Why the concept of species is more fuzzy than you might think

By Rich Feldenberg:

The term species is viewed as a fundamental unit in biology. We are the species Homo sapiens, and we love to classify ourselves and other creatures into unique categories, giving them qualities that set them apart from other creatures. Charles Darwin’s evolution by natural selection gave the first proofs that all living organisms today descended from a common ancestor, which branded into an ever growing number of different evolutionary paths, resulting in a tree of life.  The trunk being the last common ancestor (LUCA) and all the tiny twigs at the ends representing all species that have ever existed. But is this really an accurate view of the living world – each species of organism occupying its own unique little cubby, completely distinct from it’s fellows in the cubbies next door? We have learned a lot since Darwin’s important discovery of Natural Selection. Modern biology tells us that, while evolution is on firm scientific ground, the concept of the species is less so. We humans have a tendency to think in a discontinuous way – that things do fall into distinct categories – that there is a separate essence that each thing has unto itself. That may be one reason why evolution is a difficult concept to accept for some people, because if each thing has it’s own essence of being, you can’t change it into something else. This idea was demonstrated in an experiment where children were told a story about a witch that turned a frog into a rabbit. The frog now looked like a rabbit, acted like a rabbit, preferred to eat carrots and not flies, wanted to hang out with other rabbits, but when the children were asked if this animal was now a rabbit they said it was really a frog. It’s underlying froggy essence could not be altered by the witches spell.

It turns out that the concept of species is really not a discontinuous one at all. It is a continuous variable, and that may be a difficult idea to wrap your head around. In medicine some diagnoses are continuous and others discontinuous, and in some others it may be difficult to know for sure. For example, having 6 fingers on your hand is discontinuous (you either do or you don’t), but systolic blood pressure is a continuous value, with a range of anywhere from 0 to somewhere quite high like 250 or perhaps rarely 300, with most people being in a certain range, like from 100 to 140. So why is the species also a continuous variable? Isn’t a rabbit a rabbit, and a frog a frog? Certainly a human is a human, and not a chimpanzee, right?

Well, keep in mind that names are just there for our convenience. How close they approximate reality may vary depending on the purpose of the name, and how good we are at understanding what we are describing. Ideally, a name would completely describe reality, but that will never be the case because a name is just a short hand way of talking about something else. Species tells us about taxonomic ranking. This is meant to help us determine which ancestors all the members of the species have in common, and how closely related those members are to members of another species. The problem arises in that the there is no defined line in the ground where one species ends and the next begins. One definition of species asserts that members of one species can not reproduce to have fertile offspring with members of any other species. This definition isn’t technically correct. The reason that this seems true most of the time, is that the many of the ancestral species happen to have died out, so it creates the appearance of very distinct groups of organisms (each in a separate and walled off little cubby).

Every generation is the same species as its parents and the same species as its own offspring. If this is true how could new species arise? It is precisely because the changes that occur due to evolution do so over much longer periods of time than a mere few generations. An organism could reproduce with a member of the prior generation, and if transported back in time to members from tens or hundreds of generations prior. At some point, however, there will be enough structural and/or behavioral differences that reproduction would no longer be possible.

Say that we took an organism back in time (it could be any organism, even a human). When we took him or her back 50,000 generations we find that he/she was able to reproduce with the contemporary population, but couldn’t reproduce with the individuals from 100,000 generations earlier. Now if we go back 50,000 generations from our starting point and take a subject from that era (one that could easily reproduce with our original organism) and then take him or her back to 100,000 generations before our starting point (50,000 generations before this individuals time) we find that it can reproduce with an individual from that long distant time period. So the original could reproduce with a subject from 50,000 generations ago, but not 100,000 generations ago, and the individual from 50,000 generations ago could reproduce with one from 50,000 generations ahead or behind its own time.

Since in the real world, those ancestors are mostly extinct it give the illusion of a discontinuous landscape of species. Richard Dawkins gave an excellent example in his book, “The Ancestors Tale” when he described ‘the salamander’s tale’. In that example Professor Dawkins described several species of salamander that live along a ring of high elevation in Central California. The ring forms a physical geographical structure that makes the species adjacent to any salamander’s location available to them, but prevents the species from interacting with species on distant parts of the ring. At the southern end of the ring are two distinct appearing species Ensatina eschscholtzil and Ensatina klauberi. E. eschscholtzil is brown and lauberi is spotted, and the two species, while in contact with each other do not interbreed – the very definition of separate species! That’s all well and good except that as you go up north on either side of the ring there are more species still, and each of these can reproduce with the species neighboring it.

It’s likely that the ancestral species arrived at some time in the past in the north. Two descendant populations emerged, one going south by the eastern route and the other going south by the western route. If all those other species on the ring had gone extinct we would be left with two species that could not interbreed and there would be nothing very special about the story. Those other species did not die out, however, and there is a continuous ring of salamanders that can reproduce with others of similar species, except in the case of the two southern species. As Dawkins says in the book, “Strikes a blow against the discontinuous mind”. The situation for these salamanders reveals what the situation would be like for any species (human included) if all of our ancestors were alive today. There would be a continuous stream of organisms that can interbreed with those close to them in time, but only over longer time scales do differences add up that make them distinct enough that interbreeding is no longer possible.  The sides of the ring represent a common ancestor, diverging and over time becoming two separate species, but having a path of “able to interbreed” individuals all the way down.  

In another post, I’ll illustrate another problem with the “tree of life” concept.  In actuality the tree concept is complicated by “lateral gene transfer” – basically genes being swapped by other organisms of different types.  This is very common in bacteria, but also seems to happen to some extent in more sophisticated organisms.  In any case, the idea of species should be used as a useful placeholder, but has important limitations.

Reference:

1. Species, Wikipedia.
2. “The Ancestor’s Tale: A Pilgrimage to the Dawn of Evolution”, Richard Dawkins. 2004.

3. Another clever Mesign by Mother Nature.  Darwin’s Kidneys.  July 8, 2015.

 

Happy Darwin Day 2016

February 12th, 2016 is Charles Darwin’s 207th birthday. Charles also happened to share the exact same date of birth with Abraham Lincoln – so happy birthday Mr. Lincoln, as well! Since this blog is dedicated to science, with a special emphasis on evolution, and in fact, has the name Darwin in the title, I want to be sure to honor our dear Mr. Darwin properly.

There are Darwin Day celebrations planned in the USA and around the world, but no ‘Official Darwin Day’ is recognized nationally. That could change as some efforts are being made to make it official. In fact, this year the Governor of Delaware declared an official Darwin Day in his state. In some cities there are lectures or parties to celebrate.  The Center for Inquiry has a take action page, where you can send your name in a letter  to members of congress to express the importance of creating a Darwin’s Day for public education of science.

Charles Darwin’s theory of evolution was the beginning of modern biological science. As the Russian evolutionary biologist Theodosius Dobzhansky is quoted as saying, “Nothing in biology makes sense except in the light of evolution”. Evolution is the thread that binds all of biology together. Every aspect of biology, from molecular genetics, embryology, comparative anatomy, populations and ecosystems all “make sense in the light of evolution”.

Darwin’s theory was a realization of origin from common decent. Evolution does not address the emergence of life from non-biological origins, but does an excellent job explaining the illusion of design seen in the complex structures of the living world. Of course, Darwin realized that the illusion was the product of natural selection working on variations in living things. Darwin had no idea about genetics, DNA, mutations, and so on, but as those fields of biology developed they only reinforced Darwin’s big idea. It could easily have been otherwise. If evolution by natural selection was not how the world worked, then molecular genetics, phylogenetic, developmental biology, and so on would not have provided additional support to a 150 year old theory. Yet, all these modern sciences fit in perfectly, continuing to build on the original theory. Even without the fossil record modern biology would still point the way to evolution. By the way, the fossil record also supports evolution, and has only become more robust during the last 150 years as many more fossil species have now been discovered.

I’m sure Darwin would have been delighted to learn about genes, how new mutations arise by damage due to radiation, chemical mutagens, or simply errors in the normal process of DNA synthesis. He would have loved to see how the genome is cluttered with the remains of dead viruses, pseudogenes, copying errors that we have been copying and passing down to our children for geological eons. And he would have certainly understood that we can see our degree of relatedness to any living species on the planet by looking at, not just the working genes and how closely they match to us, but also these dead viruses and pseudogenes.

Darwin’s voyage on the H.M.S Beagle remains one of the most exciting and most epic expeditions of discovery in history – certainly one of the most productive, since it resulted in much of the data Darwin needed to formulate his theory over the next several decades. Darwin was an amazing naturalist and keen observer. There is hardly any area of natural science of his time that he didn’t seem to make some meaningful contributions. Not just in biology but in geology, as well.

So this Darwin’s day I plan to celebrate at home with my family. Perhaps have a piece of Common Decent Cake or Evolution Pie, learn something new I didn’t know about evolution, and honor our Dear Mr. Darwin.  Let me know how you plan to celebrate.

Other Reading:

1. Darwin Day:  Wikipedia
2. Natural Selection:  Wikipedia
3. Youtube.  Climbing Mount Improbable.  Lecture by Richard Dawkins.
4. OxoG is how radiation turns your own water against you.  Darwin’s Kidneys blog
5. Cytosine Deamination.  Darwin’s Kidneys blog.  (another mechanism of mutation).
6. Another Clever Mesign by Mother Nature.  Darwin’s Kidneys blog.  New word mesign to differentiate apparent design in nature from when we mean a designed object.
7. How our ancestors promiscuous genes became more discriminating.  ZME Science. Feb. 9, 2016.  Article on how gene families arise by gene duplications.

Diseases with an upside!

Diseases with an upside.

By Rich Feldenberg

Since life’s earliest emergence on planet earth, disease has been our constant and unwelcome companion.  Even the first single celled organisms were susceptible to break down, nutritional deficiencies, and harmful genetic mutation.  When single celled life upgraded to the multicellular stage, finally becoming large, it was then susceptible to a host of new disorders, such as cancer that interfered with the organization and growth of cells that now had to survive as part of a collective.  Humankind is no different than the rest of the animal kingdom in this regard, and throughout human existence disease has lead to untold suffering, death, and at times the threat of total extinction.  It may therefore be surprising to learn that some diseases confer protection against other types of illness, and this seems to account for the high prevalence of some of these disorders in the human population.  If the protective benefit of the disease mutation on a large portion of the population outweighs the suffering and death of a small portion of the population, natural selection will swing the balance in favor of keeping those mutations in the gene pool.  Not only may the disease mutation simply persist in the gene pool, but it may become very prevalent because it is selected for in the right environment, where the other illness it protects against is a major threat.   To illustrate how this works I’ll give some detail on two well known examples of diseases and their upside – in other words, how they protect against other threats to our species.

The first example is that Sickle Cell Anemia (SCA), which has the best documented evidence as to its evolutionary risk versus benefit ratio in its effected population.  Sickle Cell Anemia is a genetic disease that causes anemia (low red blood cell counts), and can lead to painful, and potentially deadly pain crises.  It is inherited as an autosomal recessive trait – meaning that if you receive one copy of the mutated gene from each of your parents, then you have two abnormal copies of the gene (are homozygous, in the language of genetics) and will have the disease.  Each of your parents, however, has only one mutant copy and also one normal copy (is heterozygous), and so is only a carrier (has sickle cell trait) and will not show symptoms of the disease under normal circumstances.

SCA is due to a single base switch in the DNA that codes for the beta-chain of the hemoglobin molecule.  Adult hemoglobin is made of two alpha chains and two beta chains.  This is the major oxygen carrying protein in the blood, although, there are other versions of hemoglobin that are produced (one example is fetal hemoglobin with two alpha chains and two gamma chains).    In SCA, there is a substitution of the amino acid glutamic acid for valine at the 6th amino acid in the beta chain.  Since valine is more hydrophobic than glutamic acid this has the unfortunate consequence of causing the hemoglobin molecules to polymerized and compact together, deforming the shape of the red blood cells (RBCs) that carry them, into a sickle shape – hence the name Sickle Cell Anemia.  The polymerization event is more likely to happen if the affected individual is dehydrated, in a low oxygen state (hypoxic), or otherwise ill with another illness.  The deformed red blood cells can not get through the tiny capillaries very well, causing blockages that deprive tissues of blood and oxygen.   The result is pain and organ damage.

Over time, people with SCA damage their spleen so badly that they lose the its important immune function, which normally you against encapsulated bacterial infections.  These are certain bacteria that are surrounded by a polysaccaride capsule, that helps them to escape detection by the immune system.  Someone without a functioning spleen can then die of these types of infections, whereas those with normal spleens would be able to fight off the infection easily.  The blockages to blood flow due the abnormal sickle shaped RBCs can lead to strokes and to Acute Chest Syndrome.  If people with SCA become infected with the common virus Parvovirus B19, they can develop severe life threatening anemia, with hemoglobin levels that get so low they can develop heart failure.

Sickle cell anemia is common in sub-Saharan Africa, and about 300,000 are born with disease each year.  All the complications of SCA listed above can be fatal so why would this disorder have such a high prevalence?  The answer seems to be that although people with full blown Sickle Cell Anemia are at a most definite disadvantage from a survival aspect, those who are carriers of SCA are protected against another common killer – Malaria.  Malaria is an infectious disease caused by the protozoan Plasmodium.  It has a complex life cycle, part of which is spent inside the mosquito Anopheles, and part is spent inside a vertebrate host – such as a human.  When an infected female mosquito bites a human, the organism is transmitted into the persons blood stream where it travels to the liver, infects liver cells, reproduces, and then is released back to the bloodstream where it infects RBCs.  The symptoms of Malaria include fever, vomiting, joint and muscle pain, headache, and in some cases seizures.  As the Plasmodium organism goes through its life-cycle within the host, from liver to RBC and back again (these are known as the liver phase and the erythrocytic phase respectively), the symptoms return in a cyclical fashion.  In some cases the organism passes through the blood-brain barrier leading to Cerebral Malaria, which is a very serious complication.  Malaria has a high mortality rate if untreated – as would have been the case before the age of modern medicine.

It was observed, early on, that in regions endemic to malaria, people who were carriers of the sickle cell mutation showed resistance to the malaria infection, and that full blown SCA has a high prevalence in those same regions where malaria is endemic.  Further studies confirmed that those individuals who are carries for the sickle cell mutation, do in fact, enjoy a protection due to their gene mutation.  Unfortunately, those with actual sickle cell anemia (homozygous for the gene mutation) are not protected against malaria.  Not only do they have to suffer the fate of SCA, but if they get malaria they have a worse prognosis because the malaria damages their already vulnerable RBCs.

For a long time it was thought that sickle cell trait most likely confers its malarial protection by making it difficult for Plasmodium organisms to infect the abnormally shaped RBCs, and that the abnormal RBCs are removed more readily by circulating macrophages, helping to rid Plasmodium infected cells more readily.  More recent research seems to suggest that the protective mechanism is more complex that that, and involves the up regulation of an enzyme called heme oxygenase-1(HO-1).    HO-1 causes the breakdown of heme, and the release of carbon monoxide (CO), iron, and biliverdin, resulting in an anti-inflammatory effect.  HO-1 is upregulated or produced to a greater extent in RBCs that have the abnormal hemoglobin associated with SCA, and it is the production of CO that seems to have a detrimental effect for the Plasmodium organisms.  It confers protection against cerebral malaria, and decreased mortality for those with sickle cell trait who become infected with malaria.  This might also be the answer to why several other diseases or disease traits have also been observed to offer protection against malaria, such as thalassemia trait and Glucose-6-Phosphate Deficiency.  These disorders might also increase the activity of HO-1.

We’ll move now to another deadly disease that seems to have remained in the population because it offered a survival advantage.  This is the kidney disease called Focal Segmental Glomulosclerosis (a real mouthful) or just plain old FSGS for short.  FSGS can be caused by chronic infections, such as hepatitis or HIV, but many cases are due to a genetic mutation.  It is a subset of the genetic form that may have been selected for to protect against Sleeping Sickness.  In FSGS the tiny filters in the kidneys, called glomeruli, become scarred until they can no longer filter.  This can eventually progress to kidney failure and the need for dialysis or kidney transplant.  Kidney failure is fatal without modern medical care and FSGS is one of the more common causes for young people to be on dialysis.  Its also, often more common and resistant to therapy in African Americans and other people of African descent.

Some people with the genetic form of FSGS have a mutation in a gene called APOL1, and if you are an individual with two mutated copies of the APOL1 gene, your risk of developing FSGS and kidney failure is 17 times higher than if you have two normal copies of the gene.  That adds up to around a 4% chance of developing FSGS over your lifetime if you are homozygous for mutant APOL1.  This mutation is also thought to explain 18% of all cases of FSGS that currently exist.  There are two types of mutations in the APOL1 gene that can increase risk for FSGS kidney disease.  These is the G1 variant, which contains two amino acid substitutions – one is a replacement of glycine for serine at amino acid 342 in the protein (S342G), and the other switch is a replacement of methionine for isoleucine at amino acid 384 in the protein (I384M).  You have to have both of these switches you have the G1 variant.  The other variant is the G2 variant where 6 base pairs are deleted in the DNA coding for APOL1 starting at base 388.  People can have either a G1 variant or a G2 variant, but never have both types.

APOL1 is a protein that circulates in the blood and is part of the high-density lipoprotein (HDL – otherwise known as the “good” cholesterol).  Exactly how the mutated form of APOL1 causes kidney disease is still not known.  What is known, however, is that those individuals with either a G1 or G2 specific gene mutation in APOL1 have protection against African Sleeping Sickness, caused by the protozoan Trypanosoma brucei.  This tiny single celled eukaryotic organism is transmitted to its human host by the bite of the tsetse fly.  It is a common and dangerous disease in sub-Saharan Africa.  In 1990 it caused 34,000 deaths, but the death rate dropped to 9000 in 2010, thanks to efforts of the World Health Organization to prevent and treat the infection.

Those affected by the parasite experience two distinct stages of infection.  In the first stage the victim develops headaches, fever, and severe itching.  This resolves only to eventually progress to the second stage of the disease which effects the central nervous system causing confusion, paralysis, neuromuscular weakness, and sometimes psychiatric illness.  There is a reversal of the sleep-wake cycle, giving the disorder its common name.  Infected persons often sleep in the day and remain awake at night.  Without treatment the disease always ends in the death of its victim.   It can be treated with the drug pentamidine, when in the first stage, or drugs such as eflornithine or melarsoprol for second stage disease.

Like the association of Sickle Cell Anemia and malaria, those geographic regions with a high incidence of sleeping sickness also have a high incidence in the population of APOL1 G1 or G2 variants.  This is because those gene variants protect against the ravages of the Trypanosomes.  The APOL1 variants cause the lysis (breaking apart of the cell membrane) of Trypanosomes that cause sleeping sickness.  The normal gene for APOL1 gives us resistance to other species of Trypanosomes that do infect other mammals, but are unable to harm us.  The sleeping sickness Trypanosome (Trypanosome brucei rhodesiense) is immune to the normal APOL1 since it has evolved a serum resistance-associated protein (SRA) that blocks a portion of the APOL1 protein, neutralizing its anti-trypanosomal action.  Not so for the APOL1 variants G1 or G2, however.  They are able to get around this SRA and destroy the parasite.  From an evolutionary point of view, the advantage of being more resistant to sleeping sickness in an area of high risk, outweighs the cost of having a higher than average chance of kidney disease.  There is no advantage, however, to having these variants if your ancestors originated where sleeping sickness is not a problem, so other populations aren’t found to have these gene mutations.

The two examples of Sickle Cell anemia and Focal Segmental Glomerulosclerosis (APOL1 mutation) are not the only situations where a disease mutation protect us against another illness.   I’ll just briefly mention two more.  Tay-Sachs disease, which is a lethal neurodegenerative disorder in the homozygous state, seems to protect against Tuberculosis in carriers (heterozygotes).   Also Cystic Fibrosis (CF) which usually leads to severe and chronic lung disease in the homozygous state, may have protected against the effects of cholera in the heterozygous carriers.  The CF mutation inactivates a chloride channel called CFTR, in the cell membrane.  Being a carrier for this mutation may have prevented the lethal dysentery that would have accompanied infectious cholera, by preventing water loss in the intestines due to poorly working chloride channels.  It is a very common gene mutation, with 1 in 25 people of European descent being a carrier for the CF gene mutation.

When we think disease we think of the suffering of its victims and the cost to society.  We are often unaware of the balance of the many forces involved, which influence why a particular disease may be so common in a given population.  The factors involved are typically much more complex than we appreciate, and most of them are still unknown to us.  Natural selection is working behind the scenes in ways that are difficult to detect on just a casual examination.  It may be of no consolation to the sufferers of a serious disease, or the family members devastated by a loved ones sickness and loss, but natural selection, with its cold blind eye to pain or suffering, seems to have fixed some of this in place to allow more genes to be passed onto future generations.  Evolution is not directed toward any particular goal and has no empathy or sense of compassion.  It only selects those traits that happen to give the organism the best chance to pass on its genes in its evolved environment.  This is where the human mind comes into play.  Now that we are finally learning to understand the root causes of disease at the genetic and molecular level, we can work to treat, cure, and eradicate disease.  Although we are not there yet, in theory it should be possible to cure a condition like sickle cell anemia with gene therapy.  At the same time, we shouldn’t have to worry about worsening the burden of malaria if SCA were eliminated, since we can also work on better therapies to treat the malaria, and more effective strategies to prevent infection with Plasmodium.

References and other reading:

 

1. “Mystery solved: How sickle hemoglobin protects against malaria”, ScienceDaily; April 29, 2011

http://www.sciencedaily.com/releases/2011/04/110428123931.htm

2. “Sickle Cell Anaemia and Malaria”, Lucio Luzzatoo, Mediterranean Journal of Hematology and Infectious Disease; Oct. 3, 2012.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3499995/

3. Sickle Cell disease;  Wikipedia.

https://en.wikipedia.org/wiki/Sickle-cell_disease

4. Malaria;  Wikipedia.

https://en.wikipedia.org/wiki/Malaria

5. Heme Oxygenase-1;  Wikipedia.

https://en.wikipedia.org/wiki/HMOX1

6. “APOL1 Genetic Variants in Focal Segmental Glomerulosclerosis and HIV-Associated Nephropathy”,  Jeffrey B. Kopp, et al., Journal of the American Society of Nephrology;  Nov. 2011.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3231787/

7. “Association of Trypanolytic ApoL1 Variants with Kidney Disease in African-Americans”,  Giulio Genovese, et al., Science, August 13, 2010.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2980843/

8. “A co-evolutionary arms race: trypanosomes shaping the human genome, humans shaping the trypanosome genome”, Paul Capewell, et al., Parasitology, June 26, 2014.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4413828/

9. “A risk allele for focal segmental glomerulosclerosis in African Americans is located within a region containing APOL1 and MYH9”, Giulio Genovese, et al., Kidney International, Oct. 2010.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3001190/

10. African Trypanosomiasis;  Wikipedia.

https://en.wikipedia.org/wiki/African_trypanosomiasis

Another Clever Mesign Brought To You By Mother Nature

Another Clever Mesign Brought To You By Mother Nature

By Rich Feldenberg

 

 

In the paragraphs that follow I’m going to introduce a new term, that I am calling mesign, but first let me remind you of how the world around us appears so well designed.  Almost perfectly designed, if we’re not looking too closely.  We observe the beautiful, intricate, complexity of nature everyday.  How can anyone go about their day and not be amazed by the well oiled machinery of nature, such as flowers blooming in the yard, full of nectar for busy bees.  Bees pollinating the flowers on their travels, using their compound eyes to see in ultraviolet light, markings on the pedals that are invisible to us, that guide them to where they need to go to find the nectar and pollen.   

Based on how perfectly each kind of animal and plant seems to fit into all their respective niches, it would be natural for us to assume that the world and all its living things were designed.  It would, that is, if we lived in a pre-scientific culture, but we live in a culture where we’ve fought hard to acquire a well earned understanding of the universe.  A world, where in the last 400 years, at least, the methodology of science has progressively shown us how the physical and biological phenomena that seemed so mysterious to our ancestors can be understood by human minds.  We know today that evolution works at the level of genes to shape organisms that survive and reproduce the best in their environment.  Over the billions of years that life has existed on the earth, complex biological structures have evolved such as eyes to see clearly, kidneys to maintain our internal environment in optimal chemical balance, hearts to pump blood to distant tissues, wings to soar into the sky, gills to extract oxygen from the water, and so on.  Before Darwin it was natural for people to think that all these structures, and their intricate parts, were designed to achieve their apparent purpose.  No one would deny that these things have the appearance of design.  That doesn’t mean that they were purposefully designed, however.  Evolutionary biology has revealed how complex structures, that perform complex operations, arise through the process of natural selection.  

Creationist often claim that certain biological structures are irreducibly complex, and therefore could not have evolved from any lesser evolved structure.  The eye for instance, is commonly sited by creationists as an example of a structure so perfectly made for the job it performs that it had to have been created by a divine designer.  Remarkably, it has been shown how the vertebrate eye could have very plausibly evolved in a series of small steps from more primitive kinds of eyes.  

To create a camera-type eye, like that evolved in vertebrates, you start with a simple patch of skin with light sensitive cells.  This simplest kind of eye can tell light from dark – day from night.  The next step is the formation of a slight depression at the skin surface which will then provide some ability to tell from which direction the light is coming due to shadowing in the depression.  This would seem to have obvious advantages over the creature with a simple flat eye spot.  As the depression deepened you would continue to improve the ability to discern direction.  At some point you would begin to form a pin-hole like camera eye where an image could actually be formed.  A thin transparent tissue over the pin hole might help protect the light sensitive cells inside and would act as a kind of lens as light passed through this tissue.  The shape of this lens tissue could be selected that allows for higher quality lens ability and would also allow the pin hole (now a pupil) to open wider and allow in more light and therefore a clearer image.  

 

stages of evolution for the vertebrate eye

Each step in the series outlined above, can be found in different animals in nature today, and, as Richard Dawkins, the famous evolutionary biologist has pointed out, “What use is half an eye?  Well, it is 1% better than 49% of an eye.  And 1% of an eye is better than no eye at all”.   Those creature with simple sorts of eyes, like flat worms with tiny eye spots, still use their eyes to their advantage, even though we would consider ourselves essentially blind if you suddenly saw in flat worm vision!

It is still useful for scientists to discuss the structure-function relationships of evolved features in a language that may superficially sound like a discussion of purposeful design, when in fact, they mean nothing of the sort.  For example, it is just plain simpler to use common language such as, “The eye is beautifully designed to allow light to enter through the pupil, and using the lens, focus an image precisely on the retina”.  However, for the biologist, the meaning of this sentence is, “The eye is a beautiful structure, that has evolved through natural selection in a way that allows light to enter the pupil where the lens can then focus it precisely on the retina”.  By using the word design, which is easier and more natural to use in common speech, it can give the false impression that the speaker might really mean she thinks the eye was designed by an intelligent designer when this was not her intent at all.

   

We need a new word for the illusion of design in nature.  Well, relax because that word is here – Mesign.  Mesign would be used to distinguish that the intended meaning was for the illusion of design created by a natural process, such as evolution in the case of living things.  To use our previous example, we could simply say, “The eye is beautifully mesigned to allow light to enter through the pupil, and using the lens, focus an image precisely on the retina”.  There is no misinterpreting the intended meaning of this statement.  

Mesign obviously has its root in the word design, but has been modified to look a little like the word Meme, which Richard Dawkins coined to mean an idea that spreads through a population by use of language and culture, and may even be subject to a process of natural selection, which will determine its prevalence and permanence in a particular society.  I don’t know if mesign will be a successful meme or not, but I feel it could be potentially useful.

Mesign also implies that the design process of a particular feature, being accidental through the process of natural selection, is inevitably going to contain design flaws.  Why wouldn’t it, if it was simply an evolved structure with no grand engineer making any attempt to get the design just right, or performing test and experiments on working models of the design before sending it out for prime time in the real world.  Evolution doesn’t even have any kind of a goal that it is working toward.  Only in retrospect does it seem that the purpose of the evolutionary process was to get to this particular structure, organ, or organism.  To go back to our eye example, there was no intent to go from creatures in the precambrian with light sensitive eye spots to vertebrate eyes with lens, corneas, retinas, optic nerves, and so on.  Our little precambrian worm ancestors were simply in a struggle for survival due to limited resources and the rise of predatory species.  Those creatures with eye spots able to tell day from night, and up from down,  would have had some survival advantage.  Those little guys that may have acquired a gene mutation that caused a depression at the eye spot location during their development may have been favored to survive and pass on their “mutant” genes since they would have some sense of direction due to shadowing in the eye spot depression, potentially allowing them to see a shadow of a predator approaching.  The mutation was random, but the spread of the mutation in the population is not since a favorable mutation, like the one discussed above would be selected for by natural selection.

 

Many of the features of living things, while amazing, seem poorly designed when inspected more thoroughly.  Instead of intelligent design, it seems clear this is stupid mesign.  The common passage way of the oral pharynx leading to both the esophagus and the trachea makes every meal a choking hazard.  The fetal decent of the testis from the peritoneal cavity into the scrotum leads to a weak spot in the abdominal wall, making herniation and potential death by intestinal obstruction an unnecessary threat.  And, due to our, in evolutionary terms, recent adoption of bipedalism, childbirth is an extremely deadly activity for both mom and child.  Prior to modern obstetrical care, the mortality rate for infant and mother was extremely high.   The human body would be recalled, and the designer sued if this was an engineered machine.  

When it comes to the appearance of design in the physical world, mesign could be a useful term, as well.  Consider the “fine tuning” problem in physics.  We find that the physical constants have values, such that they allow protons and electrons form hydrogen atoms, clouds of hydrogen gas to condense into stars, which then fuse into heavier elements like carbon, planets made of heavy elements form and allow for the development of life, at least here on earth.  The universe has an appearance of design, and while it is not as clear why this is the case, as opposed to the illusion of design in the living world brought about by evolution, it is still a scientific question that is being actively researched. Science continues to inch its way slowly into the unknown, and at this point, there is no reason to assume that deeper physical laws can not be found that might explain this apparent design of the cosmos.  If certain physical properties of our universe, such as cosmic inflation are found to be true, then these same theories also demand the existence of a multiverse as part of their mathematical structure.  The multiverse, while possibly not observable on its own, could be a reasonable explanation for the physical parameters in our universe.  This is basically because universes with every combination of physical parameters also exist, we just find ourselves in one that has the parameters suitable to our kind of existence because that is the only kind of universe we could find ourselves in.  

Map of the early universe showing temperature variations

To explain a physical property in the language of mesign would be to allow the reader to be clear that the author is referring to a naturalistic process, without any notion of a supernatural plan implied.  An example might be, “Stars are well mesigned to turn hydrogen into helium by nuclear fusion in their cores”.  They happen to do that very nicely, thank you, based on their physical properties of size, mass, composition, strength of gravity and the strong and weak nuclear forces, and so on, but there is no reason to suspect that they were engineered for this purpose.  In fact, most stars, such as the abundant but dim Red Dwarfs, are not efficient at synthesizing the heavy elements necessary for life.  Due to their low mass they will never explode in a supernova to produce the remainder of the periodic table.  A better design might be to have a process that guarantees every star to produce the building blocks of life.  That might be a universe where life was really thriving in every possible corner.  If someone’s intention were to suggest that the stars were designed by a designer, then design would be the proper wording in that case, and there would be no mistake about it.  

It seems better to take some of the ambiguity out of the equation when discussing question of evolution and other natural processes.  Confusion as to an author’s intended meaning, or at times, purposeful misuse of a quote to take it out of proper context might be avoided by using the word mesign when it is called for.  

References and a cool video to watch:

1.  Youtube video of Richard Dawkins demonstrating the evolution of the eye.  

https://www.youtube.com/watch?v=Nwew5gHoh3E

2.  “Evolution of the Eye”,  Trevor D. Lamb;  Scientific American collector’s edition,  July  2015.

3. Wikipedia entry on Meme:   https://en.wikipedia.org/wiki/Meme