Tag Archives: inheritance

Stephen King’s Carrie and the problem of genetics in an horror story

carrieIn the novel, Carrie, Stephen king attempts to explain telekinetic ability in terms of a real genetically inherited trait. OK, this is fiction, I have no problem with Carrie’s telekinetic ability … where would this story be without it after all?
Explaining this ability in terms of science was a mistake for two reasons. For one thing, it undermines the very idea of ‘supernatural’ that the reader has already bought into. This was exactly the problem that fans of Star Wars had with the prequel trilogy’s explanation of ‘The Force’ in terms of sub-cellular microorganisms. The second reason he shouldn’t have done this is because he didn’t understand it well himself.

Carrie White – The protagonist, who possesses telekinetic (TK) ability
Margaret Brigham – Carrie’s mother
Ralph White – Carrie’s father

From Stephen King’s Carrie (please don’t sue me Mr. King)

It is now generally agreed that the TK phenomenon is a genetic-
recessive occurrence-but the opposite of a disease like hemophilia,
which becomes overt only in males. In that disease, once called “King’s
Evil,” the gene is recessive in the female and is carried harmlessly.
Male offspring, however, are “bleeders.” This disease is generated only
if an afflicted male marries a woman carrying the recessive gene. If the
offspring of such union is male, the result will be a hemophiliac son. If
the offspring is female, the result will he a daughter who is a carrier. It
should be emphasized that the hemophilia gene may be carried
recessively in the male as a part of his genetic make-up. But if he
marries a woman with the same outlaw gene, the result will be
hemophilia if the offspring is male.

In the case of royal families, where intermarriage was common, the
chance of the gene reproducing once it entered the family tree were
high-thus the name King’s Evil. Hemophilia also showed up in
significant quantities in Appalachia during the earlier part of this
century, and is commonly noticed in those cultures where incest and
the marriage of first cousins is common.

With the TK phenomenon, the male appears to be the carrier; the
TK gene may be recessive in the female, but dominates only in the
female. It appears that Ralph White carried the gene. Margaret
Brigham, by purest chance, also carried the outlaw gene sign, but we
may be fairly confident that it was recessive, as no information has ever
been found to indicate that she had telekinetic powers resembling her
daughter’s. Investigations are now being conducted into the life of
Margaret Brigham’s grandmother, Sadie Cochran-for, if the dominant/recessive
pattern obtains with TK as it does with hemophilia,
Mrs. Cochran may have been TK dominant.

If the issue of the White marriage had been male, the result would
have been another carrier. Chances that the mutation would have died
with him would have been excellent, as neither side of the Ralph
White-Margaret Brigham alliance had cousins of a comparable age for
the theoretical male ottspring to marry. And the chances of meeting and
marrying another woman with the TK gene at random would be small.
None of the teams working on the problem have yet isolated the gene.

Surely no one can doubt, in light of the Maine holocaust, that
isolating this gene must become one of medicine’s number-one
priorities. The hemophiliac, or H gene, produces male issue with a lack
of blood platelets. The telekinetic, or TK gene, produces female
Typhoid Marys capable of destroying almost at will….


Stephen King’s explanation of the genetics of hemophilia is not quite right.

1. How is hemophilia actually inherited? Explain in terms of dominant / recessive inheritance.
2. King suggests that hemophilia is inherited from two carrier parents. Is this correct? Describe, in genetic terms, how a boy can be born with disease.
3. Is it possible for a female child to inherit the disease?


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Posted by on July 20, 2015 in Uncategorized


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Immunology’s ‘dihybrid cross’ : Antibody response to different antigens

The progress of infection can be summarized as a pathogen going through a series of steps:


Progress of Infection

The first three steps, ‘Portal of Entry’, through ‘Surviving Host Defences’ encapsulates all of the immune response. Some key events in the immunity are inflammation and the innate  response, antigen processing and presentation, adaptive immunity and memory.

Several of these topics I’ve described here before including an outline of the development of lymphocytes (B and T Cells – sorry NK Cells) in an article here. The activation of B cells here, immunological memory in several places including here.  Some of these topics I have yet to address (e.g. a good discussion of inflammation), and others (e.g. antigen processing and presentation) have been buried in other posts (see my lymphocyte development, B cell Activation or this post on Transmissible tumors). 

This time, I thought I’d prevent a sketch of the humoral immune response and how this illustrates, like Mendel’s traits in a dihybrid cross, that each immune reaction is ‘independent’. A typical immune response is outlined below showing the development of antibodies following a primary response and then a more rapid and robust secondary response. If we want to compare this response to Mendel’s monohybrid cross, we can see the same response for antigen after antigen just as Mendel saw the same pattern of inheritance for any single trait he observed.


Response to a single antigen


Before we had the ability to ‘see’ this response on a molecular level, we could see its effects on people. Those who previously contracted a disease did not contract that same disease a second time. This immunological memory is the basis for vaccination, where we separate the disease-causing agent from the immunological memory-inducing agent for any given pathogen and then use only the later to vaccinate.

However, Mendel continued to examine traits and how they were inherited individually (i.e. the inheritance of one trait had no bearing on the inheritance of another). He called this independent assortment. Is there a similar experiment that can be done to show ‘independent immunity’?


Response to two antigens independently

Borrowing a figure from Abul Abbas’ text on Cellular and Molecular Immunology, we see  that the response to one antigen has no bearing on the body’s response to a second, unique antigen. Like Mendel’s dihybrid crosses, the response to two antigens is, indeed, independent. (Note, the serum titer in this graph falls much lower than that in the first illustration – this second curve is more representative for real responses. Regardless, the antibody titer for a secondary response remains higher than that of the primary response.)

The primary response to antigen B is identical to the primary response to antigen A. The secondary response to antigen A results in a more rapid, robust response and eventually levels out to a higher steady-state of serum antibody.

To extend the analogy just a bit further, one might ask if there is such a thing in immunology that parallels the ‘linked genes’ of inheritance?

In fact, there is. The world’s first vaccine, developed by Edward Jenner in 1796, involved the use of cowpox pus to induce protective immunity to both cowpox and the related virus, smallpox. This seems to violate our rule of independent immunity, just as the Morgan lab found that genes for body color and wing formation were found to be inherited together in fruit flies, thus violating the Law of Independent Assortment (of alleles).

In the case of cowpox and smallpox, this comes from the similarity in antigens made by each of these viruses. That is, the cowpox antigens the body generates an immune response against are NOT (ENTIRELY) UNIQUE from antigens found in smallpox. When the vaccinated individual is challenged with smallpox, antibodies created to defend against a secondary challenge with cowpox react to the smallpox antigens as if this was a secondary response directed against smallpox.


Primary reaction to Cowpox antigen (A) is used for vaccination. Secondary reaction to Smallpox antigen (A’) upon challenge.

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Posted by on November 25, 2013 in Uncategorized


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Reflecting on Inheritance

Last semester I posted an essay introducing inheritance, the idea of factors/alleles, how alleles are distributed into sex cells that combine with other sex cells to bring about a new generation. Looking back on this post, I think it would be a good idea to point to it from here and suggest that all my General Biology students read through it to ensure that they understand the basics of inheritance before we go on.


Wormhole to an old post

You can go directly to that post here or drop through the wormhole on the right.

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Posted by on March 27, 2013 in Uncategorized


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Who said what about the molecular basis of inheritance? First steps towards the double helix

A workable Theory

Gregor Mendel did the first documented, accurate analysis of how one generation inherits traits from their parents’. However, being so far ahead of his time, and possibly because he may have been considered an outsider to the scientific community, the value of his work was not grasped and it was quickly forgotten. Mendel had stated a couple of theories in his paper making theoretical assumptions of how ‘factors’ responsible for inheritance are segregated during the formation of gametes and then rejoined in the zygote. Together, the two factors that every individual had for each trait determined the expression of that trait.

Colorful Bodies


From Zellsubstanz, Kern und Zelltheilung, 1882

A couple decades later Walther Flemming observed, under his microscope, some curious movements of things called ‘chromosomes’ (or colorful bodies). Unfortunately, he did so without knowledge of Mendel’s work and thus didn’t recognize the greater meaning of his discovery. At this time Germ Plasm Theory (not to be confused with Germ Theory) was being debated as a means of inheritance. This theory suggested that special germ cells carried the hereditary material from one generation to the next and that these cells were uninfluenced by the other cells of the body. The plasm itself took the place of Mendel’s idea of factors, but functioned as a more inclusive measure of material, more akin to what we call the genome today. I say ‘plasm’ is replacing ‘factors’, but it should be noted that no one intentionally renamed Mendel’s factors. The real problem was that no one knew about his work at all.

Edouard Van Beneden had been investigating similar chromosomal movements during meiosis that produced the gametes, or germ cells. However, he too was having a difficult time constructing a cogent theory concerning how these movements led to inheritance.


August Weismann

August Weismann was in the best position at the time to put the pieces together as he was already turning the available information over in his mind to construct a big picture. He recognized that the nucleus was the likely source of the ‘plasm’ and even considered the chromosomes as a possible candidate for this material. Further, he was concerned with how it was that germ cells could join in a way that did not double the heritable material with every generation.

Connecting the Dots

It was not until Sutton and Boveri  independently unearthed Mendel’s work and recognized the similarity of chromosome movement during gametogenesis (making sperm and egg cells) to his descriptions of ‘factors’ that The Chromosomal Theory of Inheritance was first seriously proposed.

Altogether, these observations led many to believe that it was, indeed, the chromosomes that carried the genetic material. Still, this did not pinpoint what molecule was responsible or how it accomplished this for chromosomes are comprised of long strings of DNA and a number of proteins. Given the simplicity of DNA, many refuted this as potential genetic material as it simply could not carry the required information. Perhaps it served as a scaffold for the more important protein molecules? This was consistent with the chromosomal theory and had the benefit of allowing for complicated proteins to bear the information required to build new cells and organisms.


Griffith with his pal Bobby

Fredrick Griffith was one of the earliest workers to begin the march to identify the specific molecules that functioned as heritable material. While working to develop a vaccine against Streptococcus pneumoniae, he discovered their curious capacity for communicating information laterally, from one organism to another.

Griffith’s Experiments: Glimpsing the Answer

Two forms of the bacteria were known: One a virulent smooth form that secreted a protective carbohydrate capsule, and Secondly, a rough strain that lacks this protective coating and is non-virulent. Predictably, mice he infected with the smooth strain died as a result of bacterial overgrowth. Mice infected with the rough strain overcame the infection and lived. Also, as one would predict, heat-killed bacteria of both strains had no ill effect on mice. But what Griffith did next was much more interesting…

He took heat killed smooth bacteria and combined it with the non-virulent rough form and found that the resulting cocktail of bacteria not only killed mice, but these mice were also found to be overgrown with the smooth form of the bacteria.

What are the possible explanations?

  1. The S strain can come back to life in the presence of R strain bacteria.
  2. Some information was taken up by the live R strain bacteria that allowed it to take on a trait from the dead S strain bacteria.

Griffith chose the simpler second option and suggested that some transforming factor was responsible. This factor was released by the dead S strain and carried heritable information.

Unfortunately, Griffith wasn’t around long enough to see the story play out as he perished during the German air raids of London during WWII. But one last experiment done by another group illustrated that he was one the right path. This experiment repeated Griffith’s work carefully, but instead of combining S strain and R strain bacteria, the S strain bacteria were spun down into a pellet using a centrifuge and only the liquid supernatant was moved in with the R strain bacteria. As Griffith might have suggested, this liquid carried his transforming factor and was sufficient to cause a change in the R strain to make it produce and secrete the carbohydrate capsule.

This last experiment and some others were done by the laboratory of Avery, MacLeod and McCarty at the Rockefeller Institute in New York and will have to be discussed in a future post.

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Posted by on November 24, 2012 in Uncategorized


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A blood typing mystery

A positive blood typing example, thanks to for the figure

A commenter raised the following as an example of a highly unusual blood type pattern within a family.


Parent #1 (female) Blood type O- (i/i,Rh-/Rh-)

Parent #2 (male) Blood type AB+ (IA/IB, Rh+/?)

Child #1 O- (i/i,Rh-/Rh-)

Child #2 Blood type AB+ (IA/IB, Rh+/?)

Is this possible?

Indeed, this is a highly questionable situation. Given that the genetics of ABO typing are fairly well described, the situation described raises a lot of flags. Assuming what is presented is an honest case, it would be extraordinarily interesting to investigate.

If I were asked to solve this, I would probably pursue the following ideas…

Before doing anything else, I would have everyone in the family re-typed. Since questions have been raised, I would insist that they were all re-typed at least three times at three facilities (or at least using different lots of the test reagents). I would also question the original typing location about the reagents used in the initial test and pursue whether any additional questionable typings were reported. Additionally, records should indicate the lots used for the original typing. I would question the company that produced these reagents about Quality Assurance and any known problems with these lots.

The commenter also indicated that he knew of several couples with this situation (which would be extraordinary). Again, this is unlikely, so the local testing facility  and its quality remain likely sources of error.

Luckily, an explanation for the Rh types of both child is possible. Assuming the father is Rh+/Rh-, and the mother is Rh-/Rh-, children could easily have either type. This is a relief, because the Rhesus gene has a large number of alleles making it more complex genetically.

Regarding ABO types, the simplest explanation for Child #1 is that it is not the father’s child. This leaves the ABO type of child#2 in question. Assuming the retyping tests suggested above come back completely supporting the original characterization, I would like to see the birth records for the child to verify that it was not adopted or even somehow ‘switched at birth’. The best verification would be an RFLP analysis of both parents and the child. This is the ‘DNA Fingerprinting’ that is talked about in the courtroom.

Probably the most interesting explanation is that the mother is a chimera. This rare condition arises when an individual starts out life as two non-identical twins that fuse early in development to become a single person. Confirming this would require a battery of RFLP tests from different locations of the body.

To be honest, I suspect this example to be apocryphal. But it provides a great example for describing how science is done. It is always important to remember that the tests we are talking about are just tools and subject to all the weaknesses of any other human pursuit. If we found fingerprints at a crime scene, we could feel quite confident that the owner of those prints was present at some time, but we don’t know with certainty that that person is actually guilty. Thank you very much for providing the topic!

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Posted by on November 19, 2012 in Uncategorized


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Blood Type Genetics and Associated Issues continued

In my last post about genetics and inheritance, I asked a question about a family:

a family comes into a clinic for their flu shots and it is found that mom had type AB blood, Dad has type O blood and they have three children with type A, B and type O blood, what are all five people’s probable genotypes and what is the problem?


                                                Genotype      Problem

Mom:AB                      IAIB

Dad: O                         ii

Child1: A                      IAi

Child2: B                     IBi

Child 3: O                    ii                  Oops! Where did this kid come from?

After a short discussion, it turns out that Child 3 belongs to one parent from a previous marriage. Which parent’s child is this? If the other parent was homozygous, what was that person’s genotype and phenotype for ABO blood type?

It turns out that blood is even more interesting than this. There is another major blood antigen that needs to be matched when doing transfusions. This antigen is called ‘Rh factor’ because it was initially found in Rhesus Macaques, a type of monkey with a lineage close to our own. Although there are a number of Rh antigens, we are typically referring to the one that elicits the strongest immune response, the D antigen. Blood types are commonly referred to as ‘positive’ if the individual has the D antigen allele or ‘negative’ if the individual does not have this allele.

Like the ABO blood types, the Rh allele is important because of the strong immune response against it after Rh- individuals are exposed to Rh+ blood. Note that this is different than the ABO types where antibodies already exist. People only generate ‘anti-Rh’ antibodies after a primary exposure to this blood type, much like when a person is vaccinated against a disease, exposure to disease-associated antigens initiates the immune response, which will be protective upon later exposures.

This sounds like I am spending too much time in the details, but they are important in this case. To illustrate, let’s discuss the most common situation where this is important:

A woman with type A- becomes pregnant from a man with type B+ blood type.

What ABO blood types are possible from this pairing? Depending upon the genotype of the parents, it could be anything (A,B,AB or O).

But we said that it would be dangerous for blood to mix between someone with A blood type, like the mother, and any type that contained the B antigen, possibly like the baby.  So, is this baby in danger?

Thankfully, not. The reason is because the antibodies that we naturally make against the A or B antigens are typically IgM, which are very large molecules that do not pass through the placenta to the baby.


The larger IgM antibody cannot cross the placenta, but the smaller IgG antibodies can


What about the Rh antigen?

The Rh alleles interact in a typical dominant / recessive manner. As you might expect, Rh+ means that you express the protein, and this allele is dominant over Rh-, which means you don’t express this protein. Given this, we know that the mother must be Rh-/Rh- in order for her to have the ‘negative’ phenotype. The man has the ‘positive’ phenotype and therefore must be either Rh+/Rh- or Rh+/Rh+. Either way, the child has a good chance of being Rh+ as well (50% or 100% respectively).

Unlike the antibodies against A and B antigens, antibodies against Rh are typically smaller, IgG molecules. These are capable of crossing the placenta into the child’s blood and can be very dangerous. But also unlike the A and B antigens, anti-Rh antibodies don’t exist prior to exposure, so the mother will not likely have any of these antibodies during her first pregnancy with an Rh+ child.

Because of the nature of childbirth, it is possible that a mother will be exposed to her child’s blood during birth and she may develop antibodies against Rh at this time. But child #1 is already out, so he/she is safe. The difficulty occurs when the mother becomes pregnant with a second Rh+ child. At this time her anti-Rh antibodies can cross the placenta and cause hemolytic disease in the developing baby.

Fortunately, there is a good safety against this. A Johnson and Johnson subsidiary company, Ortho, makes an antibody cocktail called RhoGAM that is given at the 28th week of pregnancy and then again within 72 hours after delivery (now there are a number of similar drugs made by other companies as well). This cocktail contains antibodies that bind to and ‘hide’ any Rh antigen in the mother’s system. In this way, the mother’s immune system never ‘sees’ this antigen and doesn’t make antibodies against Rh, making it safe for her subsequent Rh+ children.1,2


  1. Pregnancy (rhesus negative women) – routine anti-D (review) (TA156)
  2. Rh incompatability.

Posted by on November 12, 2012 in Uncategorized


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A first look at Heredity

Oh Boy! Clarification is definitely in order. In this week’s lecture we outlined what it is that we will be covering in Unit II and then started in on a look at inheritance.

What does it mean to inherit something?

What is it that we are inheriting?

How can we understand the principles in operation in such a way that we can even make predictions about what certain crosses will result in?

There are a lot of different ways to approach these questions. The traditional method is to imagine that we are living in the 18th century and don’t know anything about Recombinant DNA Technology or Human Genome Projects or anything about modern science. Have an open mind and just look at what we can see before us.

(material below is modified from an iBook on Inheritance to be released in 2013 from DownHouseSoftware)

For many hundreds, or even thousands, of years inheritance was something that people had an intuitive understanding of, but could not really state in a set of rules how the process operated. There were always surprises that didn’t seem to fit the pattern.

On the positive side people were wise enough to breed the big animals with good temperaments while they slaughtered the others for meat. Similarly, the seeds of larger, tastier fruit and more productive trees were replanted, while those from less desirable plants were not. With time, these guidelines resulted in improved crops and farm animals and allowed for a transition from a hunter-gatherer culture to one that was more settled and agricultural.

As the world opened up to commerce between nations, it became more important for each nation to remain competitive, which meant that they would have to work out the rules of inheritance so that they could produce the highest quality animals and crops and textiles and distilled beverages.

This was the world that Mendel was entering. One in which a man who did not seem to fit into the standard societal roles could utilize his talents in the confines of a monastery in Brno and unravel one of the most basic riddles of life. What are the rules of inheritance?

Mendel eventually chose to work with pea plants that he could exert complete control over and carry out his experiments in a slow, methodical manner and document them with copious notes and definitions that explained his work clearly.

How do you work out something like the rules of life? Put yourself in Mendel’s place. Where do you start?

What this did tell him was that there was something about pink that over-rode the instruction to make white flowers. He called this phenomenon ‘Dominance,’ and came up with a rule that whenever two true breeding strains expressing different phenotypes of the same trait are bred together, and 100% of the offspring express just one of the parents’ phenotypes, that one is Dominant. The other is Recessive.

These results would have come as a shock to an earlier naturalist, Kolreuter, who assumed that the traits of the parents are blended in the offspring. Mendel’s experiments refuted this blending theory of inheritance by demonstrating that the F1 generation (that produced from the crossing of the True breeding parentals) would all express only the dominant parent’s form of a trait. Further, when this F1 was crossed to itself, the two parental forms were produced again.

The units of heredity are particles – not a liquid that is blended!

But there is more to it! These data, and more like it, demonstrated an interesting pattern in the offspring that gave Mendel a mathematical clue. No matter what trait he followed in his flowers, the same ratio of trait expressions in the offspring appeared – always 3:1. Whatever the number of what he called the recessive trait, he always say three times that number of the dominant trait.

He reasoned that this result was due to the particles of inheritance, which he called factors. From these data he proposed his Law of Segregation:


  1. Each individual has two factors for each trait
  2. Factors separate during formation of the gametes
  3. Each gamete has only one factor for each trait
  4. Fertilization gives the new individual two factors for each trait (one from each parent)

Instead of flowers, let us imagine a human couple. Both have brown eyes, but the man is carrying two factors from brown eyes while the woman has one factor for brown eyes and one for blue. Her eyes appear brown though because the brown factor is dominant.

Let B = the Brown eye factor

b = the blue eye factor

From Law of Segregation Part 1: Each individual has two factors for each trait

The man has two factors, they are the same: ‘B’ and ‘B’.

The woman has two factors, ‘B’ and ‘b’.

Because each of them has at least one copy of the dominant factor, that is what they express – brown eyes.

From Law of Segregation Parts 2 and 3: Factors separate during formation of the gametes – and – Each gamete has only one factor for each trait

The man makes sperm that contain one of his factors. Because he has two ‘B’s, all his sperm carry the ‘B’ factor.

The woman makes eggs that contain one of her factors. Because her factors are different, some eggs have ‘B’ and some eggs have ‘b’

From Law of Segregation Part 4: Fertilization gives the new individual two factors for each trait (one from each parent)


The offspring get one factor from each parent (carried in the sex cells) resulting in new individuals with two factors. The expression of the trait depends on what factors they get.

In this example, the man always contributes a ‘B’, while the woman may contribute a ‘B’ , like she does to her son. Or a ‘b’, like she does to her daughter.  However, in either case, all the children will have at least one ‘B’, so they will all have brown eyes.

Years later, at Cambridge, Reginald Punnett devised a much simpler way to depict these interactions visually in what is called a Punnett Square.

As this post is getting long, I think I’ll lay off here. This covers the main elements of what we discussed in class this week and I’d rather start another post later to continue.

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Posted by on November 8, 2012 in Uncategorized


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Unit II (Genes, Inheritance and Evolution) ppt files posted

Money may be inherited from parents to children (as seen here in this illustration of how the Walmart fortune was dispersed following the deaths of Bud and Sam Walton. ) Why is this? What do parents have to gain by giving resources to their children? Why might some children be disinherited if it is found that they are not the biological offspring of the father? There is a very reasonable biological basis to this behavior and we will be discussing that in Unit II.

My class can find the Unit II powerpoint files posted on the blackboard site.

Note that this unit does NOT follow the chapters of Mader et al very exactly. I strongly recommend that you continue reading the chapters closely (23, 24, 25, 27 and 33) as you will be responsible for the end of chapter questions. However, it also becomes more important for you to come to class and keep up with the lectures and handbook chapters as there is material you will be responsible for that is not in the text.

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Posted by on November 1, 2012 in Uncategorized


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Another old essay – Morgan and Memes

This essay was originally published in the Osawatomie newspaper (The Graphic?) a year or two ago. It was prompted by an article in my local newspaper that showed how two ideas that have no logical connection can sometimes appear to be intimately ‘linked’ to one another.

Morgan and Memes                                                                                           

Thomas Hunt Morgan in the Fly Room

In the early 20th century, a scientist at Columbia University, named Thomas Hunt Morgan did work establishing the connection between the observations of Gregor Mendel and some lesser known scientists, Flemming, Sutton and Boveri. Mendel, an Austrian monk, was the first naturalist to see deep into the workings of nature and establish a clear, testable theory of how inheritance operates in organisms of all types. Trained in mathematics, Mendel saw that if each trait he observed was controlled by two ‘factors’ (one from each parent,) then inheritance followed a predictable pattern.

In his laboratory in Germany, totally unaware of Mendel’s work, Walther Flemming watched and documented the precise orchestration of cell division under the microscope. What he saw, less well known than Mendel’s work, was how chromosomes seem to form as threads in the cell that group along the center line of a cell before splitting and separating into each of the daughter cells formed by division. Sutton and Boveri saw the connection between these sorting chromosomes and Mendel’s ‘factors,’ but could not finish connecting the dots. Hunt’s conclusion, which seems so obvious now, was that chromosomes carry genes. To prove this he tracked two special chromosomes, X and Y and found that they determined the sex of the organism. Like humans, when flies had two X chromosomes, they were female; one X and one Y and they were male. Chromosomes were controlling the sex of the organism. This conclusion changed the way genetics was studied for years to come.

One thought that beguiled him though, was that Mendel’s work predicted that all genes sorted independently, but there were only so many chromosomes, and many, many genes. This was troubling because Mendel’s work was otherwise very clear and stood up to rigorous testing, yet it was inconsistent with what he saw with chromosomes. Mendel said that all genes are randomly inherited – and here he was, working with fruit flies and finding that it just couldn’t be true with so many genes and so few chromosomes. To skip the details, Morgan, and his lab members eventually discovered that chromosomes are tricky – and sticky. The two sets of chromosomes you get from each of your parents pair up and swap bits promiscuously. This swapping, or ‘crossing over,’ imitated randomness in all genes except those that were very close together. And so, while most genes adhered to Mendel’s law of independent assortment, those genes that lie close together on the chromosomes travel together and can be seen as traits that go hand-in-hand down the generations.

In 1976, Richard Dawkins, wrote “The Selfish Gene” in which he buried a nifty little idea. He proposed that thoughts are like genes- he called them memes– that get passed along from one person to the next, taking on a life of their own in a sort of world-wide game of telephone. He has written often about this idea, which is an interesting analogy, but not altogether useful scientifically.

Nevertheless, I had the thought of memes in my head, and when I read an article about organic farming our local county paper, I suddenly realized that memes too travel together! In the article a farmer described her farm as organic and natural – all the things that I like to hear about. I was immediately excited and wanted to join her co-op to get food that was a little more a part of the earth and a little less a product of chemistry. But then I got to some ideas that just didn’t make sense to me – things that often travel with the less well informed members of the organic food crowd: She doesn’t vaccinate her animals – or her children. She went on to suggest that cancer and autism are causally linked to genetically modified organism (GMO) foods – a completely groundless hypothesis.

Two chains of Memes (Memosome?). Memes 1-3 are all linked in some way, Memes 4 and 5 are also linked to one another, but not to Memes 1-3.

Yet, I’ve seen these memes travelling together in the past without giving it as much thought, and here they are again: The natural food meme and science-makes-us-sick meme. On one hand I see the connection and agree, I don’t think GMO foods are natural and vaccines are a way of unnaturally generating immunity without being exposed to disease. But, GMO foods are not inherently unsafe. They simply put together traits that exist in nature, but in combinations that would take breeders eons to produce ‘naturally.’

I love to know that my food comes from a natural, organic farm. And I expect to pay more for food of that sort, mostly because it is not as abundant and does not take advantage of advances in science. Advances that make it possible to feed all the billions of people on this planet. Billions that could not all be fed without modern, scientific agriculture. But there is something wholesome about foods grown in this way: the great variety of fruits and vegetables with their subtly distinct flavors and colors. Like GMOs, vaccines are also something of an unnatural creation – unnatural creations that spare us from the all too natural world of smallpox, measles, poliomyelitis.

I don’t mean to impose my values on anyone, but I do think that it can be enlightening to consider what ‘natural’ means. There are many things from the past that we should not forget and good food is one of them, but we ought not to also forget the ravages of disease that once kept children from playing outside together in the summer months or made them deathly sick only to recover and lead a life blinded, paralyzed or otherwise retarded from exposure to all things natural in the world.

I don’t think that anyone leads an entirely consistent life, but we are intelligent creatures and we don’t have to accept anything without consideration. So take some time, examine what you believe in and see just what memes are in your head just catching a ride. Maybe there’s some cleaning out to do.

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Posted by on October 24, 2012 in Uncategorized


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