cell?
July 13, 2005 9:50 PM Subscribe
How do cells form various shapes?
A lot of cells are just round blobs, but some of them have pretty complicated shapes (like nerve cells) how to cells build structures like axons and dendrites, or flagella or whatever?
Bonus question: how is gene expression regulated by chemicals in the cell. I get the idea that hormones, and other chemicals alter gene expression inside a cell How does this work? (I mean I realize its probably different for all different kind of chemicals, but is there a sort of general mechanism?)
I have an idea for a genetic cellular simulator based on some simple rules that sort of approximate real world phenomena, but I'd like to know how those two process work.
A lot of cells are just round blobs, but some of them have pretty complicated shapes (like nerve cells) how to cells build structures like axons and dendrites, or flagella or whatever?
Bonus question: how is gene expression regulated by chemicals in the cell. I get the idea that hormones, and other chemicals alter gene expression inside a cell How does this work? (I mean I realize its probably different for all different kind of chemicals, but is there a sort of general mechanism?)
I have an idea for a genetic cellular simulator based on some simple rules that sort of approximate real world phenomena, but I'd like to know how those two process work.
Best answer: Tubilin and Actin are long proteins that form chains with one another - these and other filementeous proteins (a new one in bacteria has recently [this february] been identified) - dictate cell shape.
As far as I know - the precise mechanism and how it's controlled is not currently known.
A quick search on pubmed reinforces the "we have no fricken idea" idea, although more and more protiens are being identified.
Throw in lipid rafts and endoplasmic reticulum trafficking of proteins (and how they get delivered to the right address) - you're over your head if you think you can model a cell.
If you could, though - and prove that it's a decent model - I would want you to mention my name when they give you your nobel prize.
posted by PurplePorpoise at 10:35 PM on July 13, 2005
As far as I know - the precise mechanism and how it's controlled is not currently known.
A quick search on pubmed reinforces the "we have no fricken idea" idea, although more and more protiens are being identified.
Throw in lipid rafts and endoplasmic reticulum trafficking of proteins (and how they get delivered to the right address) - you're over your head if you think you can model a cell.
If you could, though - and prove that it's a decent model - I would want you to mention my name when they give you your nobel prize.
posted by PurplePorpoise at 10:35 PM on July 13, 2005
Best answer: Oh, right- there's also contact inhibition.
Normall cells - when they contact other cells, will stop growing/dividing. Other cells don't. It's also not entirely understood why this may/may-not be true for different axes.
Also, cells in culture (will/sometimes/always - depends on cell type) be morphologically/behave morphologically-in-response-to different stimuli depending on whether it's in culture or where the cell is "supposed to be." There's also 2d vs 3d behavior - this is something that someone should be pressing NASA into doing in orbit.
Transformed ("immortalized," or "made into cancer" - it's a little more subtle than that) cells can sometimes overcome contact-inhibition (it touches another cell - it stops growing) but sometime it doesn't. It's a complicated an incompletely understood function.
posted by PurplePorpoise at 10:42 PM on July 13, 2005
Normall cells - when they contact other cells, will stop growing/dividing. Other cells don't. It's also not entirely understood why this may/may-not be true for different axes.
Also, cells in culture (will/sometimes/always - depends on cell type) be morphologically/behave morphologically-in-response-to different stimuli depending on whether it's in culture or where the cell is "supposed to be." There's also 2d vs 3d behavior - this is something that someone should be pressing NASA into doing in orbit.
Transformed ("immortalized," or "made into cancer" - it's a little more subtle than that) cells can sometimes overcome contact-inhibition (it touches another cell - it stops growing) but sometime it doesn't. It's a complicated an incompletely understood function.
posted by PurplePorpoise at 10:42 PM on July 13, 2005
Best answer: delmoi posted "Bonus question: how is gene expression regulated by chemicals in the cell. I get the idea that hormones, and other chemicals alter gene expression inside a cell How does this work?"
Wow. This is a major focus of current research in cellular and molecular biology. Regulatory pathways are immensely complex. You could probably get a lot of the background you would need to appreciate this complexity by reading The Molecular Biology of the Cell. We currently lack a complete understanding of the processes involved, though certain specific pathways are well-understood. I'd hesitate to say that there's "a sort of general mechanism".
I have an idea for a genetic cellular simulator based on some simple rules that sort of approximate real world phenomena, but I'd like to know how those two process work.
A lot of people are working on stuff like this. Be careful that you're not just replicating someone else's effort....
You mention flagella and "responding to chemicals". If you're interested in the simplest case, you might want to look into bacterial chemotaxis. It's pretty well understood for some species, at least.
posted by mr_roboto at 10:55 PM on July 13, 2005
Wow. This is a major focus of current research in cellular and molecular biology. Regulatory pathways are immensely complex. You could probably get a lot of the background you would need to appreciate this complexity by reading The Molecular Biology of the Cell. We currently lack a complete understanding of the processes involved, though certain specific pathways are well-understood. I'd hesitate to say that there's "a sort of general mechanism".
I have an idea for a genetic cellular simulator based on some simple rules that sort of approximate real world phenomena, but I'd like to know how those two process work.
A lot of people are working on stuff like this. Be careful that you're not just replicating someone else's effort....
You mention flagella and "responding to chemicals". If you're interested in the simplest case, you might want to look into bacterial chemotaxis. It's pretty well understood for some species, at least.
posted by mr_roboto at 10:55 PM on July 13, 2005
Best answer: The most basic way of putting it: cells aren't just fluid sacs. There are proteins both inside and outside that help provide structure beyond the lipid membrane. Most cells have some amount of internal protein... scaffolding, I suppose, is a reasonable way to put it. It's called the cytoskeleton, and it helps both to give the cell its shape and to allow it to move [depending on what kind of cell it is.] The composition of the cytoskeleton will vary between cell types [and even within regions of a cell], but some common components are tubulin [which forms largish microtubules], actin [which forms tiny microfilaments, and often binds with myosin to allow for intracellular movement], and keratin [which forms intermediate filaments.] As for how things are built, well, it's sort of like building stuff using one of the new fancy lego kits - only certain things will bind to certain other things, and when they bind, they're physically constrained to binding in certain ways. I'm not very familiar with the details, and I suspect that [like most things about cell function] they're still being studied.
Flagella and cilia are also made up of similar proteins. Microtubules are a large component in those structures, I believe, in the form of tubulin [or perhaps flagellin in prokaryotes.] Other proteins are also involved, but the point is that both cilia and flagella are essentially protein structures, not just "the cell squished into a weird shape." Again, I suspect that the mechanisms by which flagella assemble themselves are not yet fully known.
As for gene expression and chemical regulation: it depends on which gene system you're talking about. One classic example is the lac operon. The explanation on that site is pretty good. When there's no lactose, the repressor protein [produced by lacI] can bind to the DNA in front of the lacZ protein and prevent it from being produced. When there's lactose in the system, the lactose binds to the repressor protein and makes it incapable of binding to DNA, so RNA polymerase can bind to the DNA and produce the protein [beta-galactosidase] coded for by lacZ. This system is one of the simplest around, unfortunately - many systems include whole chains of genes, and aren't yet understood by scientists. There are a bunch of ways a chemical might start production of a protein - it might bind directly to the DNA in front of the protein sequence and encourage transcription, it might bind to another protein that does something similar, it might directly block [or bind to a protein that blocks] the production of a repressor that prevents the production of a target protein, etc.... you can see how this gets complicated real quickly. Similarly, a chemical might directly bind to the region in front of the protein sequence and block transcription, it might bind to another protein, activating it to block transcription, it might bind somewhere else and encourage the production of a protein that represses the production of the target protein, etc... It's like a game of Mousetrap, in a way, but way more touchy and complicated. Chemical pathways, signaling systems, and genetic regulation are all huge topics being studied these days, but because of the complexity even researchers have no idea how much of it works - so far, at least.
As PurplePorpoise says, if you can manage to even half-accurately model the simplest of cells, you'll be besieged by biologists. Computer models of biological systems are really popular these days as well, but due to both complexity and lack of information, accurately and completely modelling a cell is beyond everyone. Modelling the interactions of a few proteins and chemicals is about the level most people are at. You've set yourself a pretty hard task - heck, you haven't even gotten to cell division, protein production and post-translational modification, cell aging, the composition of the cell membrane, the exterior environment, cell movement [since it looks like you're considering mobile cells], etc... But good luck, and if you do end up publishing, give me a citation, eh?
posted by ubersturm at 11:02 PM on July 13, 2005
Flagella and cilia are also made up of similar proteins. Microtubules are a large component in those structures, I believe, in the form of tubulin [or perhaps flagellin in prokaryotes.] Other proteins are also involved, but the point is that both cilia and flagella are essentially protein structures, not just "the cell squished into a weird shape." Again, I suspect that the mechanisms by which flagella assemble themselves are not yet fully known.
As for gene expression and chemical regulation: it depends on which gene system you're talking about. One classic example is the lac operon. The explanation on that site is pretty good. When there's no lactose, the repressor protein [produced by lacI] can bind to the DNA in front of the lacZ protein and prevent it from being produced. When there's lactose in the system, the lactose binds to the repressor protein and makes it incapable of binding to DNA, so RNA polymerase can bind to the DNA and produce the protein [beta-galactosidase] coded for by lacZ. This system is one of the simplest around, unfortunately - many systems include whole chains of genes, and aren't yet understood by scientists. There are a bunch of ways a chemical might start production of a protein - it might bind directly to the DNA in front of the protein sequence and encourage transcription, it might bind to another protein that does something similar, it might directly block [or bind to a protein that blocks] the production of a repressor that prevents the production of a target protein, etc.... you can see how this gets complicated real quickly. Similarly, a chemical might directly bind to the region in front of the protein sequence and block transcription, it might bind to another protein, activating it to block transcription, it might bind somewhere else and encourage the production of a protein that represses the production of the target protein, etc... It's like a game of Mousetrap, in a way, but way more touchy and complicated. Chemical pathways, signaling systems, and genetic regulation are all huge topics being studied these days, but because of the complexity even researchers have no idea how much of it works - so far, at least.
As PurplePorpoise says, if you can manage to even half-accurately model the simplest of cells, you'll be besieged by biologists. Computer models of biological systems are really popular these days as well, but due to both complexity and lack of information, accurately and completely modelling a cell is beyond everyone. Modelling the interactions of a few proteins and chemicals is about the level most people are at. You've set yourself a pretty hard task - heck, you haven't even gotten to cell division, protein production and post-translational modification, cell aging, the composition of the cell membrane, the exterior environment, cell movement [since it looks like you're considering mobile cells], etc... But good luck, and if you do end up publishing, give me a citation, eh?
posted by ubersturm at 11:02 PM on July 13, 2005
Best answer: I just want to say that it is spelled tubulin. Normally I wouldn't bother but you might be doing searches and it is worthwhile to spell it correctly. I think you should read this Wikipedia article for some basics. Also, note that there are some basic molecular biology textbooks online although you can only search through them, not read them cover-to-cover.
I don't want to discourage you (especially before I've heard the idea!), but I'll note that researchers have a fair amount of difficulty trying to model even small areas within a cell.
posted by grouse at 11:42 PM on July 13, 2005
I don't want to discourage you (especially before I've heard the idea!), but I'll note that researchers have a fair amount of difficulty trying to model even small areas within a cell.
posted by grouse at 11:42 PM on July 13, 2005
Best answer: Another vote for MBOC. I could type for the next 8 hours and it'd barely put a dent in what's known.
MBOC is a fascinating book. I wish I could generally finish it before the next edition came out. Sigh.
The companion book, MBOG, answers your second question. If you really want to learn the answer, though, read Mark Ptashne's A Genetic Switch first. Once you understand how a virus that infects bacteria operates, you'll be better able to expand your understanding to higher eukaryotes like us.
You need a decent background in high school chem and biology to understand these books.
posted by ikkyu2 at 8:04 AM on July 14, 2005
MBOC is a fascinating book. I wish I could generally finish it before the next edition came out. Sigh.
The companion book, MBOG, answers your second question. If you really want to learn the answer, though, read Mark Ptashne's A Genetic Switch first. Once you understand how a virus that infects bacteria operates, you'll be better able to expand your understanding to higher eukaryotes like us.
You need a decent background in high school chem and biology to understand these books.
posted by ikkyu2 at 8:04 AM on July 14, 2005
Response by poster: Throw in lipid rafts and endoplasmic reticulum trafficking of proteins (and how they get delivered to the right address) - you're over your head if you think you can model a cell.
I'm not planning on modeling a *real* cell, but rather a simple abstract cell that was complicated enough to evolve intresting multicellular structures.
posted by delmoi at 9:38 AM on July 14, 2005
I'm not planning on modeling a *real* cell, but rather a simple abstract cell that was complicated enough to evolve intresting multicellular structures.
posted by delmoi at 9:38 AM on July 14, 2005
Response by poster: Thanks for the answers everyone, very informative. Molecular Biology of the Cell is in my amazon cart and the others are in the "save for later" section. I'm really intrested in the "nitty gritty" low-level biology stuff, and I'm starting to think I'd like to go back to school some time and get a degree in it, after I make some money :)
Let me elaborate a bit on what I want to accomplish here. Rather then a full-on cellular simulator, the goal is to try to create a sort of abstract system that is similar to a real cellular system in that multicultural systems could be constructed, or evolved. This is just for personal enrichment for now, although I have some ideas for more intresting Comp Sci research that could be based on such a system.
Anyway, fantasic answers everyone, thanks a lot :)
posted by delmoi at 9:59 AM on July 14, 2005
Let me elaborate a bit on what I want to accomplish here. Rather then a full-on cellular simulator, the goal is to try to create a sort of abstract system that is similar to a real cellular system in that multicultural systems could be constructed, or evolved. This is just for personal enrichment for now, although I have some ideas for more intresting Comp Sci research that could be based on such a system.
Anyway, fantasic answers everyone, thanks a lot :)
posted by delmoi at 9:59 AM on July 14, 2005
Response by poster: Way-late update: bought a copy of mboc, and read the first 9 or so chapters. Very facinating, and I really should read more some time.
posted by delmoi at 9:46 AM on February 13, 2006
posted by delmoi at 9:46 AM on February 13, 2006
This thread is closed to new comments.
RBC's have the "donut without a hole" shape because they have an internal "skeletal" structure made up of two structural proteins, ankyrin and spectrin, that hold the cell in that shape. It's ideal for an RBC to be that flattened shape because it increases the surface area for oxygen to attach to, and also because the flat-donut shape can twist and bend well enough to get around the bloodstream and capillaries pretty well. The two proteins build something like a scaffolding structure inside the cell to keep it shaped like that.
If there is a defect in the genes that create the ankyrin and/or spectrin protein interior structure, then the RBC would just contract to its smallest possible surface area, which is a sphere. It would be rigid and more likely to burst (high osmotic fragility) and wouldn't hold quite as much oxygen as a regular RBC. This is called spherocytosis. It is also more likely to get mistaken by the spleen for an old worn-out RBC and thus be broken down, because one way that the spleen recognizes old blood cells is that their skeletal structure is a little off and they're funny-shaped.
This constant breaking down of RBC's is known as auto-hemolysis, which is where your body is (mistakenly) breaking down your own blood supply. This leads to enlargement of the spleen (because it's working overtime), fatigue (because you have to keep creating new blood in your bone marrow at a greatly increased rate), gallstones (because the bilirubin from the broken down cell wals builds up in your gallbladder), and jaundice (because your liver has extra iron in it from the released hemoglobin from the broken down cells) . Not fun.
(Luckily, most of us do okay after a spleenectomy...)
posted by Asparagirl at 10:14 PM on July 13, 2005