|Feature Article - October 2018|
|by Do-While Jones|
A recent article about the Hox gene shows how the theory of evolution is detrimental to science.
It is commonly claimed that anyone who is anti-evolution is anti-science because many people equate “evolution” with “science.” That’s a false equivalence because the theory of evolution is unscientific.
Since it is not sufficient simply to claim that the theory of evolution is not only unscientific, but is harmful to science as well, it is necessary to give an example to substantiate the claim. So, we looked for an example in the first article about evolution we could find in the peer-reviewed journal, Science, which came in the mail today. It happened to be an article about Hox genes written by Shuonan He, and five of his associates.
In case you aren’t familiar with Hox genes (and few people are) we will tease you a little bit to grab your interest.
On page 1377 of this issue, 1 [Shuonan] He, et al., elucidate two long-standing problems in animal evolution: the ancient function of the homeobox (Hox) gene cluster, which has puzzled scientists for decades, and the centuries-old debate on the emergence of the segmented animal body. 2
Before we talk about these two specific long-standing problems, one of which has puzzled scientists for decades, and the other which has been debated by scientists for centuries, let’s establish some background.
A friend once told me the difference between a scientist and an engineer.
When a scientist makes an important discovery, the first thing he thinks is, “Where can I get this published?” When an engineer makes an important discovery, the first thing he thinks is, “How can I make a buck with this?” 3
Academia does pure, theoretical research. Private industry does impure, practical research. Both have their place.
Practical research has a goal in mind. For example, a pharmaceutical company recognizes a need to cure a particular disease and does research to figure out how to cure that disease. They hire many smart people and buy lots of expensive equipment to do the research. When they figure out how to cure it, they manufacture a medicine to cure that disease. They sell the medicine for much more than it costs to manufacture because they have to recover the research costs. In this way, the people who buy the drug to cure their disease bear the cost to discover the cure. If the pharmaceutical company didn’t make a profit, they would go out of business and not find the cures for any more diseases.
Academic research doesn’t have any goal in mind—other than to learn something new. The value in academic research comes from the fact that it is generally beneficial to know more about everything, and usually there will be a surprising payoff in the future which nobody could have predicted. Academic research is generally done by university professors who get paid through research grants from the government or wealthy philanthropic individuals.
With the distinction between theoretical research and practical research in mind, let’s consider the Hox gene research.
Hox genes, a subset of homeotic genes, are a group of related genes that control the body plan of an embryo along the head-tail axis. After the embryonic segments have formed, the Hox proteins determine the type of appendages (e.g. legs, antennae, and wings in fruit flies) or the different types of vertebrae (in humans) that will form on a segment. Hox proteins thus confer segmental identity, but do not form the actual segments themselves.
An analogy for the Hox genes can be made to the role of a play director that calls which scene the actors should carry out next. If the play director calls the scenes in the wrong order, the overall play will be presented in the wrong order. Similarly, mutations in the Hox genes can result in body parts and limbs in the wrong place along the body. Like a play director, the Hox genes do not act in the play or participate in limb formation themselves. 4
There is no obvious, immediate application for Hox research. If many children were born with feet sticking out of their necks, then parents would gladly pay for prenatal tests to determine if their child would be born with a foot sticking out of his neck, and would gladly pay for a treatment to prevent it. Despite the fact that there isn’t an immediate, pressing, obvious need that is compelling Hox gene research, the research is certainly well worth doing. Hox genes are found in just about every living thing, so it is important to learn all that we can about them. They hold fundamental secrets to embryonic development.
You have to start somewhere when beginning any research. There are two obvious starting points. You can either start with the assumption that Hox genes are found in all forms of life because they existed in a common ancestor; or you can start with the assumption that Hox genes are found in all forms of life because they were created by a common designer. Which one you pick determines how the research will proceed.
In the following quote, you don’t need to understand anything except the first sentence and the last sentence. The sentences in the middle are just there to show you how complicated the problem is, even if you don’t understand a word of it.
Hox genes were first discovered in flies and mice, where they specify different body segments along the anterior-posterior (A-P) axis. Although their expression often overlaps in posterior body regions, they show spatially distinct anterior expression boundaries. Importantly, the A-P sequence of Hox gene expression in the body matches their 3' to 5' sequential occurrence within a chromosome cluster, a principle called spatial collinearity. Moreover, the more anteriorly expressed 3' Hox genes are often expressed earlier in development, which is called temporal collinearity. In addition, individual Hox proteins are typically active close to their anterior expression boundary, because the more 5', or posterior, proteins counteract the function of the more 39, or anterior, ones whenever both products co-exist. This is called posterior prevalence.
Making sense of these rules has been challenging. 5
Comparing the Hox genes in flies and mice, scientists have noted similarities and differences having to do with where (spatial) and when (temporal) these genes do things (expression). Scientists have had (and still have) a hard time figuring out the genetic rules which determine when and where Hox genes are expressed.
Here is their explanation, which will read like gibberish followed by nonsense—but fear not, we will explain it.
Few studies revealed Hox gene expression in mesodermal structures that resemble vertebrate somites. Moreover, Hox gene clusters are active in both segmented and unsegmented invertebrates such as sea urchins. This has prompted the view that the tight link between Hox genes and body segmentation observed in vertebrates, insects, or annelids has evolved independently, that is, by evolutionary convergence. 6
They believe that because vertebrates (such as rabbits) insects (ants, for example) and annelids (earthworms) don’t have a close common ancestor, these complicated Hox genes must have evolved independently. The technical name for this wishful thinking is “convergent evolution.”
Those evolutionists who don’t have the faith to believe the unbelievable make this admission:
The best way to challenge this view [convergent evolution] is to investigate an evolutionary outgroup. Accordingly, He et al. investigated Hox gene function in the cnidarian Nematostella vectensis, the starlet sea anemone. Cnidarians are our most distant relatives to possess a Hox cluster. Their inner surface is folded, so that their primitive gut is subdivided into chambers, called gastric pouches. These are also continuous with the lumen of the tentacles. The cnidarian lineage diverged from ours when a cluster of only three Hox genes existed, with one anterior (3'), one middle, and one posterior (5') gene. The sea anemone has a fragmented version of the ancient three-gene Hox cluster, with additional, lineage-specific duplications. … [blah, blah, blah] … This is strong evidence that the link between Hox gene function and some kind of body segmentation is ancestral. But how does N. vectensis segmentation—the sequential generation of gastric pouches by epithelial folding—relate to bilaterian segmentation? … [blah, blah, blah] … One possible caveat is that the sequentially emerging N. vectensis folds are not generated from a posterior growth zone. This might represent a secondary simplification of cnidarian development, given that … [blah, blah, blah] … Examining the expression of Hox genes and of growth zone markers in these cnidarians could be especially rewarding, as it might establish a similar link between Hox spatial and temporal collinearity and the generation of body segments from a growth zone as is observed in vertebrates. Another note of caution concerns the unsolved axial relationships between cnidarians and bilaterians, which led to conflicting views about the nature of the cnidarian Hox axis. However, the data of He et al. seem to firmly settle this issue. 7
The last sentence is priceless! All those weasel words were followed by the conclusion that the issue is now firmly settled!
Thank you for sticking with us through all that technical detail in He’s report. Here’s the point in plain English:
When scientists start with the presumption of evolution, they get distracted trying to figure out when in evolutionary history Hox genes evolved, how they evolved, and which species evolved from what other species. They wind up with unsolved relationships, notes of caution, caveats, and all sorts of speculation that has absolutely no value. It wastes the valuable time of brilliant scientists.
Scientists’ time would be better spent trying to figure out how Hox genes work than trying to figure out how Hox genes evolved.
Not only is science against evolution, evolution is against science because it distracts scientists.
|Quick links to|
|Science Against Evolution
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of the Month
Shuonan He, Science, 28 Sep 2018, “An axial Hox code controls tissue segmentation and body patterning in Nematostella vectensis”, pp. 1377-1380, http://science.sciencemag.org/content/361/6409/1377
2 Detlev Arendt, Science, 28 Sep 2018, “Hox genes and body segmentation”, pp. 1310-1311, http://science.sciencemag.org/content/361/6409/1310
3 James L. Rieger
4 https://en.wikipedia.org/wiki/Hox_gene, 4 October 2018
5 Detlev Arendt, Science, 28 Sep 2018, “Hox genes and body segmentation”, pp. 1310-1311, http://science.sciencemag.org/content/361/6409/1310