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Viewing: Blog Posts Tagged with: sciwhys, Most Recent at Top [Help]
Results 1 - 12 of 12
1. Top ten OUPblog posts of 2012 by the numbers

By Alice Northover


While I already gave my opinion of the best OUPblog posts of the year, it’s only fair to see what you the reader decided. Here’s our top ten posts according to the number of pageviews they received.

(10) “Olympic confusion in North and South Korea flag mix-up” by Jasper Becker

(9) “Five GIFers for the serious-minded” by Alice Northover

(8) “Seduction by contract: do we understand the documents we sign?” by Oren Bar-Gill

(7) ““Remember, remember the fifth of November”” by Daniel Swift

(6) “Puzzling heritage: The verb ‘fart’” by Anatoly Liberman

(5) “The seven myths of mass murder” by J. Reid Meloy, Ph.D.

(4) “Oh Dude, you are so welcome” by Anatoly Liberman

(3) “How New York Beat Crime” by Franklin E. Zimring

(2) “Oxford Dictionaries USA Word of the Year 2012: ‘to GIF’” by Katherine Martin

And the number one blog post of the year is…

(1) “SciWhys: Why do we eat food?” by Jonathan Crowe

And I thought it would be interesting to note that our eleventh most popular blog post of 2012 is actually from 2009. People still enjoy arguing about unfriending.

Alice Northover joined Oxford University Press as Social Media Manager in January 2012. She is editor of the OUPblog, constant tweeter @OUPAcademic, daily Facebooker at Oxford Academic, and Google Plus updater of Oxford Academic, amongst other things. You can learn more about her bizarre habits on the blog.

Subscribe to the OUPblog via email or RSS.

The post Top ten OUPblog posts of 2012 by the numbers appeared first on OUPblog.

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2. SciWhys: How do organisms develop?

Every month OUP editor and author Jonathan Crowe answers your science questions in the monthly SciWhys column. Got a burning question about science that you’d like answered? Just email it to us, and Jonathan will answer what he can.

Today: how do organisms develop?

By Jonathan Crowe


Each of our bodies is a mass of cells of varying types — from the brain cells that give us the power of thought, to the cardiac cells that form our heart and keep our blood circulating; from the lung cells that take in oxygen from the air around us, to the skin cells that envelop the organs and tissues that lie within. Regardless of their ultimate function, however, each of these cells has come from a single source — the fertilised egg. But how can the complexity and intricacy of a fully-functioning organism stem from such humble beginnings?

At heart, the growth of any organism relies on the repeated growth and division of cells. A cell grows, then splits into two. Each of those cells grows, then splits into two… and so the cycle continues. Before long, we’ve gone from having one cell to two, from two to four, and then to eight, to sixteen, etc. In fact, after ten ‘cycles’ we already have over 1000 cells. (We still have some way to go to generate the millions of cells that form an embryo, but you get the idea.)

Initially, the egg divides to from a hollow ball of cells. However, living creatures aren’t hollow. Instead, they have a clear inside and outside, with the inside usually comprising some kind of gut, which passes the length of the body, from mouth to anus. So how do we go from a hollow ball to something with a clear internal structure? Well, imagine holding a sponge ball between the fingers of two hands, and then pushing in the bottom of the ball with your thumbs. The bottom of the ball folds up and in, almost forming a ‘tunnel’ into the ball. Our hollow ball of cells does the same thing: the cells at the bottom of the hollow ball move up and inside to form a tunnel. These cells will go on to form the digestive tract, which (as our experience tells us) runs right through the inside of our bodies.

Shortly after, a strip of cells along the back of the ball of cells roll up to form a furrow. The cells forming this furrow will go on to form the nervous system, with the furrow itself becoming our spinal cord. And, again, this fits with our experience: our spinal cord does indeed run up and along our back.

The previous paragraphs reveal an important feature of the development of a living organism. It’s not just a question of having lots of cells: to have a fully-functioning organism, we need different cells to do different things – to have different functions. After all, our bodies would be quite useless (not to mention odd-looking) if we were composed entirely of lung cells. Instead, as a population of cells grows, it also clusters into groups with common functions, forming different tissues and different organs.

So how does a cell know what kind of cell it should become? At the simplest level, it depends on the cell’s location – its position in the embryo. But how can cells tell where they are? Do they have some kind of cellular GPS system? Actually, in a way they do. Just as the GPS feature of a mobile phone can tell us our location by picking up a signal from a satellite, cells can also receive signals from their surroundings, which vary according to their location. And, because cells at different positions in the embryo — top or bottom, front or back, left or right — receive different signals, they behave in different ways.

Our everyday experience tells us that our behaviour is modified by signals in the world around us – the most obvious example being the traffic lights that tell us when to stop or go when driving. In a cellular world,

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3. SciWhys: a cure for Carys? Part Two

Over the past year, the SciWhys column has explored a number of different topics, from our immune system to plants, from viruses to DNA. But why is an understanding of topics such as these so important? In short, using science to understand our world can help to improve our lives. In my last post and in this one, I want to illustrate this point with an example of how progress in science is providing hope for the future for one family, and many others like them.

By Jonathan Crowe


In my last post, I introduced you to Carys, a young girl living with the effects of Rett syndrome. Thanks to scientific research, we now understand quite a lot about why Rett syndrome occurs – what is happening among the molecules within our cells to mean that some cells don’t behave as they should. Simply knowing about something is one thing, though; making constructive use of this knowledge is another thing entirely. During this post I hope to show you how our understanding of what causes Rett syndrome is being translated into the potential for its treatment – a cure for Carys, and the other young girls like her.

In my previous post I mentioned how Rett syndrome is caused by a faulty gene called MECP2 that affects the proper function of brain cells. However, the syndrome doesn’t actually kill the cells (unlike neurodegenerative diseases that do cause cells to die). Instead, the cells affected by Rett syndrome just function improperly. This leads us to an intriguing question: if the faulty gene that causes the syndrome could be ‘fixed’ somehow, would the cells start to behave properly? In other words, could the debilitating symptoms associated with Rett syndrome be relieved?

Obviously, researchers can’t simply play around with humans and their genes to answer questions such as these. Instead, researchers have studied Rett syndrome by using “mouse models.” But what does this mean? In short, mice and humans have biological similarities that allow the mouse to act as a proxy – a model – for a human. How can this be? Well, even though the huge variety of creatures that populate the earth look very different to a casual observer, they’re not all that different when considered at the level of their genomes. In fact, around 85% of the human and mouse genomes are the same.

Now, if the biological information – the information stored in these genomes – is similar, the outcome of using this information will also be similar. If we start out with two similar recipes, the foods we prepare from them will also be very similar. Likewise, if two creatures have similar genes, their bodies will work in broadly similar ways, using similar proteins and other molecules. (It is the bits of the mouse and human genomes that aren’t the same that make mice and humans different.)

In essence, the mouse Mecp2 gene is to all intents and purposes the same as the human MECP2 gene, and has the same function in both mice and humans. Equally, if this gene malfunctions, the consequences are the same in both mouse and human: a mouse with a mutation in its Mecp2 gene exhibits symptoms that are very like a human with a mutation in the same gene – that is, someone with Rett syndrome. In short, mice with a Mecp2 gene mutation are a model for humans with the same mutation.

With all this in mind, if we can learn how to overcome the effects of the Mecp2 mutation in the mouse, we might gain valuable insights into how we can overcome the equivalent effects in humans.

And this is wh

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4. SciWhys: a cure for Carys?

Over the past year, the SciWhys column has explored a number of different topics, from our immune system to plants, from viruses to DNA. But why is an understanding of topics such as these so important? In short, using science to understand our world can help to improve our lives. In this post and the next, I want to illustrate this point with an example of how progress in science is providing hope for the future for one family, and many others like them.

By Jonathan Crowe


Carys is an angelic-looking two-year old, with a truly winning smile. At first sight, then, she seems no different from any other child her age. Yet Carys’ smile belies a heart-rending reality: Carys has Rett syndrome, a disorder of the nervous system that is as widespread in the population as cystic fibrosis, yet is recognised to only a fraction of the same extent. (I, for one, had never heard of it until just a few months ago.)

Rett syndrome is a delayed onset disorder — something whose effects only become apparent with time. When Carys was born, she appeared perfectly healthy, and developed in much the same way as any other healthy infant. Just as she began to master her first few words, however, she lost the power of speech, and soon lost the use of her hands too. The effects of Rett syndrome were beginning to be felt.

Over time, Rett syndrome robs young girls of their motor control: they lose the ability to walk, to hold or carry objects, and to speak. But there be other complications too: there may be digestive problems; difficulties eating, chewing, and swallowing; and seizures and tremors. It is a truly debilitating disorder.

So what causes Rett syndrome? What’s happened inside the body of young girls like Carys? We know that the syndrome is caused by as little as a single error (a mutation) in a single gene. (As I mention in a previous post, it’s quite unsettling to realise that just one error in the tens of millions of letters that spell out the sequence of our genomes is sufficient to cause certain diseases. Sometimes there’s very little room for error.) The normal, healthy gene (called MECP2) contains the instructions for the cell to manufacture a particular protein; the mutated gene produces a broken form of this protein, which no longer functions as it should.

But how can a single protein affect so many processes – from speech to the movement of limbs? The answer lies in the way the protein interacts with other genes, particularly in brain cells. Essentially, the protein acts like a cellular librarian by helping the cells in the brain to make use of the information stored in their genomes (their libraries of genes). If the protein is broken, the cells can no longer make use of all of the genetic information needed for them to work properly (a bit like trying to use an instruction manual with some of the pages blacked out), so normal processes begin to break down. The broken protein doesn’t just affect the ability of the brain cells to use one or two other genes, but a whole range of them – and that’s why the effects of Rett syndrome are so wide-ranging.

But the story of Rett syndrome runs deeper than this. The mutation that causes Rett syndrome occurs in sperm; it happens after the sp

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5. SciWhys: Why do we eat food?

Every month OUP editor and author Jonathan Crowe answers your science questions in the monthly SciWhys column. Got a burning question about science that you’d like answered? Just email it to us, and Jonathan will answer what he can. Today: Why do we eat food?

By Jonathan Crowe


You may well be thinking that the question posed in the title of this blog has an all-too-obvious answer. We all know that we eat food to keep ourselves alive. But why do we find ourselves slaves to our appetites and rumbling stomachs? What is actually happening inside each of us that couldn’t happen without another slice of toast, or piece of fruit, or that most vaunted of mid-afternoon pick-me-ups, the sneakily-consumed bar of chocolate?

We’re all familiar with the concept of something needing fuel to keep it going. Just as a power station requires gas or coal to power its turbines and generate energy, so we need fuel – in the form of food – to power our continued existence.

The foods we eat provide us with a range of nutrients: vitamins, minerals, water, fat, carbohydrates, fibre, and protein. These nutrients are put to different uses — as building materials to construct the tissues and organs from which our bodies are made; as the components of the molecular machinery that keeps our cells running as they should. All of these uses are unified by a common theme: a requirement for energy to make them happen. And this is where one particular type of nutrient comes into its own. Step forward the carbohydrates.

Carbohydrates are better known to us as sugars, but in fact the sweet crystals we know as sugar are only part of this group. Carbohydrates come in very different shapes and sizes. One of the smallest is glucose, which acts as a chemical building block — multiple copies of glucose can join together to form a range of much larger molecules. For example, starch – found in potatoes and flour – is a carbohydrate formed from many individual molecules of glucose joined together in long chains. (Based on taste alone, you wouldn’t think that starch was made of glucose. Even though individual molecules of glucose taste sweet to us, once they are linked together to form starch the sweetness is lost.)

To understand how the sugar in our food can power the processes occurring in our cells every minute of every day, let’s follow some starch on its journey through the body. Many of the foods we consume aren’t in a form with which our bodies can do anything useful. Instead, they need to be digested. And so it is with carbohydrates such as starch. This process of digestion starts as soon as the food enters our mouth; our saliva contains special substances (called enzymes) that start attacking the long chains of starch, breaking it into smaller fragments.

Digestion continues as our food is swallowed and slides down into our stomach, where an arsenal of other chemical weapons set to work on the mouthful we’ve just consumed. Before long, what were initially mouth-watering morsels are reduced to something rather less appetising and leave the stomach to enter the long, snaking tunnel of our intestines. By now, the long chains of starch have been broken down into glucose, which is small enough to pass through the lining of our intestine and into our bloodstream. Our bloodstream acts as a short- and long-distance transport network, carrying the newly-arrived sugar molecules to cells all over the body.

When glucose arrives at its destination and first enters the cell, it u

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6. SciWhys: What happens when our immune system doesn’t work as it should?

This is the latest post in our regular OUPblog column SciWhys. Every month OUP editor and author Jonathan Crowe will be answering your science questions. Got a burning question about science that you'd like answered? Just email it to us, and Jonathan will answer what he can. Today: what happens when our immune system doesn’t work as it should?

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7. SciWhys: How does the immune system work?

By Jonathan Crowe Each day of our lives is a battle for survival against an army of invaders so vast in size that it outnumbers the human population hugely. Yet, despite its vastness, this army is an invisible threat, each individual so small that it cannot be seen with the naked eye. These are the microbes – among them the bacteria and viruses – that surround us every day, and could in one way or another kill us were it not for our immune system, an ingenious defence mechanism that protects us from these invisible foes.

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8. SciWhys: How does an organism evolve?

This is the latest post in our regular OUPblog column SciWhys. Every month OUP editor and author Jonathan Crowe will be answering your science questions. Got a burning question about science that you’d like answered? Just email it to us, and Jonathan will answer what he can. Today: how do organisms evolve?

By Jonathan Crowe

The world around us has been in a state of constant change for millions of years: mountains have been thrust skywards as the plates that make up the Earth’s surface crash against each other; huge glaciers have sculpted valleys into the landscape; arid deserts have replaced fertile grasslands as rain patterns have changed. But the living organisms that populate this world are just as dynamic: as environments have changed, so too has the plethora of creatures inhabiting them. But how do creatures change to keep step with the world in which they live? The answer lies in the process of evolution.

Many organisms are uniquely suited to their environment: polar bears have layers of fur and fat to insulate them from the bitter Arctic cold; camels have hooves with broad leathery pads to enable them to walk on desert sand. These so-called adaptations – characteristics that tailor a creature to its environment – do not develop overnight: a giraffe that is moved to a savannah with unusually tall trees won’t suddenly grow a longer neck to be able to reach the far-away leaves. Instead, adaptations develop over many generations. This process of gradual change to make you better suited to your environment is called what’s called evolution.

So how does this change actually happen? In previous posts I’ve explored how the information in our genomes acts as the recipe for the cells, tissues and organs from which we’re constructed. If we are somehow changing to suit our environment, then our genes must be changing too. But there isn’t some mysterious process through which our genes ‘know’ how to change: if an organism finds its environment turning cold, its genome won’t magically change so that it now includes a new recipe for the growth of extra fur to keep it warm. Instead, the raw ‘fuel’ for genetic change is an entirely random process: the process of gene mutation.

In my last post, I considered how gene mutation alters the DNA sequence of a gene, and so alters the information stored by that gene. If you change a recipe when cooking, the end product will be different. And so it is with our genome: if the information stored in our genome – the recipe for our existence – changes, then we must change in some way too.

I mentioned above how the process of mutation is random. A mutation may be introduced when an incorrect DNA ‘letter’ is inserted into a growing chain as a chromosome is being copied: instead of manufacturing a stretch of DNA with the sequence ATTGCCT, an error may occur at the second position, to give AATGCCT. But it’s just as likely that an error could have been introduced at the sixth position instead of the second, with ATTGCCT becoming ATTGCGT. Such mutations are entirely down to chance.

And this is where we encounter something of a paradox. Though the mutations that occur in our genes to fuel the process of evolution do so at random, evolution itself is anything but random. So how can we reconcile this seeming conflict?

To answer this question, let’s imagine a population of sheep, all of whom have a woolly coat of similar thickness. Quite by chance, a gene in one of the sheep in the population picks up a mutation so that offspring of that sheep develop a slightly thicker coat. However, the thick-coated sheep is in a minority: most of the population carry the normal, non-mutated gene, and so have coats of normal thickness. Now, the sheep population live in a fairly tempera

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9. SciWhys: What is gene mutation?

This is the latest post in our regular OUPblog column SciWhys. Every month OUP editor and author Jonathan Crowe will be answering your science questions. Got a burning question about science that you’d like answered? Just email it to us, and Jonathan will answer what he can. Today: what is gene mutation?

By Jonathan Crowe

In my last three posts I’ve introduced you to the world of biological information, taking you from the storage of biological information in libraries called genomes, which house information in individual books called chromosomes (themselves divided into chapters called genes), to the way the cell makes use of that stored information to manufacture the molecular machines called proteins.

But what happens when the storage of information goes wrong? If we’re reading a recipe and that recipe contains a mistake, chances are that the end-result of our culinary endeavour won’t end up as it should. And so it is at the level of cells. If the information the cell is using is somehow wrong, the end result will also be wrong – sometimes with catastrophic results.

I’ve mentioned in previous posts how biological information is captured by the sequence of the building block ‘letters’ from which DNA is constructed. The sequence of letters is ultimately deciphered by a molecular machine called the ribosome, which reads the sequence of letters in sets of three, and uses each trio to determine which amino acid – the building block of proteins – should be used next in its mission to construct a particular protein. It should come as no surprise that, if the recipe for the protein is changed – if the sequence of DNA ‘letters’ is altered – the protein that is manufactured will probably contain errors as a result. And if a protein contains errors, it won’t be able to function correctly, just as flat-packed furniture will end up being decidedly wobbly if you construct it from the wrong parts.

Imagine a snippet of DNA has the sequence GGTGCTAAG. The ribosome would ‘read’ this sequence, and would use it as the recipe for building a chain of three amino acids: Glycine-Alanine-Lysine. Now imagine that we alter just one letter in our original sequence so that it becomes GGTCCTAAG. All we’ve done is swap a G for a C at the fourth position in the DNA sequence. However, this change is sufficient to affect the composition of the protein that is produced when the sequence is deciphered: the ribosome will now build a chain with the composition Glycine-Proline-Lysine.

Surely such a small change won’t actually cause significant problems in a cell, though. Right? Wrong. Amazingly (and perhaps unnervingly) the tiniest error can have really quite significant consequences.

Let’s take just one example. Sickle cell anaemia is a condition that affects the red blood cells of humans.  Red blood cells fulfil the essential role of transporting oxygen from our lungs to all the living cells of our body: they continually circulate through our arteries and veins, shuttling oxygen from one place to another. A healthy red blood cell looks a bit like a ring doughnut (though it doesn’t actually have a hole right through the middle); by contrast, the red blood cells of individuals with sickle cell anaemia become warped into crescent-like shapes (like a sickle, the grass-cutting tool, after which the disease is named). These sickle cells no longer pass freely through our arteries and veins. Instead, they tend to get entangled with each other. As a result, the flow of oxygen round the body is impeded, and

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10. SciWhys: How is a gene’s information used by a cell?

This is the third post in our latest regular OUPblog column: SciWhys. Every month OUP editor and author Jonathan Crowe will be answering your science questions. Got a burning question about science that you’d like answered? Just email it to us, and Jonathan will answer what he can. Today: How is the information in a gene used by a cell?

By Jonathan Crowe


In my last two posts I’ve introduced the notion that DNA acts as a store of biological information; this information is stored in a series of chromosomes, each of which are divided into a number of genes. Each gene in turn contains one ‘snippet’ of biological information. But how are these genes actually used? How is the information stored in these genes actually extracted to do something useful (if ‘useful’ isn’t too flippant a term for something that the very continuation of life depends upon).

Many (but not all) genes act as recipes for a family of biological molecules called proteins: they literally tell the cell what the ingredients for a particular protein are, and how they should be combined to create the protein itself. (Proteins have a range of essential roles in the human body. Some act as building materials for different components of the body, such as the keratin we find in our hair and nails. Others act as molecular transporters: haemoglobin, which is found in our red blood cells, carries oxygen from our lungs to other parts of the body. A family of proteins called the enzymes are arguably the most important, however. Enzymes cajole different chemicals in our body into reacting with one another. Without enzymes, our bodies would be unable to generate energy from the food we eat (and you’d not be reading this blog post).)

So, somehow, the information stored in a DNA molecule is deciphered by the cell and used as the recipe for a protein. But how?

To answer this question, let’s take a journey inside the cell. We can imagine a cell to be like a factory, but one that has been divided into a series of physically separated compartments. Unlike a factory filled with air, a cell is filled with a jelly-like fluid called the cytoplasm, which surrounds the various compartments enclosed within it. In an earlier post I likened a genome to a biological library. And, inside the cell, this library is stored within a particular compartment called the nucleus.

I mentioned earlier that genes often act as recipes for proteins. But here comes a bit of a quandary: chromosomes – and the genes they contain – are locked away inside the cell’s nucleus. By contrast, proteins are manufactured by the cell in the cytoplasm, outside of the nucleus. So, for the genetic information to be used, it has to get out of nucleus and into the cytoplasm. How does this happen? Well, if we’re in a library with a book that contains information we really need, but we’re unable to take the book out of the library, we might make a photocopy of the page that holds the information we’re after. To get the information it needs out of the nucleus and into the cytoplasm the cell does something remarkably similar. The chromosome containing the gene of interest has to stay inside the nucleus, so the cell makes a copy of the gene – and that copy is then transported to where it is to be used: out of the nucleus and into the cytoplasm.

The copy of the gene generated during this cellular photocopying is made not of DNA but of a close cousin called RNA. RNA is made of three of the same building blocks as DNA – A, C and G. Instead of the T found in DNA, however, RNA uses a different block represented by the letter U (for ‘uracil’). Despite this

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11. SciWhys: What are genes and genomes?

This is the second post in our latest regular OUPblog column: SciWhys. Every month OUP editor and author Jonathan Crowe will be answering your science questions. Got a burning question about science that you’d like answered? Just email it to us, and Jonathan will answer what he can. Today: What are genes and genomes?

By Jonathan Crowe


I described in my last blog post how DNA acts as a store of biological information – information that serves as a set of instructions that direct our growth and function. Indeed, we could consider DNA to be the biological equivalent of a library – another repository of information with which we’re all probably much more familiar. The information we find in a library isn’t present in one huge tome, however. Rather, it is divided into discrete packages of information – namely books. And so it is with DNA: the biological information it stores isn’t captured in a single, huge molecule, but is divided into separate entities called chromosomes – the biological equivalent of individual books in a library.

I commented previously that DNA is composed of a long chain of four building blocks, A, C, G, and T. Rather than existing as an extended chain (like a stretched out length of rope), the DNA in a chromosome is tightly packaged. In fact, if stretched out (like our piece of rope), the DNA in a single chromosome would be around 2-8 cm long. Yet a typical chromosome is just 0.00002–0.002 cm long: that’s between 1000 and 100,000 times shorter than the unpackaged DNA would be. This packaging is quite the feat of space-saving efficiency.

Let’s return to our imaginary library of books. The information in a book isn’t presented as one long uninterrupted sequence of words. Rather, the information is divided into chapters. When we want to find out something from a book – to extract some specific information from it – we don’t read the whole thing cover-to-cover. Instead, we may just read a single chapter. In a fortuitous extension of our analogy, the same is true of information retrieval from chromosomes. The information captured in a single chromosome is stored in discrete ‘chunks’ (just as a book is divided into chapters), and these chunks can be read separately from one another. These ‘chunks’ – these discrete units of information – are what we call ‘genes’. In essence, one gene contains one snippet of biological information.

I’ve just likened chromosomes to books in a library. But is there a biological equivalent of the library itself? Well, yes, there is. Virtually every cell in the human body (with specific exceptions) contains 46 chromosomes – 23 from each of its parents. All of the genes found in this ‘library’ of chromosomes are collectively termed the ‘genome’. Put another way, a genome is a collection of all the genes found in a particular organism.

Different organisms have different-sized genomes. For example, the human genome comprises around 20,000-25,000 genes; the mouse genome, with 40 chromosomes, comprises a similar number of individual genes. However, the bacterium H. influenzae has just a single chromosome, containing around 1700 genes.

It is not just the number of genes (and chromosomes) in the genome that varies between organisms: the long stretches of DNA making up the genomes of different organisms have different sequences (and so store different information). These differences make sense, particularly if we imagine the genome of an organism to represent the ‘recipe’ for that organism: a human is quite a different organism from a mouse, so we would expect the instructions that direct the growth and function of the two organisms to differ.

B

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12. SciWhys: What is DNA and what does it do?

Today we’d like to introduce our latest regular OUPblog column: SciWhys. Every month OUP editor and author Jonathan Crowe will be answering your science questions. Got a burning question about science that you’d like answered? Just email it to us, and Jonathan will answer what he can. Kicking us off: What is DNA and what does it do?

By Jonathan Crowe


We’ve all heard of DNA, and probably know that it’s ‘something to do with our genes’. But what actually is DNA, and what does it do? At the level of chemistry, DNA – or deoxyribonucleic acid, to give it its full name – is a collection of carbon, hydrogen, oxygen, nitrogen and phosphorus atoms, joined together to form a large molecule. There is nothing that special about the atoms found in a molecule of DNA: they are no different from the atoms found in the thousands of other molecules from which the human body is made. What makes DNA special, though, is its biological role: DNA stores information – specifically, the information needed by a living organism to direct its correct growth and function.

But how does DNA, simply a collection of just a few different types of atom, actually store information? To answer this question, we need to consider the structure of DNA in a little more detail. DNA is like a long, thin chain – a chain that is constructed from a series of building blocks joined end-to-end. (In fact, a molecule of DNA features two chains, which line up side-by-side. But we only need to focus on one of these chains to be able to understand how DNA stores its information.)

There are only four different building blocks; these are represented by the letters A, C, G and T. (Each building block has three component parts; one of these parts is made up of one of four molecules: adenine, cytosine, guanine or thymine. It is these names that give rise to letters used to represent the four complete building blocks themselves.) A single DNA molecule is composed of a mixture of these four building blocks, joined together one by one to form a long chain – and it is the order in which the four building blocks are joined together along the DNA chain that lies at the heart of DNA’s information-storing capability.

The order in which the four building blocks appear along a DNA molecule determines what we call its ‘sequence’; this sequence is represented using the single-letter shorthand mentioned above. If we imagine that we had a very small DNA molecule that is composed of just eight building blocks, and these blocks were joined together in the order cytosine-adenine-cytosine-guanine-guanine-thymine-adenine-cytosine, the sequence of this DNA molecule would be CACGGTAC.

The biological information stored in a DNA molecule depends upon the order of its building blocks – that is, its sequence. If a DNA sequence changes, so too does the information it contains. On reflection, this concept – that the order in which a selection of items appears in a linear sequence affects the information stored in that sequence – may not be as alien to us as it might first seem. Indeed, it is the concept on which written communication is based: each sentence in this blog post is composed of a selection of items – the letters of the alphabet – appearing in different sequences. These different sequences of letters spell out different words, which convey different information to the reader.

And so it is with the sequence of DNA: as the sequence of the four building blocks of DNA varies, so too does the information being conveyed. (You may well be asking how the information stored in DNA is actually interpreted – how it actually determines how an organism develops and functions – but that’s a topic for a different blog post.)

You may be wondering how on earth ju

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