Photosynthesis

I could of course harp on now about how important photosynthesis is to all life on Earth and how we couldn't live without it. Of course, this is true. But you probably know that. Oh, and don't forget this: water + carbon dioxide ----> glucose + oxygen. Let's dive straight in to the chloroplast.

Photosynthesis occurs in two stages: the light dependent reaction (LDR) comes first and occurs on the thylakoid membrane of the chloroplasts, then comes the light independent reaction (LIR) which can also be called the Calvin cycle which occurs in the stroma of the chloroplast. It is also important to note the main structures in the chloroplast and their function:

• The chloroplast envelope. A double-membrane enclosure which runs around the whole chloroplast. The two membranes create a intermembrane space between them.
• The thylakoids are small disks which contain photosystems 1 and 2 (PSI and PSII) on their membrane to capture light energy and utilise it in the LDR. A stack of thylakoids is called a granum (pl. grana).
• Each granum becomes a part of an interconnected network with lamellae connecting grana between thylakoids.
• The stroma is a complex 'soup' of enzymes (for the LIR), starch grains (stores of glucose), sugars,  salts and organic acids.

In my (slightly dry) blog on ATP, I mentioned that photosynthesis is a process which both uses and produces ATP. This results in a net production of ATP of 0. It is the LDR which produces this ATP for its brother in arms, the LIR, to use in synthesising glucose. In some ways, the LDR can be thought of as the LIR's helper in that it produces two important products for it. These are ATP and reduced NADP (a photosynthetic coenzyme). The LDR is made up of three main steps:

1. Photolysis (catalytic breakdown using light) of water
2. Reduced NADP production
3. ATP production

The image above shows a model of the LDR and I suggest (strongly, very strongly because I will go off on tangents about nothing to do with this) that you use it to see how far along in the whole process we are. The sequence occurs from left (PSII) to right (ATP synthase).

We'll start at the beginning at step 1. PSII contains an enzyme which can split water into its three constituent parts: half an oxygen molecule (one O atom), two protons and two electrons. These protons and electrons will be used later, but the oxygen is released as a waste product. This is known as photolysis. However, the enzyme needs help from light to do this (hence: photo-lysis). If we can synthesis similar enzymes or inorganic catalysts, we could use them to split water into hydrogen and oxygen for use in fuel cells to make cars which only emit water as a product of use (how very considerate).

Now to step 2 (which is quite a bit longer). Two photons (particles of light energy) hit PSII which contains an array of pigments which can trap the energy of these photons. These pigments come under two categories:

• accessory pigments (xanthophyll, carotene...), which transfer the light energy to the primary pigment.
• the primary pigment (chlorophyll), which uses the energy to promote a pair of electrons (not in a you're getting a big office way - more physics than business)

These two electrons are promoted to a higher energy level (which means the electrons have more energy or are 'excited'). In their excited state, they have enough energy to escape the primary pigment. They then pass through an electron transport chain (ETC) consisting of proton pumps which use the energy of the electrons to pump protons (from photolysis) into the thylakoid lumen - creating an 'electrochemical gradient' between the thylakoid lumen and the stroma. This becomes useful later. Finally, after all that proton pumping, the electrons reach a final electron acceptor at the end of the ETC. But if all those electrons keep leaving the primary pigment, won't it run out? Nope. Remember the electrons released from water in photolysis? These are used to replenish the electrons lost from PSII or to 'reduce' the pigment. Remember that OILRIG (oxidation is loss, reduction is gain).

Once the electrons have reached the end of the ETC and the final electron acceptor, they reduce PSI. Why does it need reducing? Because two more photons excite two more electrons from PSI. These electrons are used to achieve the final goal of step two of the LDR - to reduce NADP to become reduced NADP. Each electron from the pair of promoted electrons is used, with a proton, to form reduced NADP.

NADP + proton + electron ----> reduced NADP

So, moving on to step 3. The protons pumped into the thylakoid in step 2 are now used. Because of all the positive charge and concentration of protons which has built up, the protons want to diffuse out of the thylakoid. The only way they can do this, is through the enzyme ATP synthase. In diffusing out of the thylakoid, they must donate their energy to ATP synthase which uses this energy to form ATP from ADP and an inorganic phosphate group. The movement of these protons is called chemiosmosis.

The whole process above is called non-cyclic photophosporylation. There is another version of the LDR called cyclic photophosphorylation where PSII isn't used, so the electrons promoted from PSI come back to reduce PSI back to its original state. This doesn't involve photolysis of water or reduced NADP production. It only produces small amounts of ATP, so is less preferable compared with non-cyclic photophosphorylation.

There we have the LDR, in all three stages, producing lots of ATP and reduced NADP for the LIR, which we are about to investigate.

The LIR, carbon fixation, or Calvin cycle (discovered by a scientist called Melvin Calvin - the best scientist name ever) is the next process in photosynthesis. It uses the products of the LDR with carbon dioxide to produce glucose, or in fact a whole range of organic compounds, which the plant can use later on. Below is a diagram of the Calvin cycle.

Here's a description of what's happening (the names I use don't always match up with the ones on the diagram):

1. Carbon dioxide which enters the leaf through the stomata reacts with ribulose bisphosphate (RuBP) in the presence of the enzyme, rubisco to form 2 molecules of glycerate 3-phosphate (GP).
2. 2 ATP molecules and 2 reduced NADP molecules react with the 2 GP molecules to form 2 triose phosphate (TP) molecules.
3. 5 in 6 molecules of TP then react with an ATP molecule to reform RuBP and the cycle restarts.
4. The other molecule of TP then goes to form useful organic products. If we use glucose as an example, two TP molecules are needed to make a molecule of glucose (because TP has 3 carbons and glucose has 6).

All of the reacted ATP and reduced NADP then return to the LDR to be reformed back to ATP and reduced NADP.

Because only 1/6 of all TP produced is used to make organic products, the Calvin cycle must occur 6 times to produce one molecule of glucose. This is because each carbon dioxide which is input into the cycle results in the production of 2 TP molecules. If 1/6 are formed into useful products, we need 12 TPs to make one glucose: 12 x 1/6 = 2.

Even though photosynthesis is a brilliant process which fuels all life on Earth, it can be limited by environmental conditions. The most important ones are:

• Light intensity
• Light wavelength
• Carbon dioxide concentration
• Water availability
• Temperature

If we take a look at light intensity, having a light intensity too low would result in not enough photons reaching the thylakoid membrane for a high rate of reaction for the LDR. If not enough reduced NADP and ATP can be produced, then this will also limit the rate of the LIR.

Wavelength is also a very important consideration of the light used for photosynthesis. Each pigment will only use light of a certain wavelength. This is why plants contain several different pigments; so more wavelengths of light can be used for the LDR. Despite this, not all wavelengths are suitable.

Obviously, carbon dioxide concentration is very important in photosynthesis. If it is too low, the Calvin cycle cannot occur quickly and this limits the overall rate of photosynthesis. However, an excess of carbon dioxide can cause poisoning to the plant, so the carbon dioxide concentration must be high, but not too high.

Water availability is less of an issue for plants, so long as there is some. If not enough water is available for non-cyclic photophosphorylation to occur, cyclic photophosphorylation can be used. A complete absence of water, would however result in the death of the plant.

As with all enzyme-catalysed reactions, if the temperature is too low, the rate of reaction will be low. If the temperature is too high, the enzyme will be denatured and the reaction cannot be catalysed. This is all about active sites, frequency of collision and particle energy.

Even if you were to have optimum conditions for all of these factors, photosynthesis cannot occur at an infinite rate, clearly. So there will always be one factor which limits the others. No matter how much you increase the other factors, the limiting factor will dictate the rate of photosynthesis.

And there we have photosynthesis. Even though it is a lot more complex than you might think, it does mean that we and all other life can survive, so we'll forgive it just this once.

ATP

Energy is a tricky concept when it comes to biology. Because biology is often considered a very a applied science, it is not always possible to easily describe biological processes in terms of fundamental 'pure' processes like energy transfer. Science knows a lot about energy transfer in simple, idealised situations which we can use the laws of thermodynamics for, but when we consider how complex biology is, it doesn't really make sense to talk about energy in these terms. Fortunately, that gives biologists the licence to talk slightly loosely about energy. Nevertheless, there are still some important points about energy which must be maintained. For example:

• Energy cannot be created or destroyed, only transferred between forms.
• You cannot say something has used or created energy as this contravenes the first law of thermodynamics.
• It is however, acceptable to say things like 'energy is transferred and utilised' by something.

Everything in the universe has a tendency to want to be in it's lowest energy state possible and shed its energy. This is the second law of thermodynamics and paints a scary picture for the future of the universe (but not for a few years yet). Adenosine triphosphate (ATP) - that glorious molecule - is no exception to this rule, and biology has learned to use this property to its advantage. Pretty much every active (energy-dependent) process in biology depends on ATP to function. These include:

• Photosynthesis
• Active transport
• DNA synthesis and replication
• Protein synthesis
• Cell division
• Muscle contraction
• Homeostasis

You might notice that a lot of these involve movement. Movement of course requires energy which is served up by the almighty ATP.

ATP has its origins in two antagonistic reactions: photosynthesis and respiration. These have opposing equations which can be seen in the diagram to the right. With the addition of energy, glucose can be synthesised and used as a store of energy. This is a very important feature of glucose as opposed to ATP as ATP is a very unstable molecule and cannot be stored, so must be used almost as soon as it is produced.

In order to fully understand ATP, it is important to understand its structure. In the diagram to the left, you can see that it contains a double-ring nitrogenous base (adenine) which bonds to the pentose sugar ribose. Furthermore, the ribose is bonded to three inorganic phosphate groups in a chain. Each time one of these is hydrolytically removed, there is a net exothermic reaction. So ATP-->ADP-->AMP.

When ATP is produced, it is sent (somehow) to wherever it needs to be and it will undergo a hydrolysis reaction in the presence of the catabolic enzyme ATPase. This breaks ATP down into ADP and an inorganic phosphate group. In doing so, the net enthalpy change of the reaction is negative (so it is exothermic). The energy released is then transferred to the part of the cell which needs it (e.g. a proton pump) which allows it to do useful work. 

However, if the reaction was only conducted in one direction, there would be a huge demand for adenine and a large waste of ADP and inorganic phosphate. But biology is seldom as wasteful as this. ADP and inorganic phosphate can be reformed into ATP using the enzyme ATP synthase during respiration in oxidative phosphorylation. ATP can also be reformed in cyclic and non-cyclic photophosphorylation during the light dependent stage of photosynthesis. Please note that even though ATP is produced during the LDR of photosynthesis, the same amount is used up in the Calvin cycle, so the net production of ATP in photosynthesis is 0.

You might now be wondering why ATP has been elevated to the status of 'God molecule' in biology. After al, it doesn't look particularly amazing, and surely a similar job could be carried out by other molecules. Correct, it probably could. But all known organisms have evolved around this molecule, suggesting that it arose in the simplest organisms at the dawn of life, and reap its benefits. There are some key features of ATP which make it such a good energy currency:

• It is small and soluble so can be moved easily around the cell.
• It is easily hydrolysed, so energy can be quickly released.
• It can transfer energy to other molecules.
• ATP releases small amounts of energy, so the energy can be precisely controlled.
• ATP won't leak from cells as it needs a protein pump which isn't present on cell surface membranes to pass through the non-polar hydrophobic core. 

And that mostly sums up ATP, or [(2''R'',3''S'',4''R'',5''R'')-5-(6-aminopurin-9-yl)-3,4-dihydroxyoxolan-2-yl]methyl(hydroxyphosphonooxyphosphoryl)hydrogen phosphate as UIPAC have catchily named it using systematic nomenclature. I think I'll stick to ATP though.

Population dynamics

Populations are all a game of maths really. After all, the number of individuals in a population is just an number and the growth of a population can be simulated using graphs and equations etc. So why are populations so important in biology? In fact, it is often the size of a population which determines whether a group of organisms can survive. You need to have a population size within a set of defined limits in order to live. For example, like the pandas, if a population is too small it might be hard for individuals to find mates to reproduce sexually, hence the population cannot be sustained and it will go into decline and this will only exacerbate the problem. On the other hand, populations which are too large (some say like us humans) result in a lot of interspecific competition. Competition can even be expressed as war, and not just in humans, in ants, crows and elephants too! As a matter of interest, it is only humanity's ability to innovate and adapt using technology which has allowed us to produce enough resources to keep up with our population. But anyway, let us delve into the dark recesses of populations and find out exactly why, how and who they are.

To begin, it is important to know exactly what a population means. A population is (according to AQA): "all the organisms of one species in a habitat". Within a macrohabitat (e.g. a sand dune ecosystem) there are many different populations of different species, and together these make up a community. So what is an ecosystem then? If you imagine all of these organisms interacting with each other and with the other biotic and abiotic factors in a habitat, you have an ecosystem. Speaking about all of these interactions has brought me very nicely onto my next point: niches.

The idea of a niche is a very important concept in ecology. Think of a niche as a counterpart to a habitat. Whilst a habitat is where an organism lives, a niche is exactly what the organism does there. Habitat = workplace, niche = job. Of course, the organism will not really understand what job it is doing, or why it is doing it (unless it is a particularly altruistic sea cucumber) because like all things in biology which seem to be guided by some omnipotent hand, the reason an organism falls into a niche is nothing more or less spectacular than natural selection, leading to evolution where the best adaptations survive to pass on their genes to the next generation. Now that's a big concept - it took Darwin most of his life and a letter from Wallace to realise it - so let's look at an example.

Rabbits, they're everywhere because they breed like... well, rabbits. They seem to be everywhere in the British countryside and for a good reason! Because they have found and become very well adapted to their niche and exploit it to the full. Let's look at a few adaptations of rabbits. They're brown, which camouflages them against lots of woody/muddy/leafy backdrops which means they can survive well in woodland and grassland. What do they do? They eat grass all day long. They also have highly adapted incisors for eating grass which means that they are good at it. What's more, they are fast which means they can run away from fantastic Mr. Fox. Now you don't see many other animals doing that in the woods do you? Precisely, because this is the niche of the rabbit.

But what if another species with similar adaptations were to encroach on this niche? Perhaps that evil and nefarious creature: the hare! Two species cannot occupy the same niche, because not only is it socially awkward but it means you get interspecific competition. When two species occupy the same niche, they want the same resources: food, space, water, coal, belgian chocolate etc. But of course, there isn't enough to go around so scramble competition occurs. Both species want that damn chocolate, the belgian hare of course being the finest connoisseur of chocolate, so they both gather it. But because one species will have better adaptations to gather the resource, it will outcompete the other and reclaim its niche for itself and all other members of its species (huzzah). But hang on, members of the same species also compete for the same resources, which means that intraspecific competition will also occur. Therefore only the best adapted will get their precious resources (like Golem) and this leads us back to survival, breeding and more natural selection.


Now we know this about populations, any good scientist will ask how do we know this? Well here comes the #applianceofscience (use it, you have my permission) with sampling methodology.

One way scientists can sample populations is using random quadrat placement. Very good for plants, but not so much for animals as they have a habit of moving which would produce invalid results as they could be counted twice or not at all. So here's my method:

1. Get a map of the study area and break it up into a grid using a computer/pen/sonic screwdriver.
2. Decide how many quadrats to use with the method explained here.
3. Generate random numbers using a random number simulator e.g. random.org which is cool because it uses electromagnetic noise from space to generate the numbers.
4. Turn these numbers into coordinates.
5. Place quadrats on these coordinates.
6. Go crazy counting plants and cataloguing their species.
7. You can then use these data to estimate % cover or the abundance of a species or species diversity/richness.

Never ever throw the quadrat. For one thing, nobody wants a quadrat in their eye. Also it biases the results which is exactly what random sampling aims to eliminate.

The other important quadrat method is using transects:

1. Put a long line of string in whatever direction you want to measure (e.g. distance from a cliff edge).
2. Place quadrats along the length of the string and count the species in them like in random sampling.

But what if the transect is really long and I'm really lazy? Easy, just place a quadrat at every x metre interval along the transect or every y metre height interval. This is called an interrupted transect.

But alas, we have limitations. Like I said ages back, this is rubbish for counting most animals as they like to run away. So we have capture, mark, release, recapture which is much more fun, but science doesn't care about that. But here's the method:

1. Introduce some kind of trap into the habitat e.g. a pitfall trap.
2. Have patience whilst all sorts of animals drop into it.
3. Sort out the one(s) you want and mark them using a method which wont affect them or the rate at which they are predated and note down how many were marked.
4. Release them and wait for them to mix back in with the rest of the population (a really long time if you're investigating snails/slugs/tortoises).
5. Replace the traps (under similar conditions so as not to introduce a confounding variable).
6. Wait until more animals are collected.
7. Count how many you have in total and how many of these are marked.
8. Multiply the number of animals collected on both traps together and then divide by the number which were marked on the second trap.

Wasn't that a joy? What's even more fun is carrying out risk assessments on fieldwork. Basically, don't do anything stupid and mention some hazards and appropriate steps to avoid them and you'll be fine (I don't like risk assessments - can you tell?).

Ah, but won't all this poking around in delicate ecosystems harm the environment? Yes, yes it will. So we have to take appropriate steps to mitigate our impact. For example: if we have an ultra-rare shrew and we want to know its dry biomass to construct a pyramid of biomass, heating it in an oven until dry won't do the population much good. So, maybe making an estimate from already known values of similar species would be more ethical. There are many many many ethical considerations which should be made when carrying out fieldwork, but it's really just a case of common sense.

Oh, and do you want to hear the punchline of all this investigative work? Conclusions drawn from correlations in the data have to be done so very cautiously and tentatively because as we all know correlation does not necessarily prove a causal relationship. So you might say, all of that work just means we can now say that what we thought may or may not be true, but we are a little bit more sure of it being true now than we were last week. Score: science 1-0 ignorance.

This blog is called 'population dynamics' and of course 'dynamic' means movement, so what moves in populations? The size of populations of course! They vary!

Populations can vary because of biotic and abiotic factors. Remember that, it's important, I put it in bold and everything. Let's make some more examples, shall we?

Okay, so we have our lovely squid (Sid) and his niche dictates that he can only survive in waters from 15-17˚C. Because of global warming and all that jazz, his waters are getting warmer, and his bad luck doesn't even end there. He happens to live in a closed lake, so the whole squid population is stuck there. The temperature in the water is now 17.5˚C. Some squid can survive this, but most can't. Sid is dead and the population has decreased as squid die due to warming waters.

But of course, biotic factors are also important. Let's forget Sid's unfortunate demise in the warming lake and imagine that some careless person has introduced a sperm whale into the lake (I know whales are big, but it's a big lake, go with it). Sperm whales like to eat squid - they predate it - because this large predator has been introduced, the squid population decreases and then increases again because of the classic lynx-snowshoe hare model. Sid is dead, and inside a whale. Poor Sid.

It is also worth remembering that because of interspecific and intraspecific competition, the populations will vary too. Go back to the whole hare-rabbit fiasco earlier if you want to read it again. Both of these types of competition are biotic factors.

Finally, we come to the geographical concept of human populations (woot).

Human populations grow depending on four major factors:

• Birth rate
• Death rate
• Emigration
• Immigration

Each of these factors is usually measured as a rate per 1000 of the population. For example, if per 1000 people this year, 25 die, the death rate is 25 deaths per 1000 people. Easy, right? Good, because you can also express it as a percentage. 25 per 1000 can be expressed as (25÷1000)% = 2.5%. Again, nice and easy. The total growth rate of the population (which can be negative) = (birth rate + immigration)-(death rate + emigration).

There is a very famous graph called the demographic transition model (DTM) and here it is:

It's a jolly-looking thing, but really is quite important. Because I'm feeling particularly lazy tonight, I found an annotated model which describes what is going on. Here are my explanations:

1. Only really seen in remote tribes and apocalypse survivors. There is a lack of proper healthcare and sanitation so the death rate is high and occasionally spikes due to disease or famine. The birth rate is high because there is a lack of family planning and contraception. Despite the high birth rate, the death rate keeps the population low.
2. Improved healthcare means people live for longer, so the death rate drops sharply, but the birth rate remains high due to the continued lack of family planning and contraceptives.
3. The death rate continues to fall, but more slowly now as the initial breakthroughs reach their limit of effectiveness. Birth rate begins to fall as people become more educated on sex and families and jobs begin to dictate family life.
4. Jobs dominate family life, so the birth rate levels off, occasionally spiking due to affluent periods in time. The birth rate means that the population stops growing. This is where the UK is now.
5. I know it's not on the graph, but birth rates may start to drop even further as more elderly dependents emerge so people cannot afford to have families. Only a few countries exhibit this behaviour, such as Germany and Japan.

There are many other ways to represent human populations, such as population growth curves, survival curves and age-population pyramids. Each of which can be used to find out which stage of the DTM a country is in. Each one has its own purpose and I strongly recommend that you look up the differences between them, but interpreting them is pretty straightforward. But this is starting to look more and more mathsy, and I now regret saying that populations are pretty much maths at the beginning, because this maths isn't fun maths. Nevertheless it is important, so don't disregard it so quickly as I just did!

Well, that's population dynamics. I thank anyone who managed to stick with it to the end, but it is important, regardless of how dull it can seem compared to 'proper biology' #controversy. Good night.

The game

You may of heard of 'the game'. For anyone who hasn't, the rules of 'the game' are quite simple.

• You first accept that you are a competitor in 'the game'.
• From then onwards when you think of 'the game' you have lost 'the game'.
• Every time you lose 'the game' you restart not thinking about 'the game'.
• The objective is to not think about 'the game' for as long as possible.

Easy, right? Wrong. In fact, I think it's impossible, and here's why:

When an individual, x, starts to play 'the game' they are forced to think about 'the game' in order to understand that they have started to play 'the game'. X therefore has lost 'the game'. In losing the game, they are forced to again, think about 'the game' in order to accept their loss of the game. This then renders them a loser as they have thought of 'the game'. You might, however, argue that to think of 'the game' at this point is not strictly a loss as x has not accepted that they have restarted 'the game' and therefore cannot be considered live in 'the game' so cannot have yet lost 'the game'. In which case, x accepts their initial loss and restarts 'the game'. In doing so, they are forced to think of the game, ipso facto they have lost 'the game'. This then completes a self-perpetuating, auto-catalytic, cycle of failure due to the very rules of 'the game' themselves.

If you are to model this flow into a diagram, you might argue that x's round does not start until they have first stopped thinking about 'the game', which first occurs when they start their round. Therefore, it might be considered possible to not be thinking about 'the game' when 'the game' begins. However, from an applied, realised approach, this is not possible as a thought lasts for more than an infinitesimal time in the novel property of matter known as consciousness. The abstract concept of time flow of course being one of the 'hard problems' in the fundamental understanding of consciousness; but now isn't the time to get into that, because I have neither the expertise, nor the will to explain consciousness tonight. As such, the thought which initiates 'the game' (in which is contained a though of 'the game' as an intrinsic property of the initiator function) will run over into the round, invalidating 'the game' and resulting in a loss. But due to biological variation, the time between starting a round and realising that you have invalidated 'the game' varies between people. If an individual takes longer to realise this, they are deemed 'slower' (and hence qualitatively termed more stupid). But of course, the longer this realisation takes, the longer you have lasted in the game. Hence, the less intelligent you are, the better you are at the game.

To conclude, you have to be stupid to be good at the game.

Why are genes dominant or recessive?

I found this webpage about why genes are dominant or recessive. Definitely worth a read!

Find it here!

Speciation

I live in England. In fact, i quite like it here. I like the hills and I like the clouds. I think we have the best clouds in the world. But we English are definitely a nation which likes to be angry with everything, especially the weather. Perhaps this is an adaptation of us to warn others on our little island home of adverse weather to ensure the survival of our population, in spite of the constant wind and rain.

Hop across the channel to France, and there's a completely different story. A nation with nothing but glorious weather (or at least so they tell us, relentlessly). Imagine them now, sitting outside a Marseille bar with their patio furniture. Coincidently, the French have (for the purposes of this story) become very well adapted for making and sitting on patio furniture in the light of the sun so as to suit their environment.

What does this have to do with speciation? Well, this analogy only goes so far. For one thing, I'm not suggesting that the French have evolved into a separate species, Homo Francus. How do I know this? Just a little 'voulez-vous coucher avec moi ce soir?' from an Englishman in his bowler hat and pinstripes à Paris avec une belle femme and you've produced a fertile F1 generation, and as we know two individuals who can successfully breed to produce fertile progeny are of the same species. But what I'm getting at is that the geographical isolation of Britain from France by 'La Manche' has resulted in two distinct populations with their own adaptations to suit the biotic and abiotic factors present in each of their environments. Perhaps, if we were to isolate both populations for a few hundreds of thousands of years longer, we might see changes in the two populations due to further chance mutations and natural selections so that two distinct species would arise. Then if we were to reintroduce the two populations to each other, no fertile offspring could be produced.

Perhaps this example isn't the most likely to happen in nature, but I think it illustrates speciation well. If nothing else, you'll remember this for the exam more than the CGP example of fur length - how dull!

Chromosomes

The characteristic elongated 'X' shape of a chromosome is the most familiar (perhaps with the exception of the double-helix) image of inside our nucleus and what makes us who we are. But it is a common misconception that this is the normal form of DNA. DNA only turns into this super-condensed form during the mitotic phase of the cell cycle. As we can see, this phase lasts for a short time when compared to the much longer growth and synthesis phases. Nevertheless, these short-lived gangly bundles of nucleic acid play a vital role in our everyday lives and in organising our DNA.

Another problem I've always had with pictures of chromosomes (like the diagram on the left) is that this shows a chromosome with every gene, every allele and every nucleotide doubled: it's constituent DNA has undergone replication. Therefore, whenever you see a picture like this, you need to remember that each arm (one on the left and one on the right) is absolutely identical (or thereabouts, seeing as even the best DNA synthase enzymes occasionally make a mistake) so you can think of this like two chromosomes, called sister chromatids. Each chromatid is held together by a centromere. At the time of writing, I was not sure what a centromere was, so after some googling I found that it is part of the DNA. At the centromere is a region rich in adenine and thymine which causes the two chromatids to be drawn together and causes kinetochores to form. What are kinetochores? Kinetochores are the binding sites for spindle fibres to attach to the centromere for mitosis/meiosis. Incidentally, the shorter pair of arms on the diagram are called 'p' because of the French for 'small': 'petit'.

Just one more bit on chromosome structure! Chromosomes form around bundles of proteins called 'histones'. Imagine, if you like, a cotton reel surrounded by thread. In this analogy you can imagine that the thread is like the DNA, winding around the cotton reel (the histones). Now if we extend this further, imagine that more reels are joining our original reel and the thread is continuing between the reels to make one continuous strand of DNA wrapped around many histones. This is just like the formation of a chromosome.

So, now chromosome anatomy is done it's time to explain their purpose in genetics. We humans have a grand total of 46 chromosomes (which 23 pairs, obviously). These pairs can be arranged into  a karyotype. To the left is the human karyotype, which is basically all of the chromosomes paired up into their homologous pairs (one from each parent, unless you're the result of parthenogenesis... which you probably aren't) and put onto a chart. As you move from pair 1 to pair 22 (the autosomes), the chromosomes get smaller. This suggests to me that as the pair number gets higher, the more recently that chromosome emerged in our evolutionary history - as it has had less time to accumulate more DNA as introns or mutations. Interestingly though, the sex chromosomes (pair 23, Y and/or X) are larger and look roughly the same size as pair 10. This suggests that the male mutation (how insulting, I know) arose at about the same time as pair 10 did. Therefore, find when pair 10(ish) turned up, and you're within a few million years of finding Adam.

After enough waffle to feed a small village, I've decided to move onto genes and alleles. Each chromosome carries a specific set of genes. Another important point to remember is all people have the same genes, hence same species, but have different alleles - which results in variation. NEVER say we all have different genes. But anyway, to exemplify my point the gene SERPINA1 is found on chromosome 14 and is responsible for the production of alpha-1 antitrypsin which controls the action of elastase in the lungs. An absence of the dominant allele can lead to hereditary emphysema. Each gene is also only ever found in one position on a chromosome, called a locus. Remember, each chromosome has a homologous pair, so each gene will be found twice (but maybe with different alleles) in each karyotype - but on the same locus on each chromosome.

One last thought, each DNA molecule is about 2nm wide and 50mm long. If we scaled that up to 5mm string, then it would be 125km long. So next time you are struggling to pack your suitcase, spare a thought for the size of the job for the histones.