How to join the eukaryotic chromosome “club” when you are a relative latecomer

The eukaryotic chromosome has been around for quite some time now, probably well over 500 million years. It had to start from something, did it not? Like electricity and water, life always tries to find the shortest route to achieve its ends. In layman’s terms, we call this lazy, or the mother of invention. Doing anything else just requires too much time and energy, and if you busy taking the long uphill route, don’t expect the evolutionary winners at the finish line to congratulate you on all your hard work and effort. Nice guys always finish last in this race. The classical view of eukaryotic chromosomal evolution has been one of gene duplications coupled with single point mutations. It’s kind of like monkeys typing on a typewriter and eventually writing up all the works of Shakespeare. It can be done given enough time and enough monkeys. This kind of evolution is arithmetic in nature, basically one (or perhaps several) mutations followed by others, all being edited as time progresses to check for fitness. However, there is at least one alternative model and it is the one presented throughout this blog: chromosomal sharing, followed by reduction of redundant genes. This can be accomplished through endosymbiotic events in which disparate species join up their chromosomes and basically share the best of both worlds. It’s what sex is all about. This follows a geometric progression, especially as shared chromosomes because larger over time.

So the question is this: Which of these models takes the slow boat to evolutionary change and which one takes a jet plane? You know the answer as well as I do. You can learn more about this endosymbiotic model by browsing throughout this blog. You can also learn about my hypotheses regarding the reaction and inaction of the scientific community regarding the continuation of this line of research. In the meantime, there is a fungus among us, or should I say within us, not to mention bacterial viruses, and other lower form of eukaryotes. Check out this reference for starters:

Oh, I almost forgot! What happens to latecomers when they try to join the eukaryotic chromosomal club? Well, the senior members are well established via mitosis, latecomers either find a way to integrate into the club or must reproduce like mitochondria in order to not be left behind.

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Peer review versus riding a bicycle (why the chromosome refuses to evolve)

Why does the eukaryotic chromosome refuse to evolve? For over 170 years, this staid monolithic structure stubbornly continues to exist as a single, monotonous, seemingly never-ending, tightly wound up, elongated ball of yarn; at least in the minds of scientists and their proteges, anyway. Now why is that? Is it because it’s true? Or is it something else?

Here is a very interesting video that might help explain this phenomenon. Hope you like it!

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How to Remove Bias From Scientific Peer Review

The white elephant in the room is finally being acknowledged: Peer review bias. In this instance, it relates to sex bias and the consequences in this case included termination from the editorial board. I am sure the same thing would apply to ethnic bias as well. All well and good, but what about other kinds of peer review bias? There is a more insidious kind that is very difficult to detect and difficult to talk about: I have discussed this at length in several of my postings:

Another heretical scientist dares to challenge the church of scientific orthodoxy

Are our chromosomes dumber than we are, or is it just the opposite?

Creationism versus evolution

What are they afraid of?

Posted on February 13, 2013 from: Rantings of a Mad Scientist (see excerpt below)

Many layman like to think that science is somehow above the politics of ordinary humans. Unfortunately, it is not because science is conducted by humans, not gods. These humans, like so many others, have agendas. Sometimes, discovery can get in the way of these agendas. I know this for a fact because I was once a graduate student working on a Ph.D. just like so many before me and so many after. I assumed that I should be working on discovering something new and original, otherwise why bother going after a Ph.D.?  I was soon to be rudely awakened to a brutal reality. I actually had a professor at my university tell me to my face that “they” would “KILL” me for continuing the research I was working on at Ohio State University! Of course, he didn’t mean this literally. He meant they would “kill” my career. He was very very close in his assessment. Actually, he was dead on. The research was, in fact, “killed”. All laboratory research I conducted beyond what you see on this blog was other people’s research, not my own. I had a family to feed and bills to pay, so I did what I needed to do. Throughout the years, I continued to review the literature and contact people, but it was all to no avail.

So I ask you this simple question: Is this acceptable science, or should further research be conducted into the composition of these circular structures?  Admittedly, they may just be some kind of remarkable artifact, although exactly what that really means remains untested and, therefore, unknown. Is this science at its best, or can we do better?

I believe it really boils down to this: What are they afraid of?  For many years, I believed they were simply afraid of me being wrong. I have since changed my mind. It is more than that. I believe they are afraid of me being right.

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Are you nothing more than glorified “viruses”?

What if I told you your cells’ nuclei may actually be an amalgamation of viral, bacterial, fungal, and other forms of primitive eukaryotic DNA, all working together for the common good:………..YOU!

That’s a pretty humbling thought, isn’t it? Almost on the same level as ashes to ashes and dust to dust. However, we are talking about “living” dust here. Ads on TV talk about the shingles virus already being in you, as if that is the exception rather than the rule. Think about it. Why would the shingles virus find your nuclear DNA to be such an inviting place to take up residence, along with a host of other kinds of viruses? Why indeed. My blog talks about this in quite a bit of detail. You see, I don’t think external viruses entering your body is an exception to anything. They are just “latecomers” in an age old phenomenon that has been going on since life first originated on this planet. Contrary to popular theory, I do not believe the DNA in our chromosomes is merely a long, boring, continuous molecular thread, wound up like a firehose within the nucleus. It is much much more complex than that. There are physical “switches” in the DNA, much like a railroad track, that when triggered force the DNA into different configurations that vary within cell types. These configurations force the DNA to generate RNA and hence protein that is unique to the kind of cell in which they are being generated; in other words, cellular differentiation. When these switches get seriously messed up, the cells do one of two things: they destroy themselves through apoptosis or they become genetically corrupt and capable of evolving over time into something quite sinister: cancer.

Why apoptosis, why cancer? Apoptosis is nature’s way of insuring cancer never happens. It does this by completely destroying the cellular DNA in such as way that none of it “escapes”. Escapes? What does that mean, exactly? Well, such rogue DNA may be capable of taking on a life of its own because of how it was assembled over eons of time. It may even enter normal cells and take up residence in the DNA, just like an external virus, corrupting the genetic machinery of that cell and forcing it to replicate the entire cell in order to replicate the rogue DNA. This is why apoptosis is such a complex and energy intensive process. It must never allow this to happen. The risk to the viability of the organism (in this case, you) is just too great.

You can learn more about how nuclear DNA may have been assembled over the eons by reading through this blog or contacting me.

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Circular eukaryotic DNA and cancer.

It seems the main place investigators “find” circular eukaryotic DNAs these days is when they’re looking at cancer cells which generate micronuclei and chromosomal rearrangements.  They call this DNA “pulverization” (see article link below). The chromosomes are literally “going nuts” with each cell division, breaking up and rearranging whatever is left. DNA replication becomes asynchronous, meaning a sizable number of these DNA chunks take on a life of their own, as if they were microorganisms in their own right. My question is simply this: How does this happen? Nobody seems to know. But I think I have an explanation for it. Check out the rest of my blog.

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Circular eukaryotic DNA, no longer important?

I googled circular DNA today in a variety of formats and all I could come up with is journal articles dating back to the early 2000’s or earlier. If anyone knows of more recent articles relating to this topic I would appreciate an update. Otherwise, I must assume the scientific community has moved on to better (or easier) things.

The one shown below is a 2002 article.

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Aldous Huxley

Aldous Huxley

The facts still stand: How do you generate thousands of circles with orders of magnitude size differences from 40 linear mouse chromosomes? The most obvious answer is that they were already present in a cryptic form (click photos to enlarge).

Circles  91b

Degrading mouse cells, 400x magnification

What do mouse chromosomes look like under “normal” conditions? Check out this link: mouse chromosome.


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