialized proteins. Organs are made of specialized arrangements of cell types and tissues. And body plans comprise specific arrangements of specialized organs. Yet, clearly, the properties of individual proteins (or, indeed, the lower-level parts in the hierarchy generally) do not fully determine the organization of the higher-level structures and organizational patterns (Harold 2001:125). It follows that the genetic information that codes for proteins does not determine these higher-level structures either.
The communication between the cells determines this structure. The proteins used in this communication and the proteins which determine which proteins are to be expressed are all coded in the genetic coe.
These considerations pose another challenge to the sufficiency of the neo-Darwinian mechanism. Neo-Darwinism seeks to explain the origin of new information, form, and structure as a result of selection acting on randomly arising variation at a very low level within the biological hierarchy, namely, within the genetic text. Yet major morphological innovations depend on a specificity of arrangement at a much higher level of the organizational hierarchy, a level that DNA alone does not determine.
What does he mean by major morphological inovations?
Yet if DNA is not wholly responsible for body plan morphogenesis, then DNA sequences can mutate indefinitely, without regard to realistic probabilistic limits, and still not produce a new body plan. Thus, the mechanism of natural selection acting on random mutations in DNA cannot in principle generate novel body plans, including those that first arose in the Cambrian explosion.
Of course, it could be argued that, while many single proteins do not by themselves determine cellular structures and/or body plans, proteins acting in concert with other proteins or suites of proteins could determine such higher-level form. For example, it might be pointed out that the tubulin subunits (cited above) are assembled by other helper proteins--gene products--called Microtubule Associated Proteins (MAPS). This might seem to suggest that genes and gene products alone do suffice to determine the development of the three-dimensional structure of the cytoskeleton.
Yet MAPS, and indeed many other necessary proteins, are only part of the story. The location of specified target sites on the interior of the cell membrane also helps to determine the shape of the cytoskeleton.
These are located where they are because of the structure of these sites, which are proteins. Proteins encoded in the DNA.
Similarly, so does the position and structure of the centrosome which nucleates the microtubules that form the cytoskeleton. While both the membrane targets and the centrosomes are made of proteins, the location and form of these structures is not wholly determined by the proteins that form them. Indeed, centrosome structure and membrane patterns as a whole convey three-dimensional structural information that helps determine the structure of the cytoskeleton and the location of its subunits (McNiven & Porter 1992:313-329).
The protein itself is a three dimentional structure, I have no clue why the emphasis on the 3 dimentionality.
Moreover, the centrioles that compose the centrosomes replicate independently of DNA replication (Lange et al. 2000:235-249, Marshall & Rosenbaum 2000:187-205). The daughter centriole receives its form from the overall structure of the mother centriole, not from the individual gene products that constitute it (Lange et al. 2000).
Since then it has been found that centriol formation is goverened by proteins. Proteins which are encoded in the DNA.
In ciliates, microsurgery on cell membranes can produce heritable changes in membrane patterns, even though the DNA of the ciliates has not been altered (Sonneborn 1970:1-13, Frankel 1980:607-623; Nanney 1983:163-170). This suggests that membrane patterns (as opposed to membrane constituents) are impressed directly on daughter cells. In both cases, form is transmitted from parent three-dimensional structures to daughter three-dimensional structures directly and is not wholly contained in constituent proteins or genetic information (Moss 2004).
This is an interesting area of study and is exactly what the first article was talking about. This is that the scientific community cannot focus only on genes when trying to find mechanisms for evolution. Cellular membrane and other things such as hormones in the mother effect development as well.
Ah almost finished, but I'm afraid I am out of time. In the future I would appreciate it if you could post your own opinions based on these articles instead of just tossing it on the page and expecting some form of rebuttal.
It is not length of life, but depth of life. -- Ralph Waldo Emerson
