Chromosomes (article) | Khan Academy
For a complete overview see the Issue and the Editorial of the degree of compaction of mitotic chromatin in relation to its interphase state Both types of condensins contribute to chromosome condensation with disparate. A couple of homologous chromosomes, or homologs, are a set of one maternal and one . Faulty segregation can lead to fertility problems, embryo death, birth defects, and cancer. Though the This medicine could be very prevalent in relation to cancer, as DNA damage is thought to be contributor to carcinogenesis. PDF | A chromosome is a single long DNA molecule assembled along its length with nucleosomes and proteins. During interphase, a.
One is when you're just dealing with your body cells and you need to make more versions of your skin cells, your DNA has to copy itself, and this process is called replication. You're replicating the DNA. So let me do replication. So how can this DNA copy itself?
And this is one of the beautiful things about how DNA is structured. So I'm doing a gross oversimplification, but the idea is these two strands separate, and it doesn't happen on its own.
It's facilitated by a bunch of proteins and enzymes, but I'll talk about the details of the microbiology in a future video. So these guys separate from each other. Let me put it up here. They separate from each other. Let me take the other guy. That guy looks something like that. They separate from each other, and then once they've separated from each other, what could happen? Let me delete some of that stuff over here.
Delete that stuff right there.
So you have this double helix. They were all connected. Now, they separate from each other. Now once they separate, what can each of these do? They can now become the template for each other. If this guy is sitting by himself, now all of a sudden, a thymine base might come and join right here, so these nucleotides will start lining up. So you'll have a thymine and a cytosine, and then an adenine, adenine, guanine, guanine, and it'll keep happening. And then on this other part, this other green strand that was formerly attached to this blue strand, the same thing will happen.
You have an adenine, a guanine, thymine, thymine, cytosine, cytosine. So what just happened? By separating and then just attracting their complementary bases, we just duplicated this molecule, right?
We'll do the microbiology of it in the future, but this is just to get the idea. This is how the DNA makes copies of itself. And especially when we talk about mitosis and meiosis, I might say, oh, this is the stage where the replication has occurred. Now, the other thing that you'll hear a lot, and I talked about this in the DNA video, is transcription.
In the DNA video, I didn't focus much on how does DNA duplicate itself, but one of the beautiful things about this double helix design is it really is that easy to duplicate itself.
You just split the two strips, the two helices, and then they essentially become a template for the other one, and then you have a duplicate. Now, transcription is what needs to occur for this DNA eventually to turn into proteins, but transcription is the intermediate step.
And then that mRNA leaves the nucleus of the cell and goes out to the ribosomes, and I'll talk about that in a second. So we can do the same thing. So this guy, once again during transcription, will also split apart.
So that was one split there and then the other split is right there. And actually, maybe it makes more sense just to do one-half of it, so let me delete that. Let's say that we're just going to transcribe the green side right here. Let me erase all this stuff right-- nope, wrong color. Let me erase this stuff right here. Now, what happens is instead of having deoxyribonucleic acid nucleotides pair up with this DNA strand, you have ribonucleic acid, or RNA pair up with this. And I'll do RNA in magneta.
So the RNA will pair up with it. And so thymine on the DNA side will pair up with adenine.
Chromosomes and Chromatin - The Cell - NCBI Bookshelf
Guanine, now, when we talk about RNA, instead of thymine, we have uracil, uracil, cytosine, cytosine, and it just keeps going. That mRNA separates, and it leaves the nucleus. It leaves the nucleus, and then you have translation. The transfer RNA were kind of the trucks that drove up the amino acids to the mRNA, and this all occurs inside these parts of the cell called the ribosome.
But the translation is essentially going from the mRNA to the proteins, and we saw how that happened. You have this guy-- let me make a copy here. Let me actually copy the whole thing. This guy separates, leaves the nucleus, and then you had those little tRNA trucks that essentially drive up.
So maybe I have some tRNA. Let's see, adenine, adenine, guanine, and guanine. A codon has three base pairs, and attached to it, it has some amino acid. And then you have some other piece of tRNA. Let's say it's a uracil, cytosine, adenine.
Chromatin Higher-order Structure and Dynamics
And attached to that, it has a different amino acid. Then the amino acids attach to each other, and then they form this long chain of amino acids, which is a protein, and the proteins form these weird and complicated shapes.
So just to kind of make sure you understand, so if we start with DNA, and we're essentially making copies of DNA, this is replication. You are transcribing the information from one form to another: Now, when the mRNA leaves the nucleus of the cell, and I've talked-- well, let me just draw a cell just to hit the point home, if this is a whole cell, and we'll do the structure of a cell in the future.
If that's the whole cell, the nucleus is the center. That's where all the DNA is sitting in there, and all of the replication and the transcription occurs in here, but then the mRNA leaves the cell, and then inside the ribosomes, which we'll talk about more in the future, you have translation occur and the proteins get formed. So mRNA to protein is translation. You're translating from the genetic code, so to speak, to the protein code.
So this is translation. So these are just good words to make sure you get clear and make sure you're using the right word when you're talking about the different processes. Now, the other part of the vocabulary of DNA, which, when I first learned it, I found tremendously confusing, are the words chromosome. I'll write them down here because you can already appreciate how confusing they are: So a chromosome, we already talked about.
You can have DNA. You can have a strand of DNA. That's a double helix. This strand, if I were to zoom in, is actually two different helices, and, of course, they have their base pairs joined up.
I'll just draw some base pairs joined up like that. So I want to be clear, when I draw this little green line here, it's actually a double helix. Now, that double helix gets wrapped around proteins that are called histones.
So let's say it gets wrapped like there, and it gets wrapped around like that, and it gets wrapped around like that, and you have here these things called histones, which are these proteins.
- CHROMATIN HIGHER-ORDER STRUCTURE
- Molecular Biology of the Cell. 4th edition.
Now, this structure, when you talk about the DNA in combination with the proteins that kind of give it structure and then these proteins are actually wrapped around more and more, and eventually, depending on what stage we are in the cell's life, you have different structures. But when you talk about the nucleic acid, which is the DNA, and you combine that with the proteins, you're talking about the chromatin. And the idea, chromatin was first used-- because when people look at a cell, every time I've drawn these cell nucleuses so far, I've drawn these very well defined-- I'll use the word.
So let's say this is a cell's nucleus. In general, heterochromatin tends to be located at the nuclear periphery, where specific interactions with the envelope may occur and often forms blocks surrounding the nucleolus.
These distinctions can be clearly seen in light and electron micrographs.
Transcription is largely confined to euchromatin, and it is interesting to note that Heitz presciently suggested a functional difference between the two forms. Today, the term heterochromatin is more loosely applied, and is often extended to include transcriptionally silent regions of chromatin regardless of their staining properties. An important distinction is made between constitutive and facultative heterochromatin.
Constitutive heterochromatin is always compact, and tends to be enriched in repetitive, gene-poor, and late replicating DNA sequences, whereas facultative heterochromatin can reversibly undergo transitions from a compact, transcriptionally inactive state to become more open, and transcriptionally competent.
During embryogenesis, for example, the amount of facultative heterochromatin increases as unwanted sets of genes are progressively shut down until at maturity, a cell expresses only the genes appropriate for that tissue.
The reverse occurs when, for example, differentiated cells are reprogrammed to become stem cells. These events are typically accompanied by profound changes in histone variants, histone modifications, and the presence of CAPS.
A recent comparison of properties of heterochromatin and euchromatin as diffusion barriers has yielded interesting and provocative results Bancaud et al. Measurements of diffusion constants of large polymers within these nuclear compartments confirmed that heterochromatin constitutes a more crowded environment, leading to the more efficient trapping of chromatin binding proteins such as histone H1.
The crowding effect was also suggested to assist in the maintenance of heterochromatin. Further, kinetic analyses indicated an anomalous component of diffusion that was interpreted in terms of a fractal chromatin organization at spatial scales below nm. The ubiquitous location of heterochromatin at the nuclear periphery and association with the nuclear lamina and nuclear envelope suggests that this location is both structurally and functionally important.
It was therefore surprising to read that, in the rod photoreceptor cells of nocturnal, but not diurnal, mammals, heterochromatin is concentrated in the center of nuclei Solovei et al. The authors postulate that with this arrangement, nuclei act as collecting lenses, providing additional sensitivity in very low light environments.
This unexpected finding underscores the plasticity of chromatin organization. Further, it is not at all clear whether the various loop phenomena that have been reported constitute distinct level s of chromatin higher-order structure Kadauke and Blobel It is clear, however, that loop phenomena vary in terms of their stability. For example, enhancer-promoter loops that facilitate transcription are transitory, dynamic events, whereas other types of loops appear to be more stable.
The halos were shown to consist of supercoiled DNA, suggesting that the DNA twisting that occurs when histones are removed from nucleosomes is preserved by being anchored in the residual nuclear structure. This finding is also consistent with the concept of an insoluble proteinaceous nuclear matrix or karyoskeleton to which chromatin loops are anchored by DNA sequences referred to as matrix attachment regions MARs.
However, because it has not been possible to define its composition and structure, the matrix remains a useful working concept rather than a well-accepted structure in the same sense as the cytoskeleton Pederson The supposition that these different loop phenomena reflect the same underlying chromatin organization was called into question by a surprising recent finding that halo diameter was related to the spacing of origins of replication during the previous S phase Courbet et al.
Under conditions of rapid replication, origins were widely spaced, leading to large halos, whereas slow replication triggered the firing of additional replication origins, and led to smaller halos. Halos can also be generated from metaphase chromosomes, and giant meiotic lampbrush chromosomes provide a particularly compelling example of large chromatin loops and their relation to transcriptionally coupled genes. The interaction between enhancers and promoters probably represents an unrelated manifestation of chromatin looping that is critical for transcriptional activity.
Enhancer sequences are often many Kb distant from promoters, and may be located upstream, downstream, or on a different chromosome. There seems now to be a consensus that physical interaction between enhancer and promoter is necessary to initiate transcription Visel et al. One possibility, supported by recent data Nolis et al.
Finally, the recently introduced technique of chromosome conformation capture 3C and related methods, which allow mapping of physical chromatin interactions in vivo, is providing growing evidence for physical interactions between distant loci other than enhancer-promoter juxtapositions Gondor and Ohlssen Hints that there must be mechanisms for bringing specific loci together has come from the common occurrence of some chromosomal translocations, especially those leading to human diseases. For example, Roix et al.
Human prostate cancer offers a system for tracking the physical proximity of two loci. The mechanism s involved in this large-scale motion remain unknown. Another recent study of intranuclear chromatin associations capitalizing on massively-parallel sequencing has yielded important insights into the large scale organization of chromatin Lieberman-Aiden et al.