Preaching bad design: An argument from ignorance?

Over the years many people have come with arguments that systems in nature are sub-optimal, or sub-par. These arguments were used as a means to point out that they are "dumb" designs if it was the product of mind.

An example of such an argument is given by Richard Dawkins. Take his article:
The Information Challenge

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Genomes are littered with nonfunctional pseudogenes, faulty duplicates of functional genes that do nothing, while their functional cousins (the word doesn't even need scare quotes) get on with their business in a different part of the same genome. And there's lots more DNA that doesn't even deserve the name pseudogene. It, too, is derived by duplication, but not duplication of functional genes. It consists of multiple copies of junk, "tandem repeats", and other nonsense which may be useful for forensic detectives but which doesn't seem to be used in the body itself.

Luckily science moves forward and these arguments from ignorance get left behind and the proponents of these arguments fade into history as proponents of ignorance trying to sell meaningless metaphysics.

Junk DNA is a myth.
Examples abound of research finding fascinating functions for these previously thought non-functional parts of the genome (out of ignorance and bad metaphysics-- Dawkins: "And there's lots more DNA that doesn't even deserve the name pseudogene.").

Model unravels rules that govern how genes are switched on and off

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"Since the discovery of DNA's double helical structure more than a half century ago, scientists have focused much of their attention on understanding the 2 percent of the genome that is made up of classic genes, which code for the production of proteins. However, the instructions for turning these genes on or off are generally not in the genes themselves. Rather, they are buried in the 98 percent of the genome that was once cast aside as little more than genetic "junk."

Scientists at CSHL uncover new RNA processing mechanism and a class of previously unknown small RNAs

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A very small fraction of our genetic material--about 2%-- performs the crucial task scientists once thought was the sole purpose of the genome: to serve as a blueprint for the production of proteins, the molecules that make cells work and sustain life. This 2% of human DNA is converted into intermediary molecules called RNAs, which in turn carry instructions within cells for protein manufacture. "And what of the other 98% of the genome? It has been assumed by many to be genetic junk, a massive accumulation of “code” that evolution has rendered superfluous. Now, however, scientists are discovering that the vast bulk of the DNA in our genomes, while it does not “code” for the specific RNA molecules that serve as templates for protein synthesis, do nevertheless perform various kinds of work."

'Junk' DNA May Have Important Role In Gene Regulation

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ScienceDaily (Oct. 20, 2008) — For about 15 years, scientists have known that certain "junk" DNA -- repetitive DNA segments previously thought to have no function -- could evolve into exons, which are the building blocks for protein-coding genes in higher organisms like animals and plants. Now, a University of Iowa study has found evidence that a significant number of exons created from junk DNA seem to play a role in gene regulation.

Well, it is not only supposedly "junk DNA" that was used for these kind of arguments. The vertebrate eye has been preached to be a bad design. Why? Why is it a bad design?

The human eye contain bona fide optical fibers to conduct light and here is a nice illustration. Besides the design arose 40-60 times during evolution, like evolution was biased (converged on an optimal design) towards such a structure. So why is it sub optimal? Are proponents of these arguments going to suggest a better design with all the blueprints? Thought not, arguments from ignorance are short on design.

Why was it suggested that the appendix is useless and functionless, instead of just admitting "we are still looking into it".
A few articles discussing its function:
1) Dasso JF. Howell MD. 1997. "Neonatal appendectomy impairs mucosal immunity in rabbits." Cellular Immunology. 182(1):29-37.
2) Dasso JF. Obiakor H. Bach H. Anderson AO. Mage RG. 2000. "A morphological and immunohistological study of the human and rabbit appendix for comparison with the avian bursa." Developmental & Comparative Immunology. 24:8:797-814.
3) Fisher, RE. 2000. "The primate appendix: a reassessment." The Anatomical Record (New Anatomist) 261:228-236.
4) Weinstein PD. Mage RG. Anderson AO. 1994. "The appendix functions as a mammalian bursal equivalent in the developing rabbit." Advances in Experimental Medicine & Biology. 355:249-53.
5) A more detailed survey of the evidence, with numerous references to other technical literature, showing that the appendix is not a vestigial organ can be found in J.W. Glover, The Human Vermiform Appendix—a General Surgeon’s Reflections, CEN Technical Journal, 3:31–38, 1988.

In short:
The appendix contains a high concentration of very specialized structures called lymphoid follicles (also found throughout the GIT). Lymphoid follicles in the appendix produce cells that produce antibodies that control which essential bacteria come to reside in the caecum and colon in neonatal life. The "strategic" placement of the appendix is important during the development of neonatal life in the setup of healthy intestinal flora therefore neonatal appendectomy will impair mucosal immunity.

"The appendix's job is to reboot the digestive system..." and "acts as a good safe house for bacteria,".

It might not be that important in later life and it can be removed, but so can your one kidney, your stomach, an eye, small intestines, reproductive organs etc. Are these bad designs then as well? See... these arguments have no force. Empty arguments from ignorance...



And the cilium? Until the 1990s, the prevailing view of the primary cilium was that it was merely a vestigial organelle, without important function (wiki). Seems like pretty high-tech structures to me?

Primary Cilium As Cellular 'GPS System' Crucial To Wound Repair

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ScienceDaily (Dec. 25, 2008) — The primary cilium, the solitary, antenna-like structure that studs the outer surfaces of virtually all human cells, orient cells to move in the right direction and at the speed needed to heal wounds, much like a Global Positioning System helps ships navigate to their destinations.

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What we are dealing with is a physiological analogy to the GPS system with a coupled autopilot that coordinates air traffic or tankers on open sea," says Soren T. Christensen, describing his recent research findings on the primary cilium, the GPS-like cell structure, at the American Society for Cell Biology (ASCB) 48th Annual Meeting, Dec. 13-17, 2008 in San Francisco. Christensen and his colleagues at the University of Copenhagen in Denmark and the Albert Einstein School of Medicine in the Bronx studied the primary cilia in lab cultures of mice fibroblasts, the cells that along with related connective tissues sculpt the bulk of the mammalian body.

So we think we have designed GPS systems?

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"The really important discovery is that the primary cilium detects signals, which tell the cells to engage their compass reading and move in the right direction to close the wound," Christensen explains.

Purposefully communicating information as a means to an end... wound healing.

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The researchers suspect this cellular GPS system plays roles other than wound healing. The primary cilia could serve as a fail-safe device against uncontrolled cell movement, says Christensen. Without chemical stimulation, the primary cilia would restrain cell migration, preventing the dangerous displacement of cells that is associated with invasive cancers and fibrosis, the scientists explain. On the other hand, defective primary cilia might fail to provide correct directional instructions during cell differentiation. This failure could be another link connecting primary cilia to severe developmental disorders, the researchers suggest. Protruding through the cell membrane, primary cilia occur on almost every non-dividing cell in the body. Once written off as a vestigial organelle discarded in the evolutionary dust, primary cilia in the last decade have risen to prominence as a vital cellular sensor at the root of a wide range of health disorders, from polycystic kidney disease to cancer to left-right anatomical abnormalities.

Demonstrating the vacuity of preaching sub-optimal design... an idea from faulty Darwinian reasoning?

And taking clues from original design (cellular machinery) to design our own optimal nanotechnology? Does that make the original design optimal/above par/good?

Clockwork That Drives Powerful Virus Nanomotor Discovered

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Because of the motor's strength--to scale, twice that of an automobile--the new findings could inspire engineers designing sophisticated nanomachines. In addition, because a number of virus types may possess a similar motor, including the virus that causes herpes, the results may also assist pharmaceutical companies developing methods to sabotage virus machinery.

Related article:
Biologists Learn Structure, Mechanism Of Powerful 'Molecular Motor' In Virus

One has to wonder were the next spate of these arguments are going to come from? Perhaps the low optimality of the genetic code? Perhaps not... Maybe the inefficiency of biomolecular machines? Maybe not...

Arguments from bad design should be taken with a pinch of salt as they are often made out of ignorance with hidden meaningless and mindless metaphysical propositions.

Compasses, Translational Machinery and a little epigenetics

A few more agents and biomolecular machines .
Protein Compass Guides Amoebas Toward Their Prey

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ScienceDaily (Oct. 26, 2008) — Amoebas glide toward their prey with the help of a protein switch that controls a molecular compass, biologists at the University of California, San Diego have discovered.

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Their finding, recently detailed in the journal Current Biology, is important because the same molecular switch is shared by humans and other vertebrates to help immune cells locate the sites of infections. The amoeba Dictyostelium finds bacteria by scent and moves toward its meal by assembling a molecular motor on its leading edge. The active form of a protein called Ras sets off a cascade of signals to start up that motor, but what controlled Ras was unknown. Richard Firtel, professor of biology along with graduate student Sheng Zhang and postdoctoral fellow Pascale Charest tested seven suspect proteins by disrupting their genes. One called NF1, which matches a human protein, proved critical to chemical navigation. NF1 turns Ras off. Without this switch mutant amoebas extended false feet called pseudopodia in all directions and wandered aimlessly as Ras flickered on and off at random points on their surfaces. “You have to orient Ras in order to drive your cell in the right direction,” Firtel said. In contrast, normal amoebas with working versions of NF1 elongate in a single direction and head straight for the most intense concentration of bacterial chemicals, the team reports. The biochemical components of the system match those found in vertebrate immune cells called neutrophils that hunt down bacterial invaders, suggesting that the switch might be a key navigational control for many types of cells, Firtel said. “The pathway and responses are very similar and so are the molecules.” The US Public Health Service funded this work.

Agents assemble their equipment in order to hunt down their prey. An intentional plan laid out purposefully in order to manipulate the environment as a means to an end... food.


More equipment capable of manipulating the environment as a means to an end....
New Light Shed On Molecular Machinery Required For Translation Of Histone Crosstalk

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ScienceDaily (Dec. 14, 2007) — The Stowers Institute's Shilatifard Lab has published findings that shed light on the molecular machinery required for the translation of histone crosstalk, or communication between histones.

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Histones are important components of chromatin, the packing material surrounding chromosomal DNA. Also, histones play an important role in the regulation of gene expression. Histone H3 can be modified by methylation and this modification is an essential part of gene expression. Several years ago, the Shilatifard Lab identified the first histone H3 lysine 4 (H3K4) methyltransferase, known as COMPASS, in yeast. Soon thereafter, it was established that the MLL protein in humans also existed in a COMPASS-like complex capable of methylating H3K4. In 2002, the Shilatifard Lab reported the existence of the first histone crosstalk between histone H2B monoubiquitination for the regulation of histone methylation by COMPASS. "We now know that this mode of histone crosstalk is highly conserved from yeast to humans, but until now, its molecular mechanism of action was poorly understood. Jung-Shin Lee, a Postdoctoral Research Associate in my laboratory, was able to demonstrate the molecular machinery required for the translation of this histone crosstalk," said Ali Shilatifard, Ph.D., Investigator and senior author on the paper. This work demonstrated that the Cps35 subunit of COMPASS is required to translate the crosstalk between H2B monoubiquitination and H3 methylation by COMPASS. "Given the importance of histone methylation by the MLL complex and leukemia pathogenesis, defining the molecular machinery involved in this process could be highly useful," said Dr. Shilatifard.

Cell movement

Cells Coordinate Gene Activity With FM Bursts, Scientists Find

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Proteins Have Controlled Motions, Researcher Shows[/url][/b] ScienceDaily (Oct. 2, 2008) — How a cell achieves the coordinated control of a number of genes at the same time, a process that's necessary for it to regulate its own behavior and development, has long puzzled scientists.

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Michael Elowitz, an assistant professor of biology and applied physics at the California Institute of Technology (Caltech), along with Long Cai, a postdoctoral research scholar at Caltech, and graduate student Chiraj Dalal, have discovered a surprising answer. Just as human engineers control devices ranging from dimmer switches to retrorockets using pulsed -- or frequency modulated (FM) -- signals, cells tune the expression of groups of genes using discrete bursts of activation. Elowitz, who is also a Bren Scholar and an investigator with the Howard Hughes Medical Institute, and his colleagues discovered this process by combining mathematical and computational modeling with experiments on individual living cells. The scientists looked specifically at the molecular changes within simple baker's yeast (Saccharomyces cerevisiae) cells after exposure to excess calcium, which increases in concentration in cells in response to stressful conditions such as high salt levels, alkaline pH, and cell wall damage. The scientists tracked that response using a protein called Crz1 labeled with a green fluorescent tag. Crz1 is stimulated in response to high calcium levels and activates genes that help protect the cell. The glowing of the fluorescent marker allowed Elowitz and colleagues to visualize the movement of Crz1 as it travelled within the cell from the cytoplasm into the cell nucleus and out again into the cytoplasm. Using time-lapse microscopy, they created "movies" of that movement.

Landmark Discovery Of 'Engine' That Drives Cell Movement

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ScienceDaily (Oct. 7, 2008) — How a cell assembles its internal machinery required for cell movement has been revealed for the first time.

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The researchers discovered a complex of three proteins that directly regulates the myosin network within a cell, thus generating traction force to propel the cell forward. (Myosin is the most common protein found in muscle cells, and is responsible for the elastic and contractile properties of muscle. A different form of myosin is involved in cell movement.) This action of the tripartite protein complex may be likened to a spring in a toy motorcar – when the protein complex assembles and moves backwards within the cell, it resembles the wound up "engine" of the toy car that has been pulled backwards. Subsequent disassembling of the protein complex and the resultant forward movement of the cell can be likened to the released spring which unleashes the earlier stored potential energy to propel the car forward. Michael Sheetz, Ph.D., who is William R Kenan Jr Professor of Cell Biology at the Department of Biological Sciences, Columbia University, and also Distinguished Visiting Professor at the National University of Singapore, said, "This is an exciting paper because Leung's group has discovered an unexpected step in cell migration and contractility — a complex of three proteins including a form of myosin, that is responsible for assembling most of the other myosin components involved in motile processes. The assembly mechanism has been a major mystery and is critical in a variety of diseases from cardiovascular to aging. Now we have a new tool to understand the bases of these critical processes." Of the three proteins MRCK, LRAP35a and MYO18A, MRCK was discovered by the GSK-IMCB group 10 years ago, while the other two had hitherto unknown functions. Dr. Leung of IMCB said, "The success of the work relies on the commitment and perseverance of the team. A major contributor, Dr. Ivan Tan, is a home-grown scientist who has been working on this project for many years and he has had several clues as to how the system functions for some time, but it was only recently that the jigsaw puzzle was put together. The system has the potential to unravel other as yet undiscovered mechanisms that coordinate the different 'engines' for proper cell migration."

Emphasis mine.
Hard work with spectacular results