Why are plants green?

After the greyness of winter, the arrival of spring is heralded by a splash of colour as plants emerge from the soil, and trees seemingly erupt with leaves. Soon, much of the countryside has moved from being something of a grey, barren wasteland to a sea of verdant green. But why is it that so much vegetation is green? Why not a sea of red, or blue? To answer this question let me take you on a colourful journey from the sun to within the cells of plant leaves.

As humans, our waking hours are punctuated by mealtimes: we must consume food on a regular basis if our bodies are to be able to generate the energy we need to survive. Plants, however, fuel their survival in an altogether different way. Plants don’t need to ‘eat’ as such; instead, they generate their own food supply. This manufacturing of food is powered by energy that plants capture from sunlight.

It might seem odd to say that sunlight contains energy, but our everyday experience shows this to be so: if we sit outside on a sunny day, our skin quickly becomes warm. This warmth is the result of our skin cells absorbing the energy contained in the rays of sunlight.

Sunlight is made up of millions of individual rays containing a huge range of different energies. Imagine standing on a beach, watching the waves rolling in. These waves aren’t identical in size: there will be some small waves that contain little energy, which fall gently on the sand, and other much larger ones that come crashing down; these contain a lot more energy. And so it is with the rays of sunlight: some rays have a small amount of energy; other rays have much more.

This leads us on to another, perhaps surprising, phenomenon: we see rays of light of different energies as different colours, as beautifully illustrated by rainbows, which we’ll all have seen from time to time (most often on a typical British summer afternoon, as bright sunshine is suddenly replaced by a downpour of rain). When sunlight – a mix of rays of different energies – hits drops of rain, the individual rays are separated according to their energy. Suddenly, a mix of rays that, to us, have no obvious colour become transformed into the characteristic colours of the rainbow: red, orange, yellow, green, blue, indigo, violet. We call this range of colours the visible spectrum.

Sunlight also contains rays that fall outside of the visible spectrum, none of which are visible to us, but which are visible to other creatures. For example, many insects can view ultra-violet light, which has greater energy than the violet light at the one extreme of our visible spectrum. In fact, some flowers look much more visually interesting to insects than they do to us: insects can see extra marks and patterning that show up in ultra-violet light, but which are simply invisible to us. (You can see a couple of examples here and here.)

But what has this to do with the colour of plants? Why do we see plants as green? The cells of a plant leaf contain compartments called chloroplasts, which house some special machinery that enables the plant cells to capture the energy in sunlight and to use it to power the formation of food. Chloroplasts contain a substance called chlorophyll, which is an example of a pigment – a substance with an obvious colour. This pigment isn’t there just to make the plant look pretty to the human eye: it is the component of the chloroplast that actively absorbs energy from sunlight. However, it can only absorb rays of light that have particular energies – those corresponding (in broad terms) to red and blue light. By contrast, the rays of light that fall in between red and blue light in the visible spectrum cannot be absorbed. Instead, they bounce off the surface of the leaf and into our eyes (if we’re looking at them). And what colour lies between red and blue in our spectrum? You’ve guessed it: green. The reason we see plants as green is because green is the colour of the rays of light that get bounced back by the chlorophyll in the plant cell.

In fact, this concept holds true for any colour that we see. The reason that tomatoes appear red is that they don’t absorb red light: it is bounced back from the surface of the tomato to be detected by our eyes. Tomatoes exhibit their red colour thanks to the pigment lycopene, which absorbs blue and green light, but bounces back red.

Let’s end this journey with a brief flit across the Atlantic to see why plant leaves don’t always appear green. Parts of the Eastern seaboard, in the US and Canada, are famed for the fiery displays of colour by trees in the autumn. This dramatic change in colour is a consequence of chlorophyll being degraded as air temperatures drop with the change in season, leaving behind other pigments that had previously been masked by the chlorophyll. As chlorophyll is degraded, the greenness fades, to be replaced with vivid reds and oranges. It’s now the turn of other light rays to be bounced back – giving us something truly to feast our eyes on.

Why are we told always to finish a course of antibiotics?

Most of us have at one time or another been prescribed a course of antibiotics by our GP. But how many of us heed the instruction to complete the course – to continue taking the tablets or capsules until none remain? Very often, our strict adherence to the prescription fades in line with our symptoms: the prescription may last for, say, seven days, but we’re often feeling much better after just two or three. So why bother continuing to take the antibiotic? After all, if we’re feeling better, the antibiotic has done its job, right? Well, you may think so. But, in fact, stopping a course of antibiotics early can have potentially lethal consequences. How can that be?

To answer this question, we must travel inside our body to mingle with the bacteria the antibiotics have been prescribed to kill. At face value, all the bacteria in a given population might seem identical. But look a little deeper, and you’ll see subtle differences. And one difference is the way in which they respond to a given antibiotic.

I described in a previous post how antibiotics are designed selectively to attack bacteria rather than causing harm to our own cells, which must necessarily get exposed to the antibiotic as it travels through our body in search for the alien intruder within. But different bacteria, even from within the same population, may respond differently to a particular dose of antibiotic. The ‘weak’ ones may be susceptible to a relatively low dose – they may be killed after just a few days of exposure to the antibiotic; by contrast, others may be much more resilient, and will still be alive after a few days of treatment.

The important point here is that the population as a whole is made up of bacteria exhibiting a range of tolerances – at one end of spectrum, a few real weaklings; at the other, a few really resilient ones. And, in between, we find many average, run-of-the-mill individuals, who can hold out against the antibiotic for so long – but not for very long. (I saw the same kind of distribution within a population when we grew some tomato plants this summer: some were noticeably short, some were unusually tall, but a majority hovered somewhere in between.)

But what’s causing this difference in tolerance? I mentioned in a previous post that each time a genome is copied there’s a chance a mutation (an error) will creep in to one of the genes making up that genome. Well, every time a bacterium reproduces it has to make a copy of its genome to pass on to its offspring – and, every time, there’s a chance an error will creep in. The chances are that the variation in tolerance to antibiotics that we witness in this population of bacteria is due to slight variations in their genomes; it could be that our resilient individuals show this resilience because they picked up mutations not present in their weak or average cousins.

Now, let’s return to our bacterial infection and imagine that we’ve started to take a course of antibiotics. It takes just a day or two to kill the real weaklings. And, in three or four days, even the Mr Averages will start to feel the proverbial heat. At this point, the population as a whole will have gone into noticeable decline, and we may start to feel much better as the number of alien invaders reduces.

But what has actually happened by the three or four day stage? The population as a whole may have shrunk in size – we’ll have rid ourselves of the few real weaklings and the larger number of Mr Averages – but we’ll be left with the few hangers-on at the other end of the spectrum, the real bruisers.

Before we started taking the antibiotics, the antibiotic-resilient bacteria (our ‘bruisers’) were fighting for a share of the available food with all the other members of the population. (It’s important to note that, when I talk of ‘weak’ or ‘resilient’ individuals I’m only referring to their tolerance level to antibiotics, not their ability to scavenge for food, and other aspects of survival in an antibiotic-free world.) In essence, the bruisers were being kept in check by everyone else – they remained in the minority because the whole population, including the weaklings and the Mr Averages, was growing at about the same rate. Now, three or four days in, the bruisers suddenly find themselves with much less competition for food. Imagine going to the buffet table at a wedding with 200 guests, all of whom are vying for a slice of the pie (quite literally), versus going to the same-sized buffet table with the same amount of food at a wedding attended by just 20 guests. At which wedding are you most likely to be able to fill your proverbial boots?

Now let’s consider what happens after day three or four, once the supply of antibiotic has stopped. At this point, remember, there are just a relatively small number of antibiotic-resilient bacteria left, but no weak or average ones. When the resilient bacteria suddenly find themselves the guests at an unexpected banquet – with competition for food gone – they do what bacteria do best: they reproduce. And without the previous competition for food, they can do so rapidly. So, we’ve suddenly gone from a mixed population in which the majority didn’t take kindly to antibiotics and only a few were the bruisers, to one in which virtually everyone is unusually tolerant to antibiotics. And this is where the real danger can lurk.

I mentioned above that the resilient bacteria may exhibit their resilience because they have accumulated more errors in their genomes than their weak or average cousins as successive generations have reproduced. As this resilient population now continues to thrive, it risks accumulating even more errors. And one of those errors could be what it takes to tip the balance from the bacterium being highly-tolerant of the antibiotic to it being completely resistant. You don’t need to be a medical expert to realise that complete resistance to an antibiotic is a really bad thing. If a bacterium has overwhelmed our immune system, and we don’t have an antibiotic to act as a back-up defence system, we have no weapons left to fight with.

If we carry on taking our antibiotics as prescribed, the story ends quite differently: even the resilient bacteria lose the will to live in the end. But we have to keep up the pressure by finishing the course of antibiotics. That way, any resilient individuals don’t get to dominate, and we reduce the risk of one of them picking up a mutation that makes them virtually invincible – but which is potentially lethal for us. In future, you know what you need to do…

What happens when our immune system doesn’t work as it should?

I consider myself lucky: I don’t wait for the onset of summer with trepidation, knowing that it will bring days of itchy eyes and sneezing. For others, though, the blossoming of our natural world through spring and summer is less a time for marvelling at the wonders of nature, and more a time for an annual battle with hay fever. But why do some people have to suffer such afflictions while others don’t? What’s going on?

As I’ve mentioned in earlier posts, our immune system protects us from attack from potentially dangerous alien invaders in our surroundings. But sometimes even the best systems can go awry, as hay fever demonstrates so clearly.

The symptoms of hay fever – the itchy eyes and runny noses – are a consequence of the reaction of our bodies to pollen in the air. On the one hand, pollen is an alien invader (after all, it’s not a natural part of our body), so you might think it’s a valid target for attack by our immune system. However, it’s a harmless intruder, whose presence won’t actually cause any damage if left alone. So, in fact, there is no real benefit to be had from our bodies mounting an attack against it. Indeed, this is why, for many people, no attack is mounted. (It’s a bit like having both a neighbour’s cat and a poisonous snake wandering into your garden: the cat might not belong there, but at least it won’t do much harm. You’d struggle to feel the same about the snake. It’s a question of knowing which battles are worth fighting.) For others, though, the lack of danger posed by the intruding pollen isn’t recognised by their immune system, and the familiar response I’ve noted above is triggered.

Hay fever is an example of an allergy – the inappropriate response by our body to something that isn’t actually a threat. This inappropriate response takes the form of our immune system over-producing a particular type of antibody – but it is the knock-on effect of this antibody over-production that we really notice. As I mentioned in a previous post, antibodies can summon other parts of our immune system into action. When we suffer an allergic reaction, the overabundant antibodies sound a call-to-arms that triggers inflammation – localised swelling as the white blood cells of our immune system rush in to mount an attack on the perceived intruder. 

Sometimes this over-sensitive response is little more than an annoyance, as in the case of hay fever (though I should note that it’s a significant annoyance for hay fever sufferers); other times, an over-sensitive response can be life-threatening, as in the case of asthma, where the network of tiny tubes that form our lungs swell up, making breathing very difficult. 

It’s not just invaders from outside that can trigger an inappropriate response by our immune system, however. Sometimes, our immune system can turn inwards and start to attack components of our own body, wrongly considering them to be a threat. Such a response is called an autoimmune response. For example, rheumatoid arthritis – the painful swelling and degeneration of our joints – is caused by the white blood cells of our immune system attacking the cells in our joints, as if they were dangerous intruder cells. 

Similarly, a certain type of diabetes, in which an individual’s body fails to control the level of sugar in their blood, is also associated with the misbehaviour of our immune system; in this instance, the immune system attacks a certain type of cell found in the pancreas, the part of the body that manufactures insulin. Insulin is a chemical ‘messenger’, which travels round the body, controlling how much sugar is taken up from our bloodstream. When the pancreas is damaged by attack from our immune system, its production of insulin is impeded and, with it, the vital control of our blood sugar levels.

So what causes our immune system to malfunction in these ways? While we don’t yet understand enough to have all the answers, allergies, in particular, seem to stem from the way the immune system is ‘trained’. It may seem odd to say that the immune system needs to be ‘trained’. After all, our heart doesn’t need to ‘learn’ to pump blood; our skin and nails aren’t educated in the art of growth. But our immune system does need to learn – and one way is for it to be exposed to germs and the like during childhood. Increasingly, however, this isn’t happening. 

As a child, growing up in a relatively rural part of the UK, I spent much of my time outdoors, playing in the garden, or tramping over local fields, and getting exposed to plenty of old-fashioned dirt in the process. Now, however, children spend much of their time in dirt-free zones, slumped in front of the TV, or huddled round games consoles. And this clean living comes at a price: we are seeing a significant increase in the incidence of asthma in countries of the Western world, where children are growing up in increasingly germ-free surroundings. It seems possible that, by being exposed to too sterile an environment, our immune system may not be encountering a sufficient number of potential threats to learn how properly to differentiate between harmful and harmless, and risks becoming overly-sensitive to things that are, in fact, harmless. (This is a possibility set out in the so-called ‘hygiene hypothesis’ – but is something that remains a hypothesis, rather than an irrefutable fact.)

There are also lots of questions around how our immune system fails to ignore ‘self’ – that is, why our immune system wrongly turns against the cells and tissues of our own body. Early in life, our immune system is ‘trained’ to ignore self: those white blood cells (the B cells and T cells that I mentioned in my last post) that recognise self are eliminated. But, for reasons that are still being explored, this process of education clearly isn’t quite enough. Sometimes it seems that the information stored in a person’s genes makes them susceptible to autoimmune diseases; in other cases, environmental factors such as certain bacterial and viral infections seem to be a contributory factor.

Whatever the answers prove to be, it remains the case that we would live in constant peril if we had no immune system at all, as by those with severe combined immunodeficiency (SCID). These individuals have such severe defects associated with their T cells and B cells that they can only survive, without treatment, if kept in a completely germ-free environment, as so heart-wrenchingly demonstrated by the case of David Vetter, whose childhood spent living in a plastic, sterile bubble led him being known to the world as the ‘bubble boy’. The rest of us have a lot to thank our immune systems for – even if they don’t behave quite as intended 100% of the time.