How does a cell become a baby?

Ok, a little bait and switch but not too much. What I am talking about here is something a “wee bit” more abstruse so don’t go all clicky on me and leave. Give me a chance to explain. The cute kittens can wait.

It’s tough talking to a generic audience about something as complicated as cell biology but I try my best. If I am too simplistic, the biologists get turned off, If I’m too complicated, the rest of the folks get turned off. So please bear with me while I present what will seem like complete jargon words to the average blog reader. Do not fear, I will explain everything.

The three scary words I will be talking about here are, euchromatin, constitutive heterochromatin, and facultative heterochromatin. All three are mouthfuls to say the least. Let’s start by trying to break down these seemingly indigestible words.

Eukaryotic chromosomes (our chromosomes)  are comprised not only of DNA, but DNA wrapped up in or associated with various kinds of proteins and other molecules. This conglomeration is what you see under the microscope when you’re looking at chromosomes. We call this conglomeration, chromatin. Chromatin can be loosely packaged or tightly packaged. If it is loosely packaged we call it euchromatin or true chromatin. This is the chromatin involved with gene expression as it is currently going on in a particular cell. The remaining chromatin is called heterochromatin and is not currently involved in gene expression. There are two kinds of heterochromatin: constitutive heterochromatin and facultative heterochromatin. Constitutive heterochromatin is never involved in gene expression and comprises DNA that is more structural in nature, like the DNA used to link mitotic spindle fibers to duplicated chromosomes for pulling them apart during cell division. Facultative heterochromatin can be used in gene expression, but not at the same time as euchromatin. It has to be converted into euchromatin first.

You may want to digest what I just wrote before proceeding further, unless of course you happen to be a biologist. Here is where we separate the wheat from the chaff: My models suggest that  facultative heterochromatin in one kind of cell ( e.g., neuron) is mostly different from that in other kinds of cells (e.g., liver cells). This represents a form of reversible cellular differentiation. It is what allows stem cell biologists to compress euchromatin in a cell into facultative heterochromatin while forcing other facultative heterochromatin into euchromatin within that same cell to force it to form a different cell type. This works best with stem cells and especially embryonic cells. Such a cell becomes a kind of hybrid, tenuously stuck in one kind of cell mode while masking the original cell type. This may be fine as long as no relevant genetic material has been lost in the process.

Herein comes the rub: my models suggest there is another form of cellular differentiation that is quite irreversible. This scenario is best described by what occurs when white blood cells called lymphocytes differentiate into plasma cells that secret antibodies to fight infections.  In this case, circles of DNA are pulled out of the genome and lost during a vast rearrangement of the genome in response to the infection. Something similar occurs when chromosomes are damaged by drugs or radiation, i.e., small circular chromosomes called double minutes may be pulled away from the main chromosome and lost during subsequent cell division, resulting in loss of chromosomal function and either cell death or one step closer to unregulated growth (cancer).

My models explain how this may happen in all cells, not just lymphocytes. In fact, my models also explain how our chromosomes may have evolved, how they operate during gene expression and cellular differentiation, and how they are damaged by environmental factors leading to cell death or cancer.

Personally, I think this is quite important to understand and is the reason I continue pounding away at this blog. Circles of DNA are not some curious side phenomenon that may be simply brushed aside while studying our chromosome structure. They are the very basis of it. At least, I think so, anyway. If anyone is of a different opinion, I would appreciate any constructive input they wish to provide either as a comment or via e mail at


About frankabernathy

I am a retired cell biologist and alumnus of Ohio State University. I became interested in chromosomes as far back as the 1960's when I wrote a term paper on the effects of radiomimetic drugs on chromosomes. I was fascinated at how they could break apart and reform new structures so easily. I became further involved in the early 1970's after taking a cytogenetics course at the University of Arkansas. I took that knowledge with me to Ohio State in 1980 where I eventually worked on my research and completed my Ph.D. dissertation, "Studies on Eukaryotic DNA Superstructure". My studies and later research suggested that the DNA within the eukaryotic chromosome is not the simple, linear molecular thread so widely suggested in all the classic textbooks published today. Instead, it may be the culmination of a geologically rapid set of endosymbiotic events where microorganisms plug into each other to create something greater than themselves. Feel free to contact me at
This entry was posted in cellular differentiation, evolution. Bookmark the permalink.

Leave a Reply

Fill in your details below or click an icon to log in: Logo

You are commenting using your account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s