Nessa Carey [ Imperial College, London ] You can’t talk about epigenetics without talking about genetics. This is the representation of the famous DNA double helix and back in 2001, when the human genome sequence was first released, there was this huge hoopla about it and some quite entertaining things were said.

There was this big press conference and that quote at the top left, “today we are learning the language in which God created life” that was President Bill Clinton.  I can’t imagine what it looked like for a whole roomful of scientists presenting their life’s work to have a politician rock up and start talking about God.

It must have been a great moment. The one down the bottom is not actually much less over-hyped.

It’s from Michael Dexter, who was chair of the Wellcome Trust — who poured a huge amount of money into this project, and he described the sequencing of the human genome as “the outstanding achievement in terms of human history”.

I think we might quibble with that a little.

The written alphabet, the wheel, fire, the number zero — all of those we could argue have perhaps had a bit more impact — but the human genome sequence is a big deal.

The human genome our DNA is composed of just four letters but those four letters are used over and over again to create this extraordinary volume which is us.

In fact, you inherit 3,000 million of those letters from your mother and 3,000 million from your father so three billion letters from each parent and sometimes it just takes one of those to be wrong and you can have a devastating disease.

The genome sequence is really important but it’s not all that there is and we’ve known that for a long time because we’ve known of these things called epigenetic phenomena. I’ll explain that term in a moment but let me give you some examples first.

You can breed laboratory mice, and I have to warn you — if any of you are really really fond of mice — they come up a lot in this presentation (not always in a good way), you can in breed laboratory mice and you can keep them under absolutely identical conditions.

The mice are so umbria(?) that they’re genetically the same as each other and the laboratory conditions are exactly the same and yet the mice are not identical. They will vary, for example, in things like body weight.

This has been known for such a long time, since at least the 1920s, that it was given a particular name as a phenomenon it was called intangible variation.

It’s a gorgeous example of where, in biology, we see something we don’t understand so we give it a fancy name and we just kind of park it.

A maggot and a fly. A maggot and a fly look completely different to one another and yet they have the same genetic code. There is no genome fairy that comes along and gives a maggot a new set of genes when it pupates into an adult fly.

Crocodiles and mammals.

It’s really easy to understand gender. I would take DNA from this gentleman here and this lady (and I do advise you always get that bit right. I did it in a very dark lecture theatre once. Awful. Never really recovered) if I were to take DNA from these two people and sequence it, I would be able to tell which came from the man and which from the woman because in mammals gender is determined by whether or not we have a Y chromosome.

I would take DNA from a male crocodile and a female crocodile, I’d sequence it, and I’d not be able to tell which came from the male and which from the female. Because in crocodiles, those fabulous descendants of the dinosaurs, in crocodiles gender is not determined by genetics it’s determined by the temperature at which the eggs develop – which could be a very odd consequence of global warming.

We will see a skewing in crocodile populations.

Just to add to all the other worries right?

So in all these situations we have scenarios where we have two things which are genetically indistinguishable and yet those two things are different from each other and these are known as epigenetic phenomena.

Basically two things are genetically identical and yet, in terms of their phenotype — how they look — they’re different from one another.

The word epi is simply from the Greek and it means at, on, in addition to, as well as. So it means there’s something else operating as well as the genetic code.

Now these are all lovely examples of epigenetics but there’s one that’s even better.

In fact, there’s 300 examples of it in this room — because each of us we are a masterpiece of epigenetics. Each of us started from one cell and we end up being formed from about 70 trillion cells.

Just to give you an idea of how big that is as a number, if I were to I take this lady and dissolve her into her individual cells and give them to this lady to count and I say you have to count one cell a second and when you’ve finished you can go and have a coffee — she’d get her caffeine hit in one and a half million years.

I love that figure partly because it really demonstrates how complicated we are and partly because about 15 percent of the audience are now sitting there trying to work out in their heads if I’ve got the maths right.

I can say anything I like for the next ten minutes. It’s great!

So. Huge number of cells in the human body and, with the exception of a tiny percentage of cells in our immune system, all of those cells are exactly the same as each other at genetic level. They all have exactly the same DNA code.

And yet kidney cells are different from liver cells. Skin cells are different from brain cells.

Cell types are not only different but they stay different.

This is why you do not get teeth in your eyeballs.

I wanted to call my first book No Teeth in Your Eyeballs and my publishers said it lacked a certain gravitas.

So we are epigenetic phenomena and this basically should lead us to be asking the most important question in biology. The most important question in biology is always “how?”

How can it be that a single DNA genome, one set of instructions, can lead to so many different outcomes?

Why have I got at least 200 different cell types all from the same DNA code?

The way that I think about this is, because DNA is a script (it’s not a template) and you can amend a script. By amending a script, like sticking post-it notes on a script, or writing in pencil etcetera, you can get different outcomes.

I’ve given examples of that up there. Two movies separated by about 60 years. They use the same script. What’s the movie?

Very good, Romeo and Juliet.

Okay. Who are the actors in the black and white one? Leslie Howard and Norma Shearer, I love you. That’s the first time anyone’s got that right. Marvelous.

And who are the actors in the bottom one?

You know what? It doesn’t matter the age, whenever I say who are the actors? you give me “Leonardo DiCaprio” in quite high voices.

Right. Yes. Shakespeare script completely different productions.

Okay. And that’s what our DNA does. That’s what we can do with our DNA.

So what’s new?

Well, over the last 20 years or so marvelous things have started to happen in epigenetics.

The best way I can convey this is using a still from this movie. What’s this movie? Time Machine, very very good. Time Machine. Does anyone know, that time machine that’s up there, what sitcom it appeared in recently — relatively recent?

Very good Big Bang Theory! Excellent!

So basically there’s a wonderful scene in The Time Machine. Rod Taylor, who died recently, playing the time traveler and at this point in the movie he’s only made a model of his time machine and he gathers around his scientific chums.

The movie is set in Edwardian times and it was filmed in the 60s so of course all the scientists who come to look at it or all men.

Right.

So all these blokes are sitting around the table and they say to him, as the beautiful? time traveller, “how will your time machine work?” and he says, “well the time traveller will sit in that little seat and when he wants to move into the future he’ll push that lever forwards and when he wants to travel into the past he’ll pull that lever backwards”.

And they all go, “oh, okay!” as if he’s explained it and of course he hasn’t explained it. All he’s done is described it and so far all I’ve done for you is describe epigenetics.

The reason it’s such an exciting field of biology now is because we don’t just have the description we have the explanations and the explanations are all related to this.

This is what DNA looks like in a Cell though not multi-coloured. Famous double helix of DNA we’ve got in our cells, like a long stringy molecule, it’s wrapped around eight protein molecules. Each of those protein molecules is shaped like a fist and there’s a cluster of eight of them. What you can see is that there are these tails that stick out from the protein molecules. So you’ve got eight proteins together, DNA wrapped around them, tails sticking out.

This image represented the culmination of a huge amount of work by a lot of researchers and it cost millions to generate the data that allowed this picture to be created and it’s fabulous but from my point of view of trying to communicate something about science.

It has some limitations.

One is that if you’re not used to these kind of pictures, it’s a bit overwhelming.

whenever I put this picture up I literally can see the audience going [gestures ] throughout the whole room.

So it’s a bit overwhelming.

The other issue with it, from my point of view, is that it’s very difficult to adjust it to show you the things I want to show you and so I decided I needed an improved version of this. So I created one.

Mine is an improvement because did not cost millions. I was able to adapt it to show you the things I needed to explain and then once I’d adapted it in my photograph,I ate it.

Because mine is made from strawberry laces and marshmallows and jelly tots.

I used the strawberry laces to represent DNA. Clearly I’ve not tried to make them double-stranded, because that would be taking a confectionary based joke too far, but they’re going to be the DNA.

The marshmallows represent those eight proteins, that I told youabout — those eight fish? shaped proteins — and the cocktail sticks sticking out cunningly like that are the tails that I showed you.

Now what happens is a cell DNA wraps around a cluster of eight proteins and then you get a little bit of DNA there and then it wraps around another cluster of eight proteins and so on and so on and so on.

So you have millions of these clusters of eight proteins in our cells and one gene one bit of DNA that codes for a protein will be wrapped around multiple clusters.

That’s the basic structure.

How does that help us get any further in understanding what’s happening into our genes?

Do we have any present or former teachers in the audience? Okay! You’re going to relate to this. Let’s imagine it’s getting quite far on in the term, right? And you go home and you think I’d like a little gin to take the edge off.

So you have a little gin and the term continues, what feels like endlessly, and you start finding that now you need two little gins to take the edge off.

The reason you need two little gins, where before you only needed one, is because your body is breaking down the alcohol faster. It has switched on higher expression of the gene that breaks down alcohol and the way that it does it is like this.

This is the gene for breaking down alcohol. When there’s lots of alcohol coming into your system, signals get generated in the liver and you get little modifications added to the tails of those proteins coming there — represented by the green jelly tots.

What those modifications do is they basically make it easier for that gene to be switched on.

They drive up gene expression.

Let’s say it gets to the summer holidays. After a week or two you start thinking, I should really knock it on the head a bit with the gin — there’s no point your liver continuing to make large amounts of the enzyme that breaks down the alcohol because you’re not taking in the alcohol anymore.

The green modifications, the green jelly tots, that basically said switch this gene on are removed and replaced by purple jelly tots which basically signal turn this gene off — don’t need to be breaking down alcohol at the moment.

What we have there is a way of turning genes on or turning genes off and actually it’s massively more complicated than that.

Imagine a world in which there were like 60 different flavors of jelly tots — I’m so happy when I imagine that world — so you could have 660 different colors of jelly tots on that cluster and they could occur in all sorts of different combinations

They wouldn’t have to be all green ones or all purple ones

You can see that they could all influence gene expression by different amounts. You could start having a whole range of expression, not just off and on but anywhere in between.

You can introduce enormous flexibility into how genes are expressed.

But if we have a situation where we have lots of the purple jelly tots, on lots of the protein clusters, in the same region, we can also get our modifications to the DNA itself represented by the yellow jelly tots. This says, “I’m serious about it, I don’t want this gene switched on,” you can get very high levels of that modification to the DNA.

When that happens the whole region of DNA scrunches up becomes incredibly compacted. The genes really can’t ever be switched on, so it shuts down gene expression pretty much permanently of that gene.

That’s why the genes in our brain for example do not express the gene for hemoglobin — that carries oxygen around in our blood.

They’re scrunched together in early in development and they stay switched off forever.

So we can use these sorts of modifications to switch gene expression off forever by this compaction.

We can also have a more open situation where the gene expression can vary depending on the environmental circumstances.

All of these modifications are called epigenetic modifications because they’re all in addition to the basic genetic code. And what they all do is, they change the likelihood of gene expression. But they never change the sequence. The gene still codes for exactly the same thing.

So it’s a fascinating system, and it’s fascinating in its own right, but it’s also fascinating because of the impact for us.

Epigenetic modifications really matter in human health and disease because sometimes they go wrong. We know this happens in certain types of cancer. We have drugs that actually help to change the epigenetic modifications — that are treating certain cancers very successfully — and billions of pounds are being spent in the pharmaceutical companies to discover more drugs like that.

We also see how epigenetic modifications going wrong, or being set in the wrong way, too early in life., for example, may influence lots of other aspects of human health. Particularly things like chronic diseases.

Things like rheumatoid arthritis or type 2 diabetes.

Something where someone tends to be ill for a very long time and stays ill and perhaps gets progressively worse. In those situations, gene expression is getting more and more misregulated and we think it may be due to epigenetics.

But there’s a particularly startling example of this in action that’s being explored and to think about this we have to think back to the Jesuits.

I think it was a that Jesuit said, “give me a boy until he’s seven and I will show you the man”? and that’s actually related in an odd way to one of the biggest publishing phenomena of recent years which is the rise of the Misery Memoir.

This is an actual photograph from a book shop: tragic life stories. Lovely.

The most famous example of this is this book called A Child Called It.

It was in the New York Times bestseller list for six years.

There’s been a huge appetite for these kind of books and they tend to follow the same story arc.

A child has terribly neglected. An abusive childhood and somehow they overcome it and they become happy successful adults.

I suspect one of the reasons why these books are so popular is because we actually recognize that those stories are exceptional.

All of the sociological data show that, if a child has a awful childhood, then as an adult they are at much higher risk of things like alcoholism, addiction to drugs, suicidality and mental health disorders — including severe depression and also schizophrenia.

Having a rotten childhood is a terrible start in life.

It’s true, even if a child is taken out of that awful environment and put into a more nurturing one they are still at higher risk of these adult mental health disorders.

You say to somebody why is that the case? Why did what happened in their childhood influence what happens in their adulthood? The answer you almost always get is they were psychologically damaged — which is undoubtedly true and utterly useless because it’s a description it’s not an explanation.

We can’t probe what’s happening at a molecular level in somebody’s brain but for someone like me, who’s a scientist, I have this strong belief that things have a physical basis and so something must be happening.

We can’t do this in children, but experiments have been done in a model system — which is basically rats.  Baby rats adore being loved. Absolutely adore to be loved.

And when you’re a baby rat, the way that you feel loved is that your mother licks and grooms you a lot.

Now there are rat mothers who are really good at licking and grooming, and they’ll be really good with all their litters, and there are other rat mothers who are a bit feckless and will do the bare minimum of licking and grooming.

They’re like that with all their litters as well.

Now let’s say we take a baby rat that’s been loved a lot and we let it grow up.

When it’s a baby, it’s a happy rat — and we let it get older, and rat babies are not like human babies okay after a few weeks they will leave their rat mother and not hang around waiting for their share of the mortgage.

There’s a lot to be said for rat babies.

So rat babies, a happy rat baby, grows up and when it grows up you give it a mildly stressful stimulus.

The rat adult just kind of shrugs.

It’s the whatever rat. It’s very chilled out.

However, if the rat baby was not licked and groomed a lot and you let it grow up and you give it the same mildly stressful stimulus — it jumps out of its skin.

It’s a highly stressed adult.

So we can see they are quite good analogy with the child who has had a terrible upbringing and who is a highly stressed adult.

If you look at things like levels of stress hormones in the rats, the ones that were loved as babies have low levels of stress hormones as adults. The ones that were abused, as it were, by not being licked and groomed enough, have high levels of stress hormones.

Very similar to what we see in adults who had terrible childhoods.

It’s completely dependent on whether or not the babies were loved.

If you do fostering experiments and you take a baby from one litter, a rat baby from one litter who was born to a mother who licks and grooms, and you transfer it to a mother who doesn’t lick and groom — you get the bad outcome as an adult.

What seems to be happening is that when the babies are licked and groomed a lot they produce serotonin — the Happiness neurotransmitter that sets up a particular pattern of epigenetic modifications at particular key genes involved in the stress response.

Those are set up early in the childhood, as it were, and they stay there for the rest of that rat’s life — on cells in the brain — and you get either a stressed-out or a happy adult rat depending on that early circumstance.

Quite controversial research but really quite intriguing.

I’m going to take you into something even odder.

Here we have — on this slide we have a stick insect. We have a little fish, a rather gorgeous salamander,  the lovely Komodo dragon — big fan of Komodo dragons, the zebra finch — all of those animals, in fact those precise ones — which represent a huge swathe of the animal system — can do something that mammals can’t.

Does anyone know what it is?

I think I heard it, all of these animals, including the zebra finch, can all have virgin birth

There are zebra finches, females that have been kept in captivity — never been anywhere near a male — and yet they can lay eggs that will give life — give birth.

Mammals can’t do that.

You have to have a male and a female in mammalian reproduction

Actually that seems fairly straightforward

We kind of think, “yes, of course you do” but why?

This is one of those examples of an experiment that was so beautifully designed that you kind of think oh god that’s so obvious isn’t it once someone’s done it beautiful.

Work from Azim surrani in Cambridge in the 1980s.

What he did was he took a mouse egg and took out the nucleus and then he would put back into that egg. Either two sperm nuclei, or two egg nuclei, or an egg and a sperm.

All those situations were genetically identical so that whether the egg received two egg nuclei, or two sperm nuclei, or an egg and sperm nucleus, it was exactly the same situation in terms of DNA sequence.

Then he would put the eggs back into pregnant female mice.

If he used two egg nuclei, no live mice.

If you use two sperm nuclei, no live mice.

But if you used an egg nucleus and a sperm nucleus, live mice!

What that tells you is that the reason you have to have a male and a female — when you’re doing mammalian reproduction — is because there is something on eggs and sperm in addition to the genetic information that’s necessary for development.

That information that you have to have, the additional information, is epigenetic information.

There are particular regions of our genome, and it’s true of all mammals, that come with little epigenetic modifications on them — basically the yellow jelly tots — on the DNA that say I’m from mum or I’m from dad and they control particular levels of gene expression that are absolutely crucial to maintain development.

So that’s why you can’t have virgin birth in mammals.

You have to have epigenetic information from mum and from dad.

Carrying on from that — some weird work with mice. These are my favourite mice. I don’t even know why I have favourite mice, but I just do.

There are mice called the agouti viable? yellow mice.

We have a skinny brown mouse on the right and this gorgeous fat golden one on the left and it is so cute isn’t it?

It really is.

And actually you get everything in between as well.

I’ve just shown you the extremes here.

The weird thing about these is they are genetically absolutely identical.

There is no difference anywhere in the DNA code of those two mice.

They are reared under absolutely identical conditions.

So it’s nothing to do with how they’re brought up.

So why are they so different?

It’s epigenetics.

Just one bit in their genome.

There’s a different pattern of those yellow jelly tots on the DNA and that changes expression of one gene and as a consequence you can get the skinny brown mouse or you can get the golden golden fat mouse.

And you can get everything in between, just by a few epigenetic modifications at one place in the genome.

So that shows us how significant epigenetic changes can be

But they also showed us something else

See the fat yellow mice tend to have a high percentage of fat

Yellow babies and the skinny brown mice tend to have a high percentage of skinny brown babies — essentially they’re passing epigenetic information on — so the skinny you brown mice are passing on the skinny brown epigenetic modifications and the yellow mice fat yellow epigenetic modifications.

Until you give them alcohol

Right now I just love the idea of being able to go home at night and yeah you get in and you’re other half says, “what did you do in the lab today darling?”

“Oh I got some mice absolutely ratted”

I suspect it wasn’t Prosecco. This was done in an Australian lab, so it’s probably nice Shiraz or something.

Anyway, they gave the female mouse mice alcohol. When you do that, the fat yellow mice have a different percentage of fat yellow offspring and the skinny brown mice have a different percentage of skinny brown offspring.

The alcohol has changed the epigenetics and that has changed what the offspring.

So altogether these bits of information lead us to some really straightforward thoughts

Epigenetic information is passed on from parent to child

We know that it has to be, otherwise you can’t have mammalian reproduction, and the fat yellow mice that have lots of fat yellow offspring, they’re passing on epigenetic information

We also know that epigenetic information is influenced by the environment — that’s one of the main things it does — it allows us to respond to our environment

But the totality of all of those experiments that I’ve just shown you leads us to this question, “can parents pass on environmental responses to their offspring using epigenetics?”

And that’s something that was explored beautifully in this experiment

Again anyone who’s very fond of mice put your hands over your eyes.

What they did is take mice, male mice, and they expose them to the smell of cherry blossom and when they expose them to the smell of cherry blossom they then gave them a mild electric shock

I know, somebody always goes, “ohh” at this point

They did this over and over again — it’s just a classic conditioning experiment — essentially you get to a stage where the mouse learns to associate the smell of cherry blossom with something nasty that’s about to happen and it starts to shake with fear when it’s exposed to the smell of cherry blossom

Say I took these male mice and allowed them to breed and looked at their offspring, and exposed them to the smell of cherry blossom, no electric shock, just expose them to the smell of cherry blossom — and they they shook with fear.

They had inherited the trauma, the fear response, from their parents.

And the cool thing about this experiment is that actually the group’s working on it knew a huge amount about how smell is detected, how genes get switched on using epigenetics in the brain in order to be able to detect certain smells and which brain cells to look at

They were able to show that that first generation had all the expected changes in their brain cells in terms of epigenetics and switching on particular genes but so did the offspring

It’s an extraordinary finding and it’s also completely heretical

Who’s the chap with the amazing sideburns?

Lamarck! exactly!

Who’s the other animal?

Giraffe! Yes, very good!

So as many of you no doubt know Lamarck was a predecessor to Darwin.

He came before Darwin.

He was trying to explain how you got different species and how you got different sort of inheritance.

The example he gave, amongst many, was that the long neck of the giraffe.

Lamarck’s explanation was that certain giraffes would stretch to reach the highest tree highest leaves and that would stretch their necks and then they would pass on stretch necks to their offspring.

So it’s an example of how they got a longer neck through stretching and they passed this on.

It’s an acquired characteristic.

And of course now we almost kind of life laugh at Lamarck. You know, “how ridiculous. That’s not what happens. we know what happens. it’s a Darwinian model.” Some precursors to giraffes naturally had longer necks that gave them a selective advantage that got passed on to their offspring the gene change that basically allowed them to have longer necks.

But what I’ve been describing is the opposite of that

It’s Lamarckian

It’s something that happens to the parent

They respond to it, which is an acquired characteristic, and they pass that on to their offspring

So there’s huge amounts of basically fighting about this but one of the reasons why there’s a lot of fighting about this, apart from the fact that some people are very uncomfortable with the idea that Lamarckism could ever happen, is because these experiments have to be incredibly carefully carried out.

And this is a beautiful example — again, sorry mice — take a little mouse and put it in a cage with the big mouse and you don’t let it get away. the little mouse, because mice will always run from trouble, the little mouse gets increasingly traumatized. stops eating. gets very nervous etc.

Okay so they traumatized little mice like this and then they mated them with females and the offspring were runty.

Okay and that was interpreted as the male transmitted his trauma okay he was runt.

He transmitted that — an acquired characteristic.

He was a substandard one.

But then somebody did something really clever.

They exactly repeated the experiment but instead of introducing the traumatized male mice into a cage with a female they got his semen and they artificially inseminated a female mouse.

And when they did that, all the offspring were perfectly normal size.

It was not that the male had transmitted his trauma.

What had happened was that the female, having seen this runty little specimen coming along, had realized she was being mated with a really substandard male.

I think of this as I ordered George Clooney they sent me Danny DeVito right.

Once she couldn’t see that she’d got the Danny DeVito mouse, perfectly normal offspring.

That shows you it was not epigenetic transmission from the father to his offspring.

It does raise a rather more interesting question which is how the hell does the female do that, and nobody knows.

We have no clue how the female manages to restrict the calorific supply when she think she’s been mated with a runty male but it shows you just how careful you have to be when you run these experiments.

Now there is so much science in the field of epigenetics that I wish I had time to cover with you.

I’m sure it’s of no interest to any of us in this room but it does play a role in aging not the most important thing but it does play a role.

Twins. Twins, genetically identical twins. They have exactly the same DNA code. And yet the older they get, the less similar they tend to become. That’s because they start diverging epigenetically sometimes in response to different environments.

If they’ve lived through different things sometimes just through random epigenetic drift and it can be very extreme.

If you take identical twins, if one has schizophrenia, there’s a one in two chance that the other twin will also have schizophrenia. the more interesting question, in some ways, is why is it not a 100% chance.

That’s probably at least in part due to epigenetic variation between the twins.

Tortoiseshell cats with that gorgeous black and orange coloring that’s entirely due to an epigenetic effect which is actually to do with switching off one copy of an X chromosome, the female chromosomes, in cats.

All tortoiseshell cats are female.

If you happen to have a male, he’s infertile.

It’s all to do with how epigenetics controls things.

Wheat sorry don’t we winter flowering barley and lots of other plants need a period of cold before they will flower that’s totally driven by epigenetic modifications of different genes in a particular sequence.

In fact epigenetics is totally accepted within the plant world.

Everyone’s known about a few years.

It’s just that it’s only us types who are behaving like we’ve discovered something extraordinary.

Plant people are perfectly comfortable with epigenetics.

Who’s the sheep?

Dolly! Excellent, excellent!

I always have to point out at this point she’s dead in this picture. it’s not just she was the most important sheep in the world so they just rolled her around on trolley. this is from after she’s died which is at the Royal Scottish Museum.

Epigenetics is the reason why it is possible to clone animals.

It is also the reason why it’s very difficult to clone animals and why the clones are usually less healthy than the adults.

Honeybees. Worker honeybees and Queen honeybees.

There’s nothing to distinguish them genetically. you can’t take the DNA out and tell which came from a worker and which from a queen.

Anyone remember what causes the development of Queens?

Royal Jelly, absolutely!

They get fed royal jelly for a bit longer so all that happened in the developing bees was how long they were fed royal jelly for and the phenotypic difference is extraordinary between workers and queens.

The most striking example of this is that queen bees have a lifespan about twenty times that of a worker.

If you put that into human terms we are in the reign of Queen Elizabeth the first and we’re only half way through it.

That’s how huge the phenotypic change is.

And that’s absolutely connected with epigenetic changes in gene expression.

So there’s all of this and so much more which sadly I don’t have the time to tell you about but happily I have to have written a book about it and do you know what they’ll be selling it downstairs.

Apparently there’s some nice person from Blackwell’s here and they’ve got copies of the first one The Epigenetics Revolution and just out three weeks ago was Junk DNA my new book.

There is still a huge amount we don’t understand about epigenetics and I think that’s what makes it so exciting because biology where we know everything is terribly dull biology and so all I want to do now is thank you for being such a great audience.


FEATURED IMAGE CREDIT: Ian Sane

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