How is size information encoded and preserved through generations? Given a particular set of organs and such (morphology?), how do DNA and cells say “keep reproducing and making parts up until overall, the organism is approximately this big”? If you kept force feeding a young organism while it’s growing, it still won’t grow to infinite dimensions… what’s the mechanism that limits their maximum size?
Most cells contain the whole genetic code of the body. The thing that determines whether the cell is a skin cell or a brain cell or whatever is epigenetics–processes that determine which parts of the DNA is coded into which proteins and when.
So, at some high level of generality, the answer you’re looking for is “genetics.” Conversely, the answer at a sufficient level of particularity would be to identify for any particular structure (ear, nose, liver, etc.) the particular parts of the DNA of the different cells that tells them whether and how often to divide and what the subsequent cells should do. You could also look at the various interactions among cells–some organs telling other organs what to do, as in the case of the production of growth hormone.
But there is no one answer other than genetics, I don’t think. Different cells have different genetic “rules” about whether and when to divide that are turned on by different stimuli. In extreme cases, something goes wrong, and a rule isn’t followed–which is how you get giants and cancer.
That is highly oversimplified to the point of being completely incorrect. Genetic regulation is a vast and complex collection of mechanisms, of which epigenetics is a small part.
Your second sentence is correct, but it does not contradict what I wrote (which is that epigenetics is the principal determinant of cell type).
That said, not my field. I welcome correction.
Genes aren’t blueprints, they are recipes. There’s no control that says, “When you get so big, stop growing.” Instead there has to be some sort of regulation that turns off the genes, and this is usually some sort of hormone.
So as long as the body is producing growth hormone, the cells in the bones and muscles keep growing. When that hormone slows down, growth stops and the ends of the bones calcify. What triggers the change from a juvenile level of growth hormone to an adult level?
It’s apparently really complicated and depends on a lot of factors.
But there’s no plan like “Grow until you’re 183 centimeters tall and then stop”. Your body will grow until it stops getting the signal to keep growing, and various factors can change that.
Not really oversimplified or incorrect. Epigenetics determines cell fate. Unpacking and understanding the mechanisms of epigenetics is very complex but that does not make the statement incorrect.
Are you sure about that?
I don’t think anyone knows. Even in insects, a much simpler model to study, it is not at all clear, but it does seem that there is some range of top critical size that is genetically determined with hormonal signaling modulating growth within a range (insulin being the modulating factor studied in the Drosophila model). It does seem to be that there is some control that says, “When you get so big, stop growing.”
Growth variability has also been extensively studied in dogs as there is a huge range within that single species. Variation in an IGF-1 allele seems to be the main determinant there.
Yes, it’s apparently really complicated and depends on a lot of factors.
Related to OP’s question, I’m alway amazed that the genetic mechanisms can cause separate body parts to grow in ways that are compatible with each other – the case I have in mind is the detailed shapes of all the teeth, such that the upper teeth mesh with the corresponding opposite lower teeth. It’s like those genes in the upper tooth and the opposite lower tooth are coordinating their efforts.
I think what the numerate prosimian is saying is that there is no single switch that says “when you get this big, stop growing” but that it is the overall effect of multiple interacting biochemical causes. People might envision genetics as well-written code, but it is actually layer after layer of legacy code with crude hacks and patches to keep it working at the moment. It is all duct-tape and chewing gum and and badly-mixed metaphors.
You said that epigenetics is “the thing” that determines cell fate. That is not correct. There are a vast number of inputs and processes that all contribute to the ultimate fate of any cell, including genetics, epigenetics, external inputs, hormones, etc, etc. Epigenetics (which, incidentally is NOT synonymous with “genetic regulation”) is not the be-all and end-all of developmental biology. It’s one important part out of many.
A slight tangent the OP, but to address this first:
Epigenetics tends to be wildly overhyped in the press, to the point that it’s often insinuated that nobody had any idea that genes were regulated at all until quite recently. That’s obviously a preposterous idea. As Smeghead says, epigenetics is certainly not synonymous with gene regulation. The “central processing unit” of gene regulation has long been known to consist principally of interactions among protein transcription factors and DNA. The epigenetic marks are a downstream effector mechanism. In other words, the transcription factors do most of the “thinking” and decide which genes to switch on and off, and then often place epigenetic marks at relevant positions in the DNA to mark which genes are on or off.
Epigenetic marks are rather stable within a cell, and are usually stably inherited through mitosis, i.e. in a cell lineage within the organism. Therefore, although epigenetic marks may never have done much of the “thinking” in the original decision process about which genes to switch on and off in a differentiating cell, they do tend to be the principal determinants of cell fate. Embryonic stem cells are pluripotent, having the ability to differentiate into all cell types in the body, and this essentially means that they have very few of these stable epigenetic marks. Differentiated cells (fibroblasts, neurons, etc…) have acquired stable epigenetic profiles characteristic of their cell type.
A major area of research has been the effort to wipe these stable epigenetic marks from a differentiated cell, in order to restore them to the pluripotency of stem cells.
This technology may allow (say) an adult’s skin cells to be used therapeutically to restore other damaged cell types, without any requirement to harvest stem cells from an actual embryo.
As for the OP: it’s an extremely interesting question, and one that we certainly don’t have all the answers to. The overall field is called developmental biology, and the Wikipedia article and links therein are a place to start if you want to get into the field. The classic textbook in the field is by Scott Gilbert - well worth the investment, beautifully illustrated.
It’s a huge subject with no simple answer, but one of the key ideas is that of morphogens.
(It’s interesting that the term was coined in an early speculative paper by Alan Turing.)
Morphogens are signalling molecules that diffuse across tissue in early development. The concentration gradient, often of several different morphogens on different axes, is a determinant of tissue shape and size. In other words, cells can figure out what they should be doing at their particular position in the tissue through the local concentration of morphogens.
You are responding to some pop version of epigenetics that I am not espousing, that you cannot possibly have gotten from reading my post that explicitly talks about things like growth hormone.
Please try reading my post again.
I’ve read your post and his. Sorry, but yours is the less informed version of epigenetics. Explicitly the physiologic mechanism of things like Growth Hormone and other similar hormonal influences are not typically by epigenetic mechanisms. Now epigenetic mechanisms can alter the impact of Growth Hormone … that would be stuff like this variation of CG-137 methylation in the IGF-1 promoter which is responsible for some portion of the individual variation in response to Growth Hormone … but the binding of Growth Hormone to various receptors for it and its typical function at various patterns of rises and falls and at various levels on growth is not an epigenetic issue other than in a pop version of epigenetics. Given the way “epigenetics” is presented in the media that misperception is however understandable. That’s one of Riemann’s points, well made.
You frequently do see idiotic headlines like “Your genetic fate may not be set in stone! Scientists have recently discovered that genes can be switched on and off in response to the environment! By epigenetics!”
And although your post was not like that, it did kind of say that epigenetics = gene regulation. It’s such a widespread misrepresentation that a lot of biologists (I’m certainly one of them) tend to be sensitive about it, so I’m sympathetic to Smeghead’s response.
I don’t see any significant difference between the size of an organism and other architectural or functional characteristics. Of course the optimum size range is evolutionarily defined, an example being the size dimorphism due to sexual selection. So, fitness is the ultimate cause of size, proximate causation being genetics, epigenetics, hormonal, environmental, etc. It is obviously coordinated throughout the organism, at a high enough level, so that one wouldn’t have a limb longer than the other and the eyes will fit the skull 
But the OP has certainly hit on a complex question, in the sense that there is no explicit “blueprint” of the body plan laid out in the DNA. This is the hugely silly misconception of the common sci-fi / horror movie trope that introducing the DNA of one organism into another fully-developed organism triggers transformation into some monstrous hybrid.
The body plan is established dynamically in development, and things “fitting together” is a function of cells talking to each other during development to establish relative positions and roles. It’s not as though there’s one set of genes explicitly specifying eye socket dimensions, and another set specifying eyeball dimensions.
This means that it’s challenging to work out the precise correspondence between the information about body plan that is encoded in the DNA and the phenotype. The information is obviously there, but because the body was not planned out from scratch by a designer, but by trial and error, it is not encoded in obvious ways. It may be that (for example) a substantial variation in body plan could result from subtle variation in the level or timing of expression in a cell-to-cell signalling molecule that turns on during development.
Of course, efforts to understand these things involve simple model organisms where genetics are tractable and amenable to experimentation.
Size is not attributable to any one gene, but to the combined effect of a large number of genes, most of which have pleiotropic effects (i.e. do not just affect size). This is consistent with the fact that it is generally easy to evolve substantial changes in size in response to selection.
At the same time, the fact that things fit together through cell-cell communication during development, means that some simple changes like increasing the expression of growth hormones can just make the whole body proportionately bigger. It’s not as though you need to separately tell one gene to make the torso longer and another gene to make the legs longer.
True that.
Seems though that half the variance in body size of dogs results from only 6 genes, but I understand that the biochemical signalling pathways are yet unknown, but feverishly looked for. Dogs are a perfect animal for these searches, body sizes in different breeds may vary by a factor of 40.
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The muddled popular use of “epigenetics” is sort of our collective fault, though. There are multiple biological definitions of epigenetics, as used by different fields. From the classical geneticist’s perspective, epigenetics refers to any inherited characteristic which is not directly encoded in the DNA. Many modern cell and molecular biologists use the word epigenetics to exclusively refer to chemical modifications of DNA and tightly associated proteins like histones. Usually, these two definitions overlap well enough, since with most multicellular organisms, most epigenetic inheritance occurs by DNA/histone modifications.
However, there are some other subfield-specific uses of epigenetics that really muddy the waters. There are single-celled eukaryotes which show epigenetic switches between distinctive cell states, like the C. albicans white/opaque phenotypes. This particular epigenetic switch is primarily driven by a regulatory network of transcription factors, rather than chromatin modifiers. It fits within the classical genetic definition of epigenetics, but conceptually is no different from the regulation of cell differentiation by transcription factors during animal development.
Then there are various things like the hypothesized roles of sperm/oocyte non-coding RNAs, which fits the classical genetic definition of “epigenetic” inheritance without having anything to do with chromatin. Or the role of other non-coding RNAs that are directly involved in chromatin regulation during X-chromosome inactivation, which fits the chromatin-modifier definition of “epigenetics”, but doesn’t have anything to do with inheritance.
All in all, I really can’t blame the layman, or even a student or science journalist, for picking up a vague and mixed up concept of “epigenetics” from all the conflicting uses of the word.