January 28, 2010

Jean-Paul Javerzat
Institut de Biochimie et Génétique Cellulaires
Université Victor Segalen
Bordeaux 2/CNRS UMR5095
Bordeaux 33077

Dear Jean-Paul Javerzat:

I read Directing the Centromere Guardian, Jean-Paul Javerzat SCIENCE vol. 327 no. 5962 January 8, 2010 page 150 with relish.  Five or ten years ago I presented a poster at the international genetics convention in Melbourne, Australia.  At the time I already had solid evidence that a population that becomes too large becomes infertile for genetic reasons.  My best evidence was that urban societies collapse according to a highly predictable pattern.  Since then infertility of the older urbanized societies has increased steadily, so the concept is, I feel, of great current interest.  I have amassed a lot of evidence in support since then.  Some of it is on the enclosed DVD and there is more at NoBabies.net where I also post my correspondence. 

The problem I had at the time was that there was no clearly agreed upon cause of speciation.  Obviously questions of speciation and questions of fertility are the same.  There was, so far as I could tell, not even agreement on such basics as what rules a theory of speciation should follow nor how many generations it took.  That remains unchanged. 

To my delight there was a paper published just in time for me to use it as a reference at the conference.  The theory pointed the finger at the centromere.  According to the theory the DNA of the centromere must be fine tuned to the underlying histone protein.  Because of its crucial role during meiosis, the centromere is subject to runaway evolution.  Only one of the four potential offspring of a progenitor cell becomes an oocyte.  It is to the selective advantage of the centromere to be in that cell.  Thus it is under selective pressure to outrun its sisters.  The problem is that with the detuning, when the same centromere is involved in a meiotic event leading to sperm, since four sperm are formed the whole process can break down, leading to male infertility, the hallmark of speciation.  At least so goes the theory. 

I could readily appreciate that in a small population, such runaway evolution could be kept in check.  Mutations in the DNA for the histone could adapt to any change in the centromeres.  With a larger population, there might be more than one line of centromeres that had broken free and were vying for dominance of the genome.  It would not be possible for the histone DNA to chase both at the same time in any effective fashion.  At least so goes my use of the theory.

My poster was well received, although I was not able to make contact with anyone who wanted to join the chase and produce a publishable paper.  To people who say, “Why don’t you publish?” I reply, “Why don’t you hit a home run in the World Series?”  Publishing is highly competitive, and you have my congratulations on accomplishing the publication of a paper in a major journal solo.  Few can.  Certainly not I. 

However the centromere theory was not well received. 

I took the clue myself and teaching myself C language wrote a computer program that simulated infertility arising from mutations that produced problems with meiosis.  The success of the program was to me spectacular.  It predicted results of studies that compared kinship with fertility in over a thousand animal studies and two human studies.  (These studies followed the creation of the program.)  It predicted the pattern of urban collapse that is seen in history.  (Some of these data I crunched before developing the program and some after.) It even, after much tweaking and a re-write that pushed the limits of the computational power of the strongest PC’s now available, demonstrates that societies run through two cycles; there is a roughly five generation cycle of growth and then critical decline usually followed by a second cycle ending in extinction.  (No, I can’t get the process to happen in so few generations.  And I managed to make it work after I found the data, although I had already seen that it was possible.)  The bulk of this is on the 10 minute DVD.

I have since thought that infertility might be due to a failure of timing during meiosis.  Small changes in the chromosomes could disrupt the synchronization.  But you have made clear that there is a mechanism whereby evolution has anticipated this and provided the guardian that delays separation of chromatids until all are lined up and ready.

My attention was riveted by your remark that errors in the process can result in infertility.  As I said, fertility and speciation are the same subject.  Alas over the years I have lost track of the original article I then referenced.  If you would be so kind, could you tell me whether the centromere theory of speciation has received any further attention? 

If you are interested in this, (and I fail to see how anybody with a head and a heart could fail to be interested) please let me know if I can be of further assistance. 


M. Linton Herbert MD
NoBabies.net and SilentNursery.com 

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