Genetics for skeletons or bones?

[Hoku]

Each bone evolves independantly of the others, right? I'm pretty sure that each bone has it's own gene. Assuming I'm correct, my primary question is, did each bone also evolve its density or is there a single gene that controls the density of all bones, collectively? I hope my question is clear.

 

[Andy Resnick]

Bone undergoes continuous remodeling in response to applied loads, but the mechanism is not yet understood:

http://www.ncbi.nlm.nih.gov/pubmed/20200416

You ask a good question regarding mapping the genome to specific bones- I'm not sure what is known.

 

[Pythagorean]

I was always under the impression that the "bone-builders" themselves were tied to the genetics, and the bone structures themselves are a result of:

a) environment (load, for instance)
b) how the "bone-builders" are coded to respond to that environment

 

[bobze]

Each bone evolves independantly of the others, right? I'm pretty sure that each bone has it's own gene. Assuming I'm correct, my primary question is, did each bone also evolve its density or is there a single gene that controls the density of all bones, collectively? I hope my question is clear.

Bones initially develop as a response to the morphogenetic fields during embryological development that develop most of our gross anatomical structures-Specifically ones like homeobox or HOX genes (though there are other cranial/caudalizing factors and fields, some of which we understand little) . This happens in 2 ways.

The first (well their not in order, just the first I'm talking about ) is Endochondral bone formation. The body uses "models" of bone made of hyaline cartilage. As the fetus nears birth, differential gene expression causes recruitment and differentiation of osteoblasts, which lay down a bone collar and form a primary center of ossification (in the diaphesis of the bone). Throughout the life of the organism, continued bone deposition and resorption is done--Called bone remodeling. This serves two purposes, firstly it aligns the collagen (type 2) of the bone in anti-parallel and perpendicular fashions (like plywood) which strengthens the bone. It also allows local regulatory responses to load to add more strength to bones that "need" it.

Edit: This is done with long bones.

Secondly, bones are formed de novo in a process called intramembranous bone formation. Again, expression of certain growth factors by cells (in response to their local environments) create "fields" which cause mesenchymal stem cells to differentiation into osteoblast centers, which start mineralization of the connective tissue and create bone without a cartilage scaffold.

Edit: This is done with flat bones.

Interestingly enough, we can do neat tricks (in deed sometimes mutations cause this) where morphogenetic fields are incorrectly created resulting in abnormal growth of limbs/bone structure. Like six fingers for instance. You don't have a gene for the bones in the extra finger, what you do have is an extra area on the fetal hand bud which expresses the correct "field" to start development of another finger and laying down of the hyaline cartilage that will become bone.

-Hope that helps

 

[Hoku]

Thanks for the in depth info, bobze.

I'm actually trying to understand this from an evolutionary perspective. We all know that evolution is caused by genetic mutations. I'm trying to understand the evolutionary relationship between specific bones and the skeletal system as a whole. I would think that each bone has its own gene that can mutate independantly from other bones. I think evidenced for this can be found in whales, as an example. Their vestigial hip bones have evolved useless, even if they DID have legs. But their other bones, that are still useful for them, appropriately evolved with the whale.

But there are commonalities among the entire skeletal system, like density, which varies between species. So my question is, if each bone has its own gene that can mutate independantly, are those individual genes also responsible for their bone density? I'm thinking there must be another gene in the body that is singularly responsible for characteristics like bone density, shared by the entire skeletal system.

Any further insights?

 

[bobze]

Thanks for the in depth info, bobze.

I'm actually trying to understand this from an evolutionary perspective. We all know that evolution is caused by genetic mutations. I'm trying to understand the evolutionary relationship between specific bones and the skeletal system as a whole. I would think that each bone has its own gene that can mutate independantly from other bones. I think evidenced for this can be found in whales, as an example. Their vestigial hip bones have evolved useless, even if they DID have legs. But their other bones, that are still useful for them, appropriately evolved with the whale.

But there are commonalities among the entire skeletal system, like density, which varies between species. So my question is, if each bone has its own gene that can mutate independantly, are those individual genes also responsible for their bone density? I'm thinking there must be another gene in the body that is singularly responsible for characteristics like bone density, shared by the entire skeletal system.

Any further insights?

No there isn't single genes which control bones. There is as I pointed out, fields. It is a very, very complex subject and there isn't really a short answer aside from lots of reading.

As I said before, bones in the embryo are created because of local environmental rules setup by the genes--Not specific "blue print" genes (which unfortunately lots of high school science teachers seem to giving people the impression that genes are really "blue prints").

Here's something really important about evolution. Most genes are pretty conserved, in that the gene codes for a similar protein, across taxa. What differs (and often drastically) and leads to those changes of bauplan you're wondering about is in the timing and expression of those genes-Specifically during embryological development.

Think about it like this (this is an overly simplified example). Suppose, You and I were two cells on the end of an arm bud in the developing embryo. We "know" our position because of fields of growth factors (think concentration gradients). Depending on the amount of receptors activated by these fields, then our gene expression will be differential.

Suppose on this arm bud (a 3d "pyramid") you were in a internal proximal, medial spot (inside the pyramid, toward the central line at the bottom). While I was at the "tip" of the pyramid.

Because of the different microgradients each of senses from our local environment, were going to activate different genes.

The gradient I sense leads to a cascade that says "divide and make both your progeny pluripotent stem cells)--Me being on the tip, growth needs to extend the arm.

While the field you sense activates a cascade which turns on genes that say "Divide and make one of your progeny a pluripotent stem cell and the other a mesenchymal stem cell (one capable of producing chondrocytes--which make cartilage).

By sensing the local environments around them and altering gene expression based on the local environment we can go from a single cell, to a person (or whale, or elephant).

 

[bobze]

So from an evolutionary perspective, changes to bauplan (like the whale loosing his legs) aren't because a "leg gene gets turned off", rather genes which control expression (probably better to think of them as expression cascades) get changed and that is what selection acts upon.

Maybe for instance (again, simplified) the cells which "sense" their in the developing whale leg respond less to the morphogenetic field because their genes (control of expression) says "if you find yourself in the leg, don't do this..." which leads to less expression and "less of a leg".

You also have to consider that embryological development is heavily regulated by apoptosis. Where structures do develop often, but genes are activated in those cells which say "you should commit suicide".

-I'm not sure what role, if any apoptosis plays in whale leg development (or lack there of), maybe a marine-type-biologist could answer that for us. But, you should be aware of it--Because again, depending on the cell and where it is (it knows because of fields) it may kill itself during development, altering a structure (there's lots of this in large animals like us).