Karin B. Michels | Is Epigenetics Inherited? || Radcliffe Institute
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Karin B. Michels | Is Epigenetics Inherited? || Radcliffe Institute


– Well, thank you very much. And thank you for this
extremely kind introduction. It was probably the
nicest introduction I’ve ever got for any talk. And I’m also extremely
privileged to be a hero among all these
unbelievable Fellows, and I’m very, very
flattered to be having been selected as a Radcliffe Fellow. When I found out that
I got this fellowship, I was actually somewhere in
rural Vietnam about a year ago, on a public bus with
spotty internet. And I got this
email, and it didn’t open for about seven minutes. And when it finally opened,
I started to scream, and all these Vietnamese
people on the public bus looked at me like, these
foreigners are so weird. So anyway, it’s been
great to be here, and I hope I can share with
you a little bit of what I do this afternoon. So thank you very much
for being here today. I want to also think Professor
Gelles for setting up my topic last week in
last week’s lecture, where he actually showed
you this picture, which becomes very handy to me today. Because he already gave
you an introduction into genetics and
transcription and translation and what happens, very
basically, with our DNA as it is transcribed into
RNA and translated into the proteins
that make us alive and makes our body
function, such as hormones and other proteins. Professor Gelles also
showed you this picture, and as he was
explaining, his work– and the work he does with
RNA, and telling you– and RNA polymerase, and telling
you that all the mechanisms that I showed you before work
in all different cell types the same– set me up for my journey today. I want to go down
a different path. I want to ask the
questions, what makes these cells
different given that they do have all
the same DNA and all the same transcription and
translation of processes? How come, then,
they are different? And they all arise, of
course, from the same stem cells with the same
genetic information. And remember, each one of
us, as we are sitting here, is a former stem cell. So the answer to the question
why we have different cells– one is a muscle cell,
and one is a blood cell, and one is a kidney cell– is that while every cell
has the same potential due to their genetics– potential
in expression and forming proteins– every cell activates
different genes. So your DNA is basically
little compartments which are the genes that
then can be translated into different proteins. And not every cell
reads the entire genome. In fact, no cell reads
the entire genome. Every cell decides
which of the genes are necessary to produce
the cell, the protein, that makes the cell the cell and
its particular function. Now, I’m interested
in the mechanism that makes this possible. And that is basically
epigenetics. So what is epigenetics? Epigenetics is a mechanism that
shuts on and off these genes in the different cell types. And epigenetics uses
three different mechanisms to do this. One is DNA methylation, which
is possibly the best known epigenetic mechanism, which
is essentially just adding something– an adduct– onto the DNA. And that also explains the
name “epigenetics,” “epi-” meaning above, on
top of, the DNA– an additional layer
of information on the DNA that tells the DNA
whether it’s active or passive. And in addition to this
DNA methylation– which is basically adding methylation
groups to certain parts of the DNA, depending
on whether you want to silence it by
adding a methyl group, or activating it by not
adding this blockade. In addition, there’s also
the chromatin structure of your DNA, which
basically means– you all know that the DNA is
an incredibly long molecule, but it has to fit into this
unbelievably tiny cell. So it’s curled up. And this curling up,
if it’s really dense, this messenger RNA Professor
Gelles told you about last week cannot get there and do the
transcription and then go on to do the translation
and the protein. So depending on how
it’s curled up– we call this the
chromatin structure– it is possible to read
these genes or not. And then also, curling them
around the histone molecules in your cell also
allows, potentially, whether these genes are
going to be read or not. The third mechanism
was only later added to the understanding
of epigenetics, and that is microRNAs. MicroRNAs also
contribute to being able to read this
information on the DNA. So what the microRNA does
is, it potentially binds to messenger RNA and therefore
blocks the translation process, so the protein is not created. So we have DNA methylation,
chromatin and histone modification, and
microRNAs as to the three fundamental functions
in epigenetics. By far the best studied
is DNA methylation, and most of what I’m
going to talk about today is about DNA methylation. DNA methylation is the
most stable mechanism. First of all, it is more
like the long-term mechanism, whereas the chromatin structure
can change very quickly and the microRNAs can too. The other thing is that it
is just easier to study, because it is stable
in samples that we all have in our refrigerators
or freezers. So that’s why a
lot more insights have been accomplished in the
context of DNA methylation. And this is just a simple graph
on how DNA methylation works. So if you have methylation,
which is signified here by these solid lollipops, in
certain regions of your DNA, then the gene
expression is repressed, and your gene is not
expressed and not translated into a protein. But if you don’t have
this methylation, if your DNA area
is unmethylated, then you have
expression, and the gene is basically used in that cell. So now we have genetics
and epigenetics. So how do they relate? So we have the
genetics, the DNA, and for those of you
who have done 23andMe, you get a result
about your genetics, but there’s very little
you can do about it. You have your genes,
and that’s it. Epigenetics is
much more dynamic. It does enable the
genetics to be used or to be silenced
with the mechanisms that I just told you about. So epigenetics is
something much more dynamic and also opens up new
opportunities for us for disease prevention,
as I’m going to allude to, and also how we deal as a result
and response of the environment we are exposed to. Let me give you a few
examples to illustrate the importance of epigenetics. Butterfly development– three
different developmental stages, same genome, different
what we call phenotype. It looks different. And this is enabled
by epigenetics. Another example from
the animal world, the so-called jumping ant. Just like the bees, they
have a queen and worker ants. The queen is large,
only reproduces, and has low brain function. Don’t need much brain
for reproduction. Whereas the worker
ants have to be smart, because they keep the
whole thing going, maintaining the colony,
but they do not reproduce. Now, what happens
when the queen bee– the queen ant, that is– dies? So if the queen dies, the
workers fight for the throne. And the winner
upregulates some genes– in particular,
telomerase and SIRT1, which are longevity
genes, because the queen has about 10 times the
lifespan of the worker ants. Now, what does that tell you? All these ants have the same
genome, but they’re able to up- or downregulate some of their
genes depending on their needs. And so a worker can
become queen just by upregulating some genes– and also downregulating,
again, brain function, upregulating
reproductive function. So these are some of the
wonders of the animal world– all epigenetic phenomena. And finally, the well-known
queen bee from the honey bees. Also here, we have queen
bee and worker bees, but here it’s a
little bit different, because it depends on the diet
now, which is very interesting. They all have the same genome,
again, but in the larva stage, it depends what food you get. Do you get the royal
jelly or the worker jelly? And if you get the royal
jelly, you become a queen, but if you get the worker
jelly, you become a worker. Again, the queen– bigger,
much longer lifespan, only reproduces, not
much brain function. Very similar to the ants. All of this due to the
effect of the diet. And a very different
example now. You may have noticed
that it’s become pretty quiet in the area of cloning. You know, there
was a lot of talk about cloning some
time ago, and Dolly the sheep was a little clone. And then Dolly didn’t make it,
because Dolly died prematurely. So not much has happened
since in cloning, due to the fact that the
cloning researchers realized that there was one thing that
they couldn’t accomplish. While they could
faithfully copy the genome, they were unable to
copy the epigenome. It is due to the failure to
faithfully copy the epigenome that we cannot clone– at least so far. So epigenetics has moved
much into the public eye, as you can see here. “Why Your DNA
Isn’t Your Destiny. The new science of
epigenetics reveals how the choices you make
can change your genes– and those of your kids.” And I will come back
to that in a minute. But it has become sort of
a more common interest area to think about epigenetics
and not only about genetics. Now, why is that? Because we are,
with our epigenome, responding to the environment. What we eat can potentially
influence our epigenome– the histone modification, the
DNA methylation, the microRNAs. And that is in fundamental
difference to genetics. Genetics doesn’t change– unless
you have a mutation, which happens very rarely. Epigenetics changes as a result
of the environment we live in– not only what we eat,
but many other things. Whether you smoke is one of
the most potential challenges to your epigenome. Smokers have a substantially
altered epigenome. Other things, whether
it’s exercise, taking drugs, social
interactions, air pollution, viruses, or the microbiome– all of those are
influencing our epi genome. Why is that so important? Because an aberrant epigenome
predispose you to disease. And many diseases
have been associated with a malfunctioning
epigenome– most well known
and best studied, cancer, but it is
becoming apparent that many other
diseases are associated with a malfunctioning epigenome. So given that we
have this plasticity to adjust our epigenome
to the environment, and given that the epigenome
is associated with disease probability, I think
it is very important to understand the epigenome
as well as we could. Now let’s go back to the basics. To understand
epigenetics, we have to understand how it works. And I just went to the internet,
and I put in “epigenetics,” and I looked up the first
definition that came up. And this is what came up. “The term epigenetics refers
to the heritable change in gene expression
that does not involve changes in the
underlying DNA sequence.” Now, the word “heritable”
here is extremely important because it has led to
a lot of confusion. This definition is not correct. It’s not incorrect, but it’s so
imprecise that it is confusing. So the definition should
say, “the mitotically heritable variation.” And “mitotically”
means cell division. So what I’m trying to
say is that epigenetics, when it is connected
with the word “heritable” means from one cell to
the next in your body. The muscle cell wants
to stay a muscle cell. And as the cells and
the muscle cells divide, the epigenome stays the same. It is faithfully produced
within the muscle cell, because the muscle
cell does not want to become the kidney cells. Of course, the stem
cell researchers want the muscle cell to
become a kidney cell, but that’s a different topic. For your body to
function properly, your muscle cell has to
stay the muscle cell. And that’s where the word
“heritable” is justified. But carry that outside,
lose the word “mitotic”– people think of “heritable”
from one generation to the next, mother to the child. And that is what I
am interested in. Is that actually
the case, that we are inheriting an
aberrant epigenome that resulted from us smoking
to our children, or not? When I said to some
people I was going to give the talk “Is Epigenetics
Heritable,” they said to me, what’s the question? Of course it is– isn’t it? That is because people think
of “heritable,” from one generation to the next. So the current field
of epigenetics, within and outside,
is completely confused by this word, because it is
never used, or rarely used, precisely. Whenever I go to a conference
and people use this word, I get up and I say,
“mitotically, yes?” Because people forget
to insert this word. Now, when is our epigenome set? Our epigenome is determined very
early on, which makes sense, because the muscle cell needs to
know early that it is a muscle cell, and the kidney
cell needs to know early that it is a kidney cell. So the epigenetic code
is set in the embryo, around the stage
of the blastocyst. Now you are sort of a
little advanced stem cell. But these cells that are
undifferentiated, meaning they don’t know their destiny
and their function yet– they need to learn what
they are going to be. At that time, the genome
kicks in, is developed. Makes sense. So in utero. Now, interestingly– so
what you see on this graph is actually the male
and the female germline. So you inherit one gene from
Dad and one gene from Mom. The blue one is the
one you get from Dad, and the red one is the one
you get from your mother. And here you have
low methylation and high methylation. As you can see here, in
this embryonic stage, your initially
unmethylated genes– some of them will
become methylated. And depending on what
the cell is going to be, the certain parts of the DNA
will be methylated or not. Now, what’s interesting is
what happens before this. So here, the male
and female germline come together during the
fertilization process. But in the actual sperm cell
and oocyte, as you can see here, there is what we call a round
of re- and demethylation. So what that means is,
your entire methylation is completely wiped out. Then you establish another
round of methylation. And after fertilization,
bing, another complete wipeout of the DNA methylation. So Mother Nature makes
you go through two cycles of completely wiping
out your epigenetic memory. There must be a reason for that. Double insurance by evolution
that you’re not inheriting epigenetics information
from Mom or Pop. That’s how I would interpret
what’s going on here. Why otherwise would there
be a double wipeout? So evolution, as
I see it, does not plan for transgenerational
inheritance of the epigenome. So you would not suffer from
the fact that mom has smoked or grandma has smoked, but
the record is set straight and you have a new start. So if it is there, if
transgenerational inheritance of the epigenetic
information happens, it would require that the
epigenetic information is not completely wiped out. So incomplete erasure of
these epigenetic marks– that would be required for
transgenerational inheritance off the epigenome
if it then exists. So if it does exist, the other
question is, is it permissive? So is it sort of
planned for that not everything is wiped out? Or is it an error? Is it a mistake? That’s big questions. And I’m not claiming
to have the answers, but I’m going to show you
some other data that we have. This is actually a
very famous experiment. So this is an experiment that
caused a lot of news articles. So we have what we
call an agouti mouse. That’s a certain
subtype of mouse. And you can see that the agouti
mouse has a light coat color, and it’s a fat mouse. So depending on what you feed
this mouse during pregnancy– so mother being pregnant– the mother may have different
distribution of offspring. So this is two potential
examples of offspring. If you feed the mother
during pregnancy a diet that is very rich in methyl donors– and you may remember DNA
methylation, the methyl groups going on the DNA– so you must have these methyl
groups to go on the DNA. And they come from somewhere. And diet– in particular,
folic acid, methionine, cytosine– they provide these
methyl groups with your diet. Now, if you have lots of
them, you can use them, and they can go in your DNA. So this mother was fed a
lot of these methyl donors, and then she had offspring that
had very few representatives of the fat agouti trait
with a light fur color, whereas more offspring
with brown color. If she was fed a regular
diet low in methyl donors, she had more of the
agouti offspring. So what happened here? Well lots of methyl
groups, like the mother that has lots of the
brown agouti offspring, silences the agouti gene. Methylation, silencing. Agouti, yellow,
cannot be expressed. Now, hypomethylation, meaning
no blockage of the agouti, agouti’s expressed–
more of the yellow ones. So here is the
distribution of the two. So this was a
revolutionary experiment, because it showed
it does matter what the mother eats for the
phenotype of the offspring. Plus, it was shown it’s
actually epigenetic. It’s a methylation effect. Now, my question
to you is, now, is this transgenerational
inheritance of epigenetics or not? Yes or no? Is it? Is it not? Well, I would say no. What it is is simply
intrauterine exposure. These mice were,
in utero, exposed to whatever the mother eats. And as a result, it changed
the genome of the offspring. We don’t know anything about
the epigenome of the mother. It changed the epigenome
of the offspring. I mean, I’m not saying it is not
completely impossible that it is transgenerational
inheritance, but my primary guess it’s a
simple intrauterine exposure to diet of the
mother that changed the epigenome of the child. And there’s probably no
inheritance going on here. So the induced
DNA methylation is a result of the maternal diet. OK, let’s talk about
some other examples– identical twins. Epidemiologists love
identical twins to study– in particular, those who
are discordant for disease later in life. Why, if the two have identical
genome, why does one of them develop cancer
and the other not? Very interesting to
study identical twins, because genetics cannot
be the explanation. Now, can it be epigenetics? Well, I think it could
be a variety of things. First of all, it
starts in utero. Oftentimes, identical twins have
very different birth weight, because they have
very different room. So one has better room to grow,
the other one’s very small. So already, in utero, the
conditions are different. And birth weight is
a very good predictor of chronic disease risk
60, 70 years later. So that’s one thing. The other thing is, all
these lifestyle factors that happen between birth and
adulthood, of course, could contribute. And if these twins
are reared apart, they’re even more different. Nevertheless, it is important
to note that identical twins, as they are born, they
have a very similar epigenetic profile. But as they grow older, this
epigenetic profile grows apart. So they develop further
and further apart in their epigenetic
profile, so there could be some epigenetic
mechanism in this disease discordance of the
identical twins. Again, is that
transgenerational inheritance? Probably not. There is a whole
field of research that’s called developmental
origins of health and disease and that basically talks about
the intrauterine reprogramming of propensity to disease. So what you have here is,
during a critical period of development, you have
a transient environmental stimulus. And a very good example of
this is much-studied famines. There are natural
and less natural famines that occur
throughout the world and that have led
to malnutrition of the mother, which is
a transient environmental stimulus. But the offspring has
been shown to have permanent long-term damage,
ranging from obesity to psychiatric diseases
and other chronic diseases. Again, people have
talked about, what are the mechanisms
for these findings? And we are still
talking about this, because we still
haven’t understood what the mechanisms are. One prime candidate
is epigenetics. And it could very
well be epigenetics, but it may not be, again,
transgenerational inheritance, but simply intrauterine
exposures that may have changed the
epigenetics of the offspring. So I think we really
have to differentiate between the
intrauterine exposure versus the transgenerational
inheritance, and there is unbelievable
confusion about that in the scientific community. So I’m going to show
you three scenarios. One scenario is, you have
an intrauterine exposure to a stressor, due to whatever
happens to you in utero– behavior of the mother
or something else– that leads, via mechanisms
that we don’t understand well, to a particular
phenotype or disease. The other scenario is that
the same exposure indeed does lead to an
epigenetic modification, like in the agouti mouse, that
then changes the phenotype, like the light fur color. Now, what I’m interested
in figuring out is the transgenerational
inheritance. That would start with an
epigenetic modification that would then be inherited to
the next or next-after-next generation and then cause
a difference in phenotype. And this epigenetic
modification is probably the result of some
exposure that we undergo. So these are different
scenarios that we have to distinguish between,
but they are completely confused in the scientific literature. OK, which scenario of the three
I just showed you is this? Grandmother smokes,
obesity in the grandchild. We find this in
epidemiologic studies. Is this transgenerational
inheritance, necessarily? Well, remember, I
added a generation now. It’s not mom, it’s grandma. I added a generation. I’m sorry? – Grandma lives at home. – Yes, yes. OK. I should have been more concrete
in saying grandmother smokes during pregnancy with daughter,
and granddaughter has obesity. – But also, the eggs that the
child’s going to come out of were all developed while– – You got it. Thank you. What happens is,
grandmother smokes, so that’s the first generation. Second generation is the fetus. But the fetus already carries
the reproductive cells for the grandchild. So you already damage
the reproductive cells for the third generation. So even with three
generations, we cannot prove transgenerational inheritance,
because it can still be intrauterine exposure. So this is only true
for females, though. For male germline,
we really only need two generations,
because as you know, sperm’s produced
nearly all the time. OK So intrauterine exposure
along the female germline can reach three generations,
for the male germline can reach two. To prove transgenerational
inheritance, you would need four generations
along the female germline and three along
the male germline. And don’t get me wrong– I’m not saying this could not
be transgenerational inheritance along this line. I’m just saying to prove
that it is, you need this. This is very hard to get. When you do this in
humans, it would certainly exceed the lifetime
of one researcher. So to do a study like this is
very difficult to do in humans. You can do it,
potentially, in mice. OK, so the question
comes back to, is there incomplete
erasure of the epigenome? I looked a little bit
into the literature. I’m just going to give you
three quick examples from what’s published in the literature. You can already see
“transgenerational” is in the headline
here of this paper. “Epigenetic information
can be inherited through the mammalian
germline and represents a plausible
transgenerational carrier of environmental information.” So they are out to prove the
transgenerational inheritance of epigenetics. What do they do? Well, they exposed the
paternal animal here to a low-protein
diet, and then they found, in the next generation
that there was a difference in DNA methylation. Is there anything
transgenerational? Not in the sense we
just established it. There’s absolutely no proof for
transgenerational inheritance. It’s pure intrauterine exposure. Yet these authors
conclude, “these results, in conjunction with recent
human epidemiological data, indicate that parental diet can
affect cholesterol and lipid metabolism in offspring,
and define a model system to study environmental
reprogramming of the heritable epigenome.” There is no heritable
epigenome here. Nothing whatsoever. Next paper. This paper caused
a lot of attention. So what the investigators
here did is, they used– basically, they used a model
of associating a certain smell with trauma, and looked
whether also they could find this in
the next generation. So if they exposed the next
generation to the same smell, did they express fear? So they did these experiments. In F1, they exposed,
basically, the sperm. They did an IVF conception. But they did absolutely
no epigenetic experiments whatsoever in this paper. But they concluded that these
transgenerational effects are inherited via parental gametes. “Our findings
provide a framework for addressing how environmental
information may be inherited transgenerationally at
behavioral, neuroanatomical, and epigenetic levels.” They did absolutely
no epigenetics. So this happens all the time. And there is just
a third example where they did exactly
the same thing. “Epigenetic germline
inheritance” is in the title. They did an experiment. There was no
epigenetics done at all, yet “epigenetics”
is in the title. At this point, I got so annoyed,
I wrote a letter to the editor. After all, this is
Nature Genetics, which is, like, the paper
everybody wants to publish in. And I say, like, what
is it with you editors? And they say, we
are not interested. Basically, you
publish your paper better if it has “epigenetics”
in the title, as we know. This is how you get your
grants, your tenure, and your papers published. OK. So far so good. We haven’t found anything
that is transgenerationally inherited. Now, I’m going to give
you the one example where I’m convinced that there is
transgenerational inheritance, which is genomic imprinting. Let me introduce you
to genomic imprinting. We have some interesting
subgroup of genes– very few– that do not
follow the normal pattern. Normally, you get Mom’s
allele, Pop’s allele, and you express them both
or you silence them both. They both do the same thing. Now, the imprinted genes
are a little different, because only one
allele is expressed– either the father’s
or the mother’s. The best known
imprinted gene is IGF2. IGF2 is the most important
intrauterine growth gene. It is very important for
the growth of the fetus– makes the fetus big or not. What’s important about
these imprinted genes is that they are
faithfully always expressed from the same allele. So IGF2, for example,
is only expressed from the paternal chromosome,
from the paternal allele– never from the mother’s. And that is generation after
generation after generation after generation. And you can ask– and this is another
picture showing you more of the mechanisms. You may ask, why do we
have genomic imprinting? Well, there is the
Haig hypothesis. And I’m very honored that
Professor Haig actually came himself. If I had a hypothesis
named after me, I would probably rest and
enjoy, but he’s so prolific that he prints out
his papers for me and he writes a new
paper every day. It’s unbelievable. Anyway, so Professor
Haig came up with the following reason for
why genomic imprinting exists, and I’m very impressed
by the theory that he came up with, because I
think it makes a lot of sense. Remember, intrauterine growth–
and many of the imprinted genes are actually responsible
for intrauterine growth. That means growth,
good for the baby, good for the
survival of the baby. The father, of course, has one
sole interest in reproduction– passing on his genome. The father doesn’t
know whether he’s going to get another
chance, so he’s going to put all his eggs in one
basket and make that baby big. OK The mother, of course,
knows she can have as many as she wants anytime–
just go around the corner, you get another one. Right? So she probably has 18 others
at home to take care of. So she needs to balance
the survival of that one child versus her own survival,
to take care of the 18 others. And she can have
another 18 if she wants. So they have
different interests, so there is a conflict–
all of this very elegantly explained by Professor
Haig in his work. There is this conflict,
where the mother has a very different
interest than the father in this evolutionary conflict. The father doesn’t really
care about the mother. The father cares
about the genome. He doesn’t care whether
the mother dies. So the bigger the better. So the mother shuts
off the growth genes, the father shuts them on. And that is true for all these
intrauterine growth genes. The father shuts them
all on– not only IGF2, but there are others– whereas the mother
shuts them all off. And that’s the imprinted genes. But what’s
fascinating– of course, fascinating in terms of an
evolutionary hypothesis– what’s fascinating besides
“why do we have this” is that this parent of origin,
the mother shutting them off, the father turning them on for
many of these imprinted genes– not all, but many– is faithfully passed from
one to the next generation and maintained. So this is the
one example that I would accept as
transgenerational inheritance of epigenetic information. We do not well understand
how it works, though. And that’s something that
I’m extremely interested in. And Professor Haig has
some thoughts on this. I had some thoughts. We discussed this the other day. But I think the jury’s
not out how this works. So there must be something– some mechanisms– that
obviously makes this possible. And to come back to
our graph, the one thing I did not explain to you
previously is the black line. The black line are
the imprinted genes. And what you can see here
is that imprinting only has one cycle of
demethylation, and it’s not it’s not wiped out
again after fertilization. That already means something
in the context of evolution in that the imprinted
genes seem to escape some of this de- and
remethylation cycle. So in conclusion, we have
intrauterine exposures that can affect our
phenotype many decades later. These intrauterine
exposures can impact on the epigenome of the fetus. Whether epigenetics is one
of the mechanisms underlying these intrauterine exposures
and how they relate to phenotype or disease later in
life remains to be established. But we need to distinguish
between epigenetic changes as a consequence of
intrauterine exposures and transgenerational
inheritance of epigenetic marks, which is
something totally different. So on the transgenerational
epigenetic inheritance, I think there is insufficient
evidence from human studies to suggest that
there is such thing, except for the imprinting. But on all the other
examples that I’ve shown you, I’m not saying it’s not there. I’m saying we don’t
have evidence. The data from animal
studies is very limited. Most of the studies are
interpreted incorrectly, because there is confusion about
in much of the terminology. And to prove it, we need four
generations down the female and three generations down the
male line, which is very, very hard to do in humans. And even in animals,
it seems nobody seems to bother to
do this, but still claim that they have
transgenerational inheritance. So the exception is the
parent-of-origin mechanism of imprinting, which
I would completely subscribe to as
transgenerational inheritance of epigenetic information. But we do not well understand
how this actually works. There must be some
memory that always tells the paternal
allele to be turned on and the maternal
allele to be shut off. So once we understand
that better, maybe we also understand
the entire transgenerational inheritance better. So for the future, I think
we need to understand better the evolution of imprinting
and epigenetics– and that is, of course, much of what
Professor Haig also deals with– design the perfect human and
animal studies to actually show transgenerational epigenetic
inheritance; consolidate the existing evidence better;
and also, for some of the other marks that I have not
talked about today, they, of course, also
play into this question. Now, finally, what if
epigenetics is inherited? We are probably
at the worst stage of our evolutionary development. So if all the bad traits
that we have been managed to include our lifestyle,
et cetera– if all of this is leaving marks in the
epigenome, which is then transmitted to the
next generation– is that actually a good idea? And where is this
going to lead us? Well, maybe not everything
is in the epigenome. And I always tell people
that while epigenetics is very fashionable
to do and to research, the answer is not always
in the epigenetics. But it is oftentimes used as
an explanation when we don’t understand what’s going on. So I hope I was able to give
you a little introduction into the world of
epigenetics and why I’m here and what I’m interested in. And I thank you
for your attention. [APPLAUSE]

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