Posted on 07/29/2002 6:35:04 PM PDT by Tribune7
Printer-friendly format July 26, 2002, 6:11PM
A bone to pick: Missing link is evolutionists' weakest By JEFF FARMER
It has been said that if anyone wants to see something badly enough, they can see anything, in anything. Such was the case recently, but unlike some ghostly visage of the Madonna in a coffee stain, this was a vision of our ancestral past in the form of one recently discovered prehistoric skull, dubbed Sahelanthropus tchadensis.
Papers across the globe heralded the news with great fanfare. With words like "scientists hailed" and "startling find" sprinkled into the news coverage, who couldn't help but think evolutionists had finally found their holy grail of missing links?
For those of us with more than a passing interest in such topics as, "Where did we come from? And how did we get here?," this recent discovery and its subsequent coverage fall far short of its lofty claims. A healthy criticism is in order.
Practically before the fossil's discoverer, the French paleoanthropologist Michel Brunet, could come out of the heat of a Chadian desert, a number of his evolutionary colleagues had questioned his conclusions.
In spite of the obvious national pride, Brigitte Senut of the Natural History of Paris sees Brunet's skull as probably that of an ancient female gorilla and not the head of man's earliest ancestor. While looking at the same evidence, such as the skull's flattened face and shorter canine teeth, she draws a completely different conclusion.
Of course, one might be inclined to ask why such critiques never seem to get the same front-page coverage? It's also important to point out that throughout history, various species, such as cats, have had varying lengths of canine teeth. That does not make them any closer to evolving into another species.
A Washington Post article goes on to describe this latest fossil as having human-like traits, such as tooth enamel thicker than a chimpanzee's. This apparently indicates that it did not dine exclusively on the fruit diet common to apes. But apes don't dine exclusively on fruit; rather, their diet is supplemented with insects, birds, lizards and even the flesh of monkeys. The article attempted to further link this fossil to humans by stating that it probably walked upright. Never mind the fact that no bones were found below the head! For all we know, it could have had the body of a centaur, but that would hardly stop an overzealous scientist (or reporter) from trying to add a little meat to these skimpy bones. Could it not simply be a primate similar to today's Bonobo? For those not keeping track of their primates, Bonobos (sp. Pan paniscus) are chimpanzee-like creatures found only in the rain forests of Zaire. Their frame is slighter than that of a chimpanzee's and their face does not protrude as much. They also walked upright about 5 percent of the time. Sound familiar?
Whether it is tooth enamel, length of canines or the ability to walk upright, none of these factors makes this recent discovery any more our ancestral candidate than it does a modern-day Bonobo.
So why does every new fossil discovery seem to get crammed into some evolutionary scenario? Isn't it possible to simply find new, yet extinct, species? The answer, of course, is yes; but there is great pressure to prove evolution.
That leads us to perhaps the most troubling and perplexing aspect of this latest evolutionary hoopla. While on one hand sighting the evolutionary importance of this latest discovery, a preponderance of these articles leave the notion that somehow missing links are not all that important any more.
According to Harvard anthropologist Dan Lieberman, missing links are pretty much myths. That might be a convenient conclusion for those who have been unable to prove evolution via the fossil record. Unfortunately for them, links are absolutely essential to evolution. It is impossible for anything to evolve into another without a linear progression of these such links.
The prevailing evolutionary view of minute changes, over millions of years, is wholly inadequate for the explanation of such a critical piece of basic locomotion as the ball-and-socket joint. Until such questions can be resolved, superficial similarities between various species are not going to prove anything. No matter how bad someone wants to see it.
Farmer is a professional artist living in Houston. He can can be contacted via his Web site, www.theglobalzoo.com
Seems you are as ignorant as your friend. Read a book instead of the garbage in TalkOrigins.
Suppose you give us the facts and tell us how it disproves anything I have said. I am sure you will not. You are too lazy to read anything as your ridiculous statement on Y chromosomes showed.
The observable physical or biochemical characteristics of an organism
Protein expression is observable you putz.
Run along and look up western blotting in your little book.
Unlike evolutionists scientists
All scientists, save for a handful of crackpots, are evolutionists.
Get a clue.
Mutations in the HOX genes cause changes in the developmental program (and changes in morphology.)
Gore3000 was given FOUR examples of this which he was either too stupid, lazy, or scared to read.
You can't. You are illogical.
we are talking facts
Fact: Only mosquitoes with the duplicated genes have increased esterase levels.
Fact: Non-mutant mosquitoes do not overproduce esterase.
Fact: The mosquitoes with the duplicated genes are resistant to organophosphates.
Fact: Wild type mosquitoes die in the presence of organophosphates.
These facts have been observed in many different mosquito populations all over the world. There is an unquestionable link between gene duplication, esterase production and organophosphate resistance. Draw your own conclusions.
If this is the only 'logical' conclusion why don't they say it?
They DID. If they didnt that paper wouldnt have been published!
As usual you failed to READ anything I gave you.
Lenny, we had this SAME exact conversation a few weeks ago.
You were completely shot down. Was it that traumatic for you? No recollection at all?
Read it again and have it tattooed to your chest this time so you dont forget it again.
The EbgA mutations were both novel AND conferred a major survival advantage. This is ALL evolution claims. Youre completely out of any wiggle room.
Your math has been rendered irrelevant. Try to follow:
The individuals with the beneficial mutation are having all of the fun and most of the children.
The non-mutants are losers in the grand game of life.
Do you sympathize with the non-mutants?
You just asked me this five posts ago.
Cant you keep track of your own dishonesty anymore or have you gone mad reflecting upon your life?
Here is the original post (from over a month ago): #2104
Here are the posts from yesterday: #791, #800
Distilled for you in post#847
But I am sure you will have absolutely no trouble ignoring all of this for the tenth time.
Nicely put.
Why are you now trying to bring up other mutations?
Because that is what happens in real life. Inbreeding brings out the worst in the species. If you remember your genetics, it brings out the bad recessive genes in the population. That is what happens with small inbreeding populations.
You can look it up. I knew it was just a smoke screen. Only lame evos expect opponents to prove their case for them.
The observable physical or biochemical characteristics of an organism
Scientists (and that does not include confusionist evolutionists) speak of changes in phenotype as changes in the structure of the organism. When they talk about protein expression they protein expression. Science does not play fast and loose with words as evolutionists do.
You really are a bore. Changes in the Hox genes have been shown to result in unfavorable mutations. The famous case is the one in the flies where a change in the Hox genes destroyed the stabilizers of a fly and replaced them with wings. This made the fly less able to fly. The scientists won a Nobel Prize for it. Here is the previous discussion about us on the matter:
The only thing the mutation did was destroy the production of some of the legs of the insect- in the same way that drug use by the mother destroys the brains of their children. In addition, turning off genes is not creating a more complex organism - as evolution requires - it is destroying complexity. If you were trying to prove that bacteria devolved from humans, you might have a point, but you are trying to prove the opposite. That you (and evo 'scientists') claim that a destructive mutation is a proof of evolution shows quite well the utter desperation of evolutionists in trying to prove their theory.
Further, you and your evolutionists continue to ignore the challenge which I posed. All I am asking for is a concrete example, a real example of a single species which has transformed itself from a simpler species to a more complex one. If evolution were true there should be numerous examples of such transformations amongst the millions of species living and dead. Numerous examples should have been found in the 150 years in which evolution has been claiming that it is true. Just one example showing "Macro-evolution is a transformation requiring new genes, more complexity and new faculties. In terms of genetics, it requires at a minimum the creation of more than one new gene. In terms of taxonomy it would require an organism to change into a different genus."
The problem is not that a mutation can destroy something - such as the legs of insects as this study shows. We all know that mutations can destroy things and that is one of the strongest arguments against evolution. Mutations in the developmental program, such as from women who take drugs can destroy the brains of babies also, I guess you wall that a proof of evolution also?????? Here's your link again so that all can see this mutation deletes information, it does not add anything to the organism.
Here is the proof that the developmental process of an organism is a program:
23. Cell Interactions in Development
In Chapter 14, we learned that regionalization along the anteroposterior axis in the early Drosophila embryo is largely determined by gradients of transcription factors generated through translation of spatially restricted maternal mRNAs and subsequent diffusion of the encoded proteins through the common cytoplasm of the syncytial blastoderm. These transcription factors, in turn, control the patterned expression of specific target genes along the anterioposterior axis. In contrast, local interactions between cells, mediated by secreted or cell-surface signaling molecules, determine regionalization along the dorsoventral axis in Drosophila and along both major axes in early vertebrate embryos. Such local interactions also are the primary mechanism regulating the formation of internal organs such as the kidney, lung, and pancreas. Likewise, the vast number of highly specialized cells and their stereotyped arrangement in different tissues is a consequence of locally acting signals.
The importance of cellular interactions in development was demonstrated first in the early part of twentieth century through two complementary experiments. In one, destruction of an optic-vesicle primordium in developing frogs prevented formation of the lens from the overlying ectodermal cells. Conversely, transplantation of an optic-vesicle primordium to a region of ectoderm that normally does not give rise to a lens induced formation of a lens in an abnormal (ectopic) site (Figure 23-1). In modern biology we now use the term induction to refer to any mechanism whereby one cell population influences the development of neighboring cells.
In some cases, induction involves a binary choice. In the presence of a signal the cell is directed down one developmental pathway; in the absence of the signal, the cell assumes a different developmental fate or fails to develop at all. In other cases, signals can induce different responses in cells at different concentrations. For instance, a low concentration of an inductive signal causes a cell to assume fate A, but a higher concentration causes the cell to assume fate B. The concentration at which a signal induces a specific cellular response is called a threshold.
In many cases, an inductive signal induces an entire tissue containing multiple cell types. Two models have been proposed to account for these properties of extracellular signaling molecules. In the gradient model, a signaling molecule induces different fates at different threshold concentrations. A cells fate, then, is determined by its distance from the signal source. In the alternative relay model, a signal induces a cascade of induction in which cells close to the signal source are induced to assume specific fates; they, in turn, produce other inductive signals to pattern their neighbors.
Although inductive interactions often are unidirectional, they sometimes are reciprocal. Prominent examples of reciprocal induction include the formation of internal organs such as the kidney, pancreas, and lung. Many inductive interactions occur between non-equivalent cells; that is, the signaling and responding cells are already different. However, interactions between equivalent cells often are crucial in assuring that some cells in a developing tissue assume a specific fate and others do not. An evolutionarily conserved class of ligands and receptors regulates such interactions in C. elegans, Drosophila, and vertebrates.
Another feature that distinguishes various developmental pathways is the nature of the extracellular inductive signals. Many are freely diffusible and hence can act at a distance, whereas some are tethered to the cell surface and are available only to immediate neighboring cells. Still others are highly localized by their tight binding to the extracellular matrix. Early embryologists noted that cells differed in their ability to respond to inducing signals. Cells that can respond to such signals are referred to as competent. Competence may reflect the expression of receptors specific for a given signaling molecule, the ability of the receptors to activate specific intracellular signaling pathways, or the presence of the transcription factors necessary to stimulate expression of the genes required to implement the developmental program induced.
In this chapter, we first describe examples of various types of inductive signals and cellular interactions that regulate cell-type specification in several different developmental systems. Specific extracellular signals also control the migration of certain cells, which occurs during development of some tissues. As an example of this phenomenon, we discuss the role of extracellular signals in the assembly of connections between neurons. Another common feature of developmental programs is the highly regulated death of certain cells. In the final section of this chapter, we examine the conserved pathway leading to cell death and how it is controlled. The examples presented in this chapter were chosen to illustrate key concepts in this rapidly advancing field.
From: Cell Interations in Development
Note how complicated it is. Note that these scientists call it a program. Note that small changes or mistakes lead to disastrous results.
We are talking about mutations. Show proof that these duplicated genes are mutations. You refuse to back up your statements every time. You are just throwing a smoke screen.
They DID.
No they did not and that is why you will not repost the article. Come on, repost the article so all can see I am correct.
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