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| subject: | Re: Endoderm, Mesoderm, E |
On Sat, 3 May 2003 23:59:38 +0000 (UTC), "Robert Karl Stonjek" wrote: >>norman: >You are perfectly correct about the evolution of lungs. I was simply >careless in my description. The lung did not evolve from a swim >bladder. Rather, both the bony fish swim bladder and the tetrapod lung >erived from a respiratory structure in an early form of lungfish. The >point is still valid, though, our lungs derive from a structure >developed from the digestive tract and so are endodermal in origin. > >Thyroxine and the steroid hormones, in particular, are well known to >influence gene expression. In fact, "the mechanism of action of these >hormones is to modulate gene expression in target cells" >http://arbl.cvmbs.colostate.edu/hbooks/pathphys/endocrine/moaction/intra >cell.html >or "The overall mechanism of steroid hormone action is the regulation >of gene expression" (http://www.people.vcu.edu/~urdesai/estr.htm) > >RKS: >Thanks, Norman. Say, you wouldn't happen to know if there is any >relationship between the human endocrine system and gene expression?? I >suspect that the relationship between hormones and gene expression is >restricted to the cellular level, but then hormones in the blood can >eventually impact on individual cells, I guess. The point of thyroxine and the steroid hormones is that they are directly connected to gene expression. That is exactly how they work, by controlling the expression of genes. Other hormones ordinarily work though the "signaling system" I originally referred to. That is, you are exactly correct in saying that the only ways that hormones in the blood can act is by their impact on individual cells and the effect is restricted to the cellular level. The way this works is that the hormone (a non-thyroxine or non-steroid hormone anyway) binds to a protein receptor on the outside of the cell membrane. This leads the piece of that protein sticking inside of the membrane to become altered in structure and function and initiate a process that eventually leads to the activation of enzymes (protein kinases) that cause protein phosphorylation (the addition of a phosphate group to a tyrosine or methionine or threonine). The modified protein then has modified properties. Since you can phosphorylate just about every kind of protein found inside a cell, you can influence enzyme reactions, membrane transport, secretion, contractility, excitability, cell division, and gene transcription that way. That is, hormones can influence anything and everything that a cell does. One specific mechanism might be a hormone that binds with what is called a "G-protein coupled receptor". That activates a G protein which activates an enzyme called adenyl cyclase. That enzyme produces a chemical called cAMP. cAMP activates a protein called PKA (protein kinase A) which can phosphorylate other proteins. One protein it can phosphorylate is called CREB (cAMP response element binding protein) which can bind to a specific segment of DNA called the cAMP response element to turn on or turn off transcription of specific genes. Yes, it does seem like a rather overelaborate and complex process, but don't blame me! I didn't design it. In fact that is, in my mind, one very powerful argument against "intelligent design". No competent designer in his/her right mind would every dream up such a complex and cockeyed scheme. So, yes, hormones very definitely can and do influence gene transcription. In general, hormones are examples of one cell "sending a signal" to another cell by means of a chemical. And cell signaling systems very definitely can and do influence gene transcription. This is exactly what is going on during cell differentiation and development, when one cell influences the way a nearby cell develops. --- þ RIMEGate(tm)/RGXPost V1.14 at BBSWORLD * Info{at}bbsworld.com --- * RIMEGate(tm)V10.2áÿ* RelayNet(tm) NNTP Gateway * MoonDog BBS * RgateImp.MoonDog.BBS at 5/4/03 3:26:52 PM* Origin: MoonDog BBS, Brooklyn,NY, 718 692-2498, 1:278/230 (1:278/230) SEEN-BY: 633/267 270 @PATH: 278/230 10/345 106/1 2000 633/267 |
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