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Why the genome is divided into several chromosomes and not just a single big chromosome?

Why the genome is divided into several chromosomes and not just a single big chromosome?


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In many eukaryote species, there are several chromosomes. In humans, for example, there are 23 pairs of chromosomes.

Why are there several chromosomes and not just a join of all chromosomes into a single big chromosome?


The leading contender of "why" in my former lab, is that if a chromosome becomes too long, a cell cannot fully isolate the chromatid to a daughter cell. Ie in a giant chromosome, the chromosome arms trail so far behind centromere, that the arms are of two sister chromosome are still touching each other even through the centromere have reached the opposite poles of a dividing cell. This prevents nuclear reformation. It would also mean, that the size of the cell will determine the chromosome maximum size.

At present this is a hypothesis. We have only just created the method to make ultra large synthetic chromosomes. I expected an answer is 3-5 years (2021-2023). However we say there is nothing special to a chromosome number.


Short Answer: Humans reproduce sexually and evolution, with some random effects, has led to 23 pairs of chromosomes.

Explained:

Reproduce Sexually - Bacteria do have one large piece of DNA. This works for bacteria because they will copy all their DNA, and split the two copies creating two "clones" of each other. Humans, on the other hand, half the amount of genetic material in their sex cells (sperm and egg), which when combined together in a zygote sums to the full or normal amount of DNA. This is why nearly every cell in the human body has 23 pairs, or 46 total chromosomes. To have sexual reproduction we therefore need at least 2 chromosomes in the normal, or diploid, cells.

Randomness - While evolution is often taught as a very directed process, there is actually a great deal of randomness that shift outcomes. The best example is that apes, our closes descendent have 24 chromosomes. In becoming human, two of theses chromosmes somewhat randomly fused together into the human chromosome 2. While there could be some selection advantage, what it would be is unclear. Similarly, many other species have a variety of chromosome number. Biologists have been unable to directly relate a cause for the number of chromosomes in each species (see UCSB and Museum of Innovation), and have therefore determined that the number is mostly based on random effects. A good metaphor is that a chromosome is a bookshelf and genes books, the character of a library is not defined by the number of bookshelves or books, but rather the contents of the books.

Evolution - Chromosomes fill several important roles in a cell. Firstly, during normal cell life they unravel partially and gain/lose different markers (histone marks), which can direct different proteins as to which genes should be transcribed. Secondly, during mitosis the chromosomes must become very compact, and split exactly along the mitotic plane, and during meiosis the chromosomes crossover, exchanging DNA with the other pair. The mechanics of each event is inherently based on the size and number of chromosome. For all of these roles, the number of chromosomes clearly has some impact, although the exact relationship is unclear. So while evolution may select for an optimal number, the strength of the selection is likely very weak and overpowered by the random effects.


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Hi - I've recently become interested/fascinated by genetics my basic question is:- 'why' is the [human] genome split into separate chromosomes rather than being one long strand and what determines[ed] which genes went to which chromosome?

-A curious adult from the United Kingdom

You're right that these questions are basic. But this doesn't mean they are simple. Sometimes the simplest questions about biology and genetics are the hardest to answer.

To some extent the number of chromosomes and which genes are on each chromosome may be due to blind evolutionary chance. But that's not the whole story.

Why is the human genome split into separate chromosomes rather than being one long strand?

First let me remind you that we humans have 46 chromosomes in each of our cells. So why 46 chromosomes? Why not one giant one?

Some of the simplest forms of life, like bacteria, keep all of their DNA in a single chromosome. However, more complex creatures (like humans!) divide their DNA into lots of different chromosomes.

One reason for this difference may have to do with how each kind of beast makes babies. Bacteria make new bacteria asexually. This means that when they make new bacteria, they just split in two with each half getting a copy of the same DNA.

Most other creatures make new offspring sexually. What this does is combine DNA from two parents to make the child.

We all have two copies of every chromosome (except males who have one X and one Y plus 22 other pairs). Mom and dad give us copies of half their DNA -- one of each chromosome. At the end, we all have two copies of each of our chromosomes just like mom and dad. But our DNA is a mix of mom's and dad's.

Each egg or sperm gets 23 chromosomes (half of each pair). Which chromosome they get in the pair is totally random. When you do the math, this comes out to 10 trillion different possible combinations. If we had only one pair of chromosomes, the number drops to 4.

Of course, none of this would matter if the chromosomes were exactly the same between mom and dad. Luckily they're not. In fact, there is on average 6 million differences between any two people's DNA.

The mixing of DNA in this way generates lots of these differences. This 'genetic diversity' is very important for survival. Not necessarily the survival of any one individual, but for the species as a whole.

Say, for example, a new deadly disease hits (think of the plague during the Middle Ages). Lots of people would die, but some would live. Some of these survivors would live because they had the right set of DNA differences.

And reproducing sexually increases genetic diversity hugely. Without it, we'd have to rely on random DNA changes which wouldn't cause as much mixing. And random changes can cause lots of problems with "bad" mutations that mixing doesn't.

So this addresses the question of why we don't simply have one long strand of DNA. We need more than one to increase genetic diversity.

But why 46 exactly? How (or why) we ended up with exactly 46 chromosomes is somewhat of an evolutionary mystery.

Generally speaking though, species that are closely related have a similar number of chromosomes. For example, chimpanzees and other great apes, our closest evolutionary cousins, have 48.

Over time, pieces of chromosomes break off and stick to other chromosomes. Sometimes whole chromosomes stick to other chromosomes. At some point in the last 6-8 million years, two of our chromosomes fused together to make our chromosome 2. We know this because our chromosome 2 is really just two chimpanzee chromosomes fused together.

It is this sort of rearrangement that helped to give our current number of chromosomes. As you can see from this example, this number is certainly not fixed, it can and does change.

So similar species tend to have a similar number of chromosomes. But aside from this general rule there is very little rhyme or reason to how many chromosomes a species has.

For example, the number doesn't have to do with how complicated the species is. We have 46 chromosomes but a goldfish has 94, and a certain type of fern (Ophioglossum reticulatum) has 1,260. And it's safe to say we're more complex than a fern!

What determines which genes are on which chromosome?

This is another interesting question for which I'm afraid I don't have a straightforward answer. To some extent it may be that which genes are on which chromosomes is the luck of the evolutionary draw.

We know that chromosomes contain different genes or "chunks" of the genome. Genes are simply stretches of DNA that contain instructions in a 4 letter, 64 word code for making a protein.

Proteins are the workers in the cell. Almost anything that needs doing is done by a protein. They carry our oxygen, help us see and even think!

In bacteria, those simple organisms with only one chromosome, the genes are organized into groups based on what the genes do for a living. For example, all the genes needed to digest lactose, the sugar found in milk, are grouped together on the chromosome.

When there is lactose around, all the genes can get used together. Our genes may have started out similarly a billion years ago or so. But then those rearrangements we talked about earlier started happening. Also, for reasons we won't go into, virus-like DNA picked up genes and moved them around. The end result is that our genes started getting separated and moved around.

In humans for example, the gene for alpha globin, a part of the hemoglobin protein that carries oxygen in red blood cells, is found on chromosome 16. However, the gene for beta globin, the other part of the hemoglobin protein, is found on chromosome 11.

Of course, our genes aren't just a jumbled mess. Some parts of our chromosomes are organized by function.

The infamous Y chromosome contains all the genes needed for 'maleness'. Since both males and females have X chromosomes, the genes for 'femaleness' are not grouped on the X chromosome but instead are spread throughout the genome.

Chromosome rearrangements and gene hopping may make the order of our genes less organized. But there is another process at work that makes groups of genes that are more organized on our chromosomes. This is called 'gene duplication'.

Like it sounds, gene duplication is when a region of DNA on a chromosome containing a gene gets copied. This new version of the gene becomes part of the genome and lives very close to its parent gene on the chromosome (unless a rearrangement happens!).

Gene duplication is one way that new genes are born. Over time, small changes build up in human DNA. These random changes, or mutations, occur differently in the DNA of each version of the gene.

What can happen is that the mutations cause the two genes to evolve different jobs. After awhile, you end up with a new gene having a new function.

But these two genes are near each other and usually do pretty similar sorts of jobs. This results in more organization as genes that are doing similar things are near each other.

I hope these answers help you to understand a little bit about why our genes and chromosomes are set-up the way they are. As you can see, we scientists are just beginning to understand the answers to these very interesting and important questions ourselves. Thanks for asking!


Why Do Most Humans Have 23 Pairs of Chromosomes?

You may have heard that 137 is the magic number, but if you ask a geneticist, they'll tell you the real magic is in 46. Why 46? Because that's the total number of chromosomes found in almost every human cell — 23 pairs to be exact — and those little thread-like structures pack all the information about who you are and what makes you unique.

DNA and Chromosomes

To understand what chromosomes are, you first have to understand what DNA is. Formally known as deoxyribonucleic acid, DNA is a complex molecule found in all plants and animals. It's found in almost every cell of an organism's body, and it contains all the information necessary to keep that organism up and running (and developing and reproducing). DNA also is the primary way organisms pass on hereditary information. In the process of reproduction, a portion of DNA is passed along from parent to offspring. In short, DNA is what tells the story of your totally unique biology.

As you can probably imagine, DNA has to be pretty long to hold all that important info. And it is — if you stretched the DNA in just one cell all the way to its full length, it would be about 6.5 feet (2 meters) long, and if you put the DNA in all your cells together, you'd have a chain about twice the diameter of the solar system.

Luckily, cells are pretty smart and have an ingenious way of packaging all that info into space-efficient parcels. Enter: the chromosome.

With its name rooted in the Greek words for color (chroma) and body (soma), the chromosome is a cell structure (or body) that scientists can spot under a microscope by staining it with colored dyes (get it?). Each chromosome is made up of protein and — you guessed it — DNA.

Every chromosome contains exactly one molecule of DNA, to be exact, and that long string of genetic info is tightly wrapped around the protein (called a histone), which acts like a spool, efficiently bundling the lengthy, info-rich molecule into the perfect size and shape to fit inside the nucleus of a cell. Every human cell has 23 pairs of chromosomes for a total of 46 (aside from sperm and egg cells, which each contain only 23 chromosomes).

Why 23 Pairs?

The magic number of 46 (23 pairs) per cell isn't universal among living things. First, though, humans also happen to be a "diploid" species, which means that most of our chromosomes come in matched sets called homologous pairs (the two members of each pair are called homologues). A lot of animals and plants are diploid, but not all of them have a total number of 46. Mosquitoes, for example have a diploid chromosome number of six, frogs have 26 and shrimp have a whopping 508 chromosomes!

But why do humans have 23 pairs? It happened during evolution. "Humans have 23 pairs of chromosomes, while all other great apes (chimpanzees, bonobos, gorillas and orangutans) have 24 pairs of chromosomes," Belen Hurle, Ph.D., says via email. Hurle is a research fellow at the National Human Genome Research Institute at the National Institutes of Health. "This is because in the human evolutionary lineage, two ancestral ape chromosomes fused at their telomeres [tips], producing human chromosome 2. Thus, humans have one fewer pair of chromosomes. This is one of the main differences between the human genome and the genome of our closest relatives."

Now let's go back to that sperm and egg issue — these cells only have one homologous chromosome from each pair and are considered "haploid." Here's why: When a sperm and egg fuse, they combine their genetic material to form one complete, diploid set of chromosomes. And if you think about it, that makes perfect sense. It means each parent contributes one homologue to a homologous pair of chromosomes in their child's cells.

Consider blood type as a clear example: People with AB blood type inherited two different gene variations on their two homologous chromosomes — one for A and one for B — that, when combined, produced AB.

Too Many or Too Few Chromosomes

Now you know the textbook example of a healthy human has 23 pairs of chromosomes in almost every cell of their body, but life isn't always a textbook. What happens if something causes more or less chromosomes to develop? A gain or loss of chromosomes from the standard 46 (called aneuploidy) occurs either during the formation of reproductive cells (sperm and egg), in early fetal development or in any other cell of the body after birth.

One of the more common forms of aneuploidy is "trisomy," which is the presence of an extra chromosome in the cells. One well-known result of trisomy is Down syndrome, which is a condition caused by three copies of chromosome 21 in each cell. This extra chromosome leads to a total of 47 chromosomes per cell, rather than 46.

The loss of one chromosome in a cell is called "monosomy," and describes a condition in which people have just one copy of a specific chromosome per cell as opposed to two. Turner syndrome, in which women have only one copy of the X chromosome per cell versus the regular two, is considered a form of monosomy.

There are other variations of aneuploidy as well, and in extreme cases, they may compromise a person's life. Additionally, cancer cells also have alterations in their number of chromosomes. Unlike the variations that happen in reproductive cells, these changes occur in other cells of the body, so they're not inherited.

The X and Y chromosomes weren't named randomly — their shapes actually resemble the letters X and Y, respectively.


How many chromosomes do humans have?

The typical number of chromosomes in a human cell is 46: 23 pairs, holding an estimated total of 20,000 to 25,000 genes. One set of 23 chromosomes is inherited from the biological mother (from the egg), and the other set is inherited from the biological father (from the sperm).

Of the 23 pairs of chromosomes, the first 22 pairs are called "autosomes." The final pair is called the "sex chromosomes." Sex chromosomes determine an individual's sex: females have two X chromosomes (XX), and males have an X and a Y chromosome (XY). The mother and father each contribute one set of 22 autosomes and one sex chromosome.

The typical number of chromosomes in a human cell is 46: 23 pairs, holding an estimated total of 20,000 to 25,000 genes. One set of 23 chromosomes is inherited from the biological mother (from the egg), and the other set is inherited from the biological father (from the sperm).

Of the 23 pairs of chromosomes, the first 22 pairs are called "autosomes." The final pair is called the "sex chromosomes." Sex chromosomes determine an individual's sex: females have two X chromosomes (XX), and males have an X and a Y chromosome (XY). The mother and father each contribute one set of 22 autosomes and one sex chromosome.


The demise of men?

As we argue in a chapter in a new e-book, even if the Y chromosome in humans does disappear, it does not necessarily mean that males themselves are on their way out. Even in the species that have actually lost their Y chromosomes completely, males and females are both still necessary for reproduction.

In these cases, the SRY “master switch” gene that determines genetic maleness has moved to a different chromosome, meaning that these species produce males without needing a Y chromosome. However, the new sex-determining chromosome – the one that SRY moves on to – should then start the process of degeneration all over again due to the same lack of recombination that doomed their previous Y chromosome.

However, the interesting thing about humans is that while the Y chromosome is needed for normal human reproduction, many of the genes it carries are not necessary if you use assisted reproduction techniques. This means that genetic engineering may soon be able to replace the gene function of the Y chromosome, allowing same-sex female couples or infertile men to conceive. However, even if it became possible for everybody to conceive in this way, it seems highly unlikely that fertile humans would just stop reproducing naturally.

Although this is an interesting and hotly debated area of genetic research, there is little need to worry. We don’t even know whether the Y chromosome will disappear at all. And, as we’ve shown, even if it does, we will most likely continue to need men so that normal reproduction can continue.

Indeed, the prospect of a “farm animal” type system where a few “lucky” males are selected to father the majority of our children is certainly not on the horizon. In any event, there will be far more pressing concerns over the next 4.6m years.


Forget single genes: CRISPR now cuts and splices whole chromosomes

Imagine a word processor that allowed you to change letters or words but balked when you tried to cut or rearrange whole paragraphs. Biologists have faced such constraints for decades. They could add or disable genes in a cell or even—with the genome-editing technology CRISPR—make precise changes within genes. Those capabilities have led to recombinant DNA technology, genetically modified organisms, and gene therapies. But a long-sought goal remained out of reach: manipulating much larger chunks of chromosomes in Escherichia coli, the workhorse bacterium. Now, researchers report they've adapted CRISPR and combined it with other tools to cut and splice large genome fragments with ease.

"This new paper is incredibly exciting and a huge step forward for synthetic biology," says Anne Meyer, a synthetic biologist at the University of Rochester in New York who was not involved in the paper published in this week's issue of Science. The technique will enable synthetic biologists to take on "grand challenges," she says, such as "writing of information to DNA and storing it in a bacterial genome or creating new hybrid bacterial species that can carry out novel [metabolic reactions] for biochemistry or materials production."

The tried and true tools of genetic engineering simply can't handle long stretches of DNA. Restriction enzymes, the standard tool for cutting DNA, can snip chunks of genetic material and join the ends to form small circular segments that can be moved out of one cell and into another. (Stretches of linear DNA don't survive long before other enzymes, called endonucleases, destroy them.) But the circles can accommodate at most a couple of hundred thousand bases, and synthetic biologists often want to move large segments of chromosomes containing multiple genes, which can be millions of bases long or more. "You can't get very large pieces of DNA in and out of cells," says Jason Chin, a synthetic biologist at the Medical Research Council (MRC) Laboratory of Molecular Biology in Cambridge, U.K.

What's more, those cutting and pasting tools can't be targeted precisely, and they leave unwanted DNA at the splicing sites—the equivalent of genetic scars. The errors build up as more changes are made. Another problem is that traditional editing tools can't faithfully glue large segments together. These issues can be a deal-breaker when biologists want to make hundreds or thousands of changes to an organism's genome, says Chang Liu, a synthetic biologist at the University of California, Irvine.

Now, Chin and his MRC colleagues report they have solved these problems. First, the team adapted CRISPR to precisely excise long stretches of DNA without leaving scars. They then altered another well-known tool, an enzyme called lambda red recombinase, so it could glue the ends of the original chromosome—minus the removed portion—back together, as well as fuse the ends of the removed portion. Both circular strands of DNA are protected from endonucleases. The technique can create different circular chromosome pairs in other cells, and researchers can then swap chromosomes at will, eventually inserting whatever chunk they choose into the original genome. "Now, I can make a series of changes in one segment and then another and combine them together. That's a big deal," Liu says.

The new tools will bolster industrial biotechnology by making it easier to vary the levels of proteins that microbes make, Liu and others say. They also promise an easy way to rewrite bacterial genomes wholesale, Meyer adds. One such project aims to alter genomes so they can code not just for proteins' normal 20 amino acids, but also for large numbers of nonnatural amino acids throughout the genome. That could lead to synthetic life forms capable of producing molecules far beyond the reach of natural organisms.


Why the genome is divided into several chromosomes and not just a single big chromosome? - Biology

When comparing prokaryotic cells to eukaryotic cells, prokaryotes are much simpler than eukaryotes in many of their features (Figure 1). Most prokaryotes contain a single, circular chromosome that is found in an area of the cytoplasm called the nucleoid.

Practice Question

Figure 1. A eukaryote contains a well-defined nucleus, whereas in prokaryotes, the chromosome lies in the cytoplasm in an area called the nucleoid.

In eukaryotic cells, DNA and RNA synthesis occur in a separate compartment from protein synthesis. In prokaryotic cells, both processes occur together. What advantages might there be to separating the processes?

The size of the genome in one of the most well-studied prokaryotes, E.coli, is 4.6 million base pairs (approximately 1.1 mm, if cut and stretched out). So how does this fit inside a small bacterial cell? The DNA is twisted by what is known as supercoiling. Supercoiling means that DNA is either under-wound (less than one turn of the helix per 10 base pairs) or over-wound (more than 1 turn per 10 base pairs) from its normal relaxed state. Some proteins are known to be involved in the supercoiling other proteins and enzymes such as DNA gyrase help in maintaining the supercoiled structure.

Eukaryotes, whose chromosomes each consist of a linear DNA molecule, employ a different type of packing strategy to fit their DNA inside the nucleus (Figure 2). At the most basic level, DNA is wrapped around proteins known as histones to form structures called nucleosomes. The histones are evolutionarily conserved proteins that are rich in basic amino acids and form an octamer. The DNA (which is negatively charged because of the phosphate groups) is wrapped tightly around the histone core. This nucleosome is linked to the next one with the help of a linker DNA. This is also known as the “beads on a string” structure. This is further compacted into a 30 nm fiber, which is the diameter of the structure. At the metaphase stage, the chromosomes are at their most compact, are approximately 700 nm in width, and are found in association with scaffold proteins.

In interphase, eukaryotic chromosomes have two distinct regions that can be distinguished by staining. The tightly packaged region is known as heterochromatin, and the less dense region is known as euchromatin. Heterochromatin usually contains genes that are not expressed, and is found in the regions of the centromere and telomeres. The euchromatin usually contains genes that are transcribed, with DNA packaged around nucleosomes but not further compacted.

Figure 2. These figures illustrate the compaction of the eukaryotic chromosome.


Conclusion

Many large-scale studies with vast Hi-C data have given us important insights into possible mechanisms of looping, subsequent higher order chromatin organization, and functional significance of domain formation and chromosomal interactions in different processes including transcriptional regulation. Given that these observations encourage a shift in perspective regarding how 3D organization of the genome impacts biological processes, it is of much interest to understand the underlying mechanistic rules governing causation of the folded architecture. Though cohesion and CTCF have been implicated in the formation of chromosomal loops, these proteins are absent in a fraction of loop loci (

10–14%) suggesting a role of other factors in determining how chromosomal interactions arise and how these contribute to specific cellular and context-specific functions.


Affiliations

Department of Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge, CB3 OES, UK

Willem Rens, Patricia CM O'Brien, Oliver Clarke, Daria Graphodatskaya, Vladimir A Trifonov, Helen Skelton, Mary C Wallis, Frederic Veyrunes & Malcolm A Ferguson-Smith

School of Molecular and Biomedical Science, The University of Adelaide, Adelaide, 5005, SA, Australia

Frank Grützner & Enkhjargal Tsend-Ayush

Institute of Cytology and Genetics, Russian Academy of Sciences, Siberian Department, 630090, Novosobirsk, Russia

School of Animal Sciences, Currumbin Sanctuary, Queensland University, Brisbane, QLD, 4072, Australia

Research School of Biological Sciences, The Australian National University, Canberra, ACT, 2601, Australia


CONSTRUCTION RULES FOR CHROMOSOMES

Insertion of single genes or even gene clusters into existing genomes will generally be tolerated and the novelty maintained in the respective chromosome. This is especially true for bacteria because they are naturally prepared to take up and integrate foreign DNA into their genomes. Horizontal gene transfer is a profitable enterprise in the microbial world. When thinking about a synthetic chromosome consisting of building blocks from many different organisms or of entirely novel synthetic sequences, many questions arise. To date, most scientists tend towards a gene-centric view on synthetic chromosomes. Frequently asked questions are: What is a minimal set of genes needed, or, what fancy characteristic of the new organism should I encode? However, chromosomes are much more than simple gene arrays. They also need to carry all the necessary information to direct replication, orderly folding and segregation. Such processes are collectively referred to as chromosome maintenance. Knowledge of chromosome maintenance systems has rapidly accumulated in recent years and we suggest using this knowledge to formulate construction rules for synthetic chromosomes. Below we will outline two main aspects that we consider to be important.

Chromosome maintenance systems

Many systems which maintain bacterial chromosomes consist of a DNA motif and respective proteins which recognize this motif. Interestingly, the chromosomal distribution of such motifs is often not random and often related to the function of the respective system (Fig. 7 Touzain et al. 2011 Messerschmidt and Waldminghaus 2014). One example would be the Ter sites responsible for termination of the replication fork in E. coli or B. subtilis (Bussiere and Bastia 1999). Such sites occur at positions opposite the replication origin and are oriented towards the dif site. The dif site is important for chromosome dimer resolution through the site-specific recombinase XerCD (Blakely and Sherratt 1994). For these nucleases to find the dif site, another chromosome maintenance system is required consisting of the DNA translocase FtsK and so-called FtsK orienting polar sequences (KOPS). These sites are oriented from the replication origin to the terminus and recognized by FtsK as arrows pointing in the dif direction (Bigot et al. 2005 Ptacin et al. 2008). Considering only these Ter- and KOPS-systems illustrates the need for a smart chromosome design (Fig. 8). A chromosome constructed without consideration of KOPS orientation will mislead the FtsK DNA translocase and prohibit chromosome dimer resolution. Although this might not be generally lethal, it leads to an unstable situation, and a proportion of cells in a population will be lost (Liu, Draper and Donachie 1998 Bigot et al. 2005). More severe effects are expected in chromosome designs with Ter sites in the wrong orientation. Ter sites block the replication machinery in one direction but permit it in the other direction (Mulcair et al. 2006 Duggin and Bell 2009). Accordingly, a chromosome might not be able to form a viable cell if Ter sites are included in the non-permissive orientation at wrong locations (Fig. 8).

Chromosome maintenance DNA motifs and their distribution on the E. coli chromosome.