How Jumping Genes Shape the Placenta and Pregnancy Health

Name: How does epigenetics impact the placenta? - with Jennifer Frost
Uploaded: 2026-04-29T18:00:41+00:00
Duration: 35 min 7 s
Channel: The Royal Institution
Description: Summary and key takeaways on How Jumping Genes Shape the Placenta and Pregnancy Health, covering to Transposons Transposons, often called “jumping genes,”

The Royal Institution

Apr 29, 2026

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35 min video

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2 min read

YouTube video ID: boj1lLDXBJw

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Transposons, often called “jumping genes,” occupy roughly half of the human genome, while protein‑coding genes make up only about five percent. The term “jumping” is misleading; most transposon copies are now fixed and no longer move. Discovered by Barbara McClintock in the 1950s, these elements were later recognized as remnants of ancient viral infections. Over evolutionary time, the host can “domesticate” viral DNA, retaining sequences that confer a survival advantage. Functional transposons are frequently co‑opted to act as regulatory switches that turn other genes on or off.

The Placenta as a Research Subject

The placenta is a uniquely disposable organ that connects the developing fetus to the mother’s blood supply, handles waste removal, and provides immune protection. In humans and great apes the organ is highly invasive, remodeling maternal vessels to secure nutrients. Its structure varies dramatically across mammals, a pattern that points to rapid evolution driven by species‑specific transposons. Because the placenta is normally discarded after birth, historical sample collection is difficult, making modern laboratory work essential for understanding its biology.

Mechanisms of Gene Regulation

Long terminal repeat (LTR) retrotransposons carry regulatory “caps” at their ends. The host cell exploits these caps to recruit transcriptional machinery, effectively using viral remnants as gene‑control modules. One celebrated example is syncytin, a protein derived from a viral envelope gene. Syncytin mediates the fusion of trophoblast cells into a multinucleated syncytium, a layer critical for nutrient exchange in the placenta. This viral‑derived gene illustrates convergent evolution: a once‑harmful virus becomes essential for mammalian reproduction.

Research Methodology

Jennifer Frost’s lab at King’s College London employs human trophoblast stem cell lines to dissect transposon function. By knocking out specific transposon regions, researchers observe changes in cell differentiation and gene expression. Complementary analysis of frozen placental samples from complicated pregnancies—such as those affected by preeclampsia—provides real‑world relevance. Long‑read sequencing technology enables precise mapping of the ~1,500 transposon copies that appear to regulate genes in the human placenta. Notably, a transposon insertion that drives overexpression of endoglin is linked to preeclampsia and is present only in Old World monkeys.

Future Clinical Applications

If transposon activity can be monitored non‑invasively, it may serve as a biomarker for early detection of pregnancy complications through prenatal testing. Moreover, targeted interference with pathogenic transposon‑driven pathways could open therapeutic avenues to correct placental development errors. The ultimate goal is to translate the evolutionary story of viral DNA co‑option into practical tools that improve maternal and fetal health.

Takeaways

Transposons make up about 50% of the human genome and are frequently repurposed to regulate other genes.
The placenta, a disposable organ essential for fetal development, is a hotspot for transposon activity and rapid evolutionary change.
LTR retrotransposon caps serve as regulatory modules, with syncytin—a viral‑derived protein—being crucial for placental cell fusion.
Long‑read sequencing of trophoblast stem cells and placental samples reveals dozens of transposon copies that influence gene expression and are linked to conditions like preeclampsia.
Detecting transposon‑driven signals could enable non‑invasive prenatal biomarkers and future therapies to correct placental dysfunction.

Frequently Asked Questions

What are transposons and how do they influence gene regulation in the placenta?

Transposons are DNA elements that comprise roughly half of the human genome and often originate from ancient viral infections. In the placenta, their long terminal repeat caps act as regulatory hubs that attract transcription factors, allowing the host to turn nearby genes on or off, as exemplified by the viral‑derived syncytin protein.

How could transposon activity be used as biomarkers for pregnancy complications?

Specific transposon insertions can alter expression of genes linked to disorders such as preeclampsia; for example, a transposon‑driven increase in endoglin is associated with the condition. By detecting these altered transposon‑derived signals in maternal blood, non‑invasive prenatal tests could identify at‑risk pregnancies early.

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The Gene An Intimate History Book Recommended

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High Quality Laboratory Notebook For Research

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Full Transcript YouTube

The placenta [music] is the only
disposable organ found in the human
body, and yet none of us could have
survived without one.
>> [music]
>> Jennifer Frost leads a research group at
King's College London [music]
investigating the genetic elements of
placental function and the [music]
impact these can have on pregnancy.
Jenny, thank you for having me in your
lab at Guy's Hospital today. [music]
You lead a group here at King's College
London and that research is funded by a
research grant through the Welcome Trust
and you're investigating the effects of
ancient transposons on the placenta
and how this can lead to complications
in pregnancy.
There's a lot to unpack there, but I
wanted to start with the genetic element
and then work our way through to the
placenta.
So, transposons are also known as
jumping genes, which is how people might
have heard of them before, which gives a
little bit of an indication about what
they do, but
what do they do? I think the term
jumping genes is a bit of a misnomer
because usually these elements aren't
genes at all.
So, transposons were originally
discovered in the 1950s by
a female Nobel laureate, Barbara
McClintock, and she identified them as
being regulatory elements, which has
only really come to be known as
absolutely correct sort of 50 years
later. And basically, these are genomic
elements that are called transposons
because they can move. So, the jumping
part is correct. And some of them can
move by themselves, some of them need
other machinery for them to jump around.
And these make up around 50% of your
whole kind of genome component. Genes
are only about 5%, so a gene is usually
something that codes a protein that goes
on to have a specific function. And
those are well studied as parts of our
genome because those are the things that
if they go wrong, they cause disease,
and so they're very well characterized,
whereas transposons don't usually code
for genes. They're sequences that are
throughout our genomes and most of them
can't jump around anymore. So, they're
fixed in our genomes. So, some of them
probably don't do anything, but what is
becoming
researched much more now and what my lab
works on are those that are functional.
And there are a subset of transposons
that are genes and they have become
domesticated throughout evolution for
function. So, transposons have
particular sequences that the cell might
think, "Oh, that that looks useful. I'm
I'm going to use that." And so, some of
them actually now encode proteins. And
in some cases, these proteins have come
from viruses. So, some transposons are
from viruses and viruses have genes in
their DNA that encode particular viral
proteins, and so there are a few really
nice examples of viral genes that have
been domesticated in the species that
these these viruses infect.
Your research is specifically looking at
ancient transposons. So, are these
those transposons that have been
integrated, say, by viruses or things
way back when?
And how do they differentiate from
modern transposons if that's the right
>> terminology? [laughter]
I Yeah, that's a really good question
and I think modern transposons is
something that is very difficult to
study. So, there's lots of different
families of transposons that correspond
to from whence they came and how they
move around when they did move around
and they have different sequences, the
sorts of different families. So, some of
them predate eukaryotes and some of them
are a bit more recent. And the ones that
we're particularly interested in
in my lab are a class called long
terminal repeat retrotransposons.
And these have come from viral
infections. So, viruses have infected
species since the dawn of time and
they bring with them bits of their DNA
and they insert their DNA into your into
your genome.
These bits of DNA are sometimes kept and
over millennia, they've built up and so
these viral bits of DNA now make up
about 10% of our genomes.
A lot of these are ancient, the ones
that we know about and the ones that we
can study are so-called ancient because
they have been in our genome for
millions of years.
And there are transposons that are, as
you say, modern and that have arrived
more recently.
So, probably we have transposons in us
from COVID-19, for example, and
basically any other virus will insert
its DNA into your genome.
But those are going to be bits of DNA
that will die out with you. So, they're
specific to you as a person.
The ones that stick around are the ones
that go into your germline and then they
can continue
in in human DNA.
But these ones are really difficult to
study because some of them are going to
be unique to people, some of them are
going to be unique to populations. Even
those transposons that are unique to
humans are really hard to study because
they're repetitive. So, we call them
repeat regions because there are many
copies of them and the sequence of them
can be completely identical. And the
technologies that we use to to identify
them and look at them
can't differentiate between these
different sequences. And so, there there
might be thousands of copies, there
might be hundreds of copies, there might
be one and we can't tell that with the
most used technologies.
There There's a recent fairly recent
set of technologies called long read
sequencing, which is becoming much more
used now in biology, and that can
sequence your entire genome from end to
end, from telomere to telomere, all of
the sequences
in between. And using that, we can
finally really drill down into these
people's genomes, into animal genomes,
and find these weird repetitive kind of
hidden sequences. And so, I think in the
future, we'll be able to tell how much
of your transposon portion is is modern,
is brand new, is specific to you, is
specific to your family, specific to
this country, things like that.
So, you've identified these transposons.
The next
step, if you like, is how they then
influence gene expression. And this is
what you're specifically looking at. How
do these sequences have an impact on
gene expression? What does that process
look like?
So, the as I said, the sequences in this
in this lab that we're looking at are
these long terminal repeat or LTR
retrotransposons.
And they come from viral infections. So,
the specific group of transposons are
from from viruses, from historical viral
infections, and in our case, ancient
ancient ones, sort of primate specific,
perhaps.
Um
And the sequences come in with a
particular structure. They have kind of
two end pieces, like caps on the end,
and then genes in the middle.
And these caps on the end are
regulatory sequences. So, in the virus,
they're used to to regulate gene
expression and they are they can do the
same thing in the host, in in in humans,
for example. And often over time, the
gene sequences in the middle of these
caps are lost and so you're left with
only this regulatory sequence.
And so, the human cell can use it in the
same way the virus did to attract
molecules that turn on genes or turn off
genes. And so, our cells use them for
that exact purpose. And there's lots of
evidence accumulating now that this
happens across tissues, across species,
where these pieces of viral DNA are
co-opted by the host to to regulate
genes.
Why is the placenta an organ of
particular interest with gene expression
and this area of study? So, the placenta
is a fetal tissue. It develops with the
fetus. Absolutely required for mammalian
pregnancy. And mammals are defined by
having a placenta as part of their
reproductive process.
And it is a a
a kind of conduit between the mother and
the baby. It regulates the blood supply,
waste disposal, the immunity, protection
for the fetus because the fetus is half
dad. And so, why the mother doesn't
reject it is still
a huge source of interesting research.
And the placenta's part of that. So, the
structure of it and the the hormones
that produces and um
and the protection it provides is is
really key. And it's it's sort of a
a bit of a like a big plate shape. It's
this big disc. They look really
disgusting. And
so, no, you know, this is one of the
reasons that nobody talks about them cuz
they're hideous. And you do you deliver
after the baby? And it sometimes comes
as a surprise, you know, you've
delivered this baby. It's like, "Right,
okay, you've got to deliver the placenta
now." I was
>> Yeah. You think you've done the hard
work and there's more.
>> work here.
And it's it can be, you know, it can be
it's quite a big organ and
um
unfortunately, it's it's not really well
studied. It For a long time, it would
just be discarded
and so it's quite difficult to to do
research on it because finding samples
is is quite difficult. But it's a kind
of a structure made up of in primates,
in most primates, sort of these these
villi trees of blood vessels with fetal
blood in and that exchanges with the
maternal blood. So, it provides an
exchange surface. It's on one side of
the uterus, kind of connecting the fetus
via the umbilicus to the to the maternal
blood supply. And it's very invasive.
So, especially in in humans and in great
apes, the level of invasion of this
structure is is huge. It goes right into
the maternal musculature, remodels her
vessels so that the baby gets enough
blood.
And it's a really important part of
pregnancy. And if the development of the
placenta goes wrong, then the the
pregnancy will also go wrong.
As you said, this is a difficult area to
study because of the lack of backlog, if
you like, of samples to research from.
But when you think about researching a
tissue and then thinking about this
genetic element of transposon activity,
they seem to be immediately quite
different areas of research. So, how was
that
overlap first identified of transposon
activity being impactful in the
placenta? And yeah, where did where did
that come from? So, um several research
groups over over the last kind of 10 to
15 years have been interested in
transposons and their role in gene
regulation.
And there's
a really lovely study actually looking
in the maternal kind of side of the
placenta as in the decidua. So, at the
beginning of pregnancy, the uterus
decidualizes and forms this very
glandulous structure that is that allows
an embryo to implant. And this process
of forming this decidualized tissue and
allowing pregnancy to begin actually
relies on certain transposable elements
that are switched on during this process
and allow progesterone to signal to the
uterus to be receptive to the embryo.
And so, without these transposons in
uterine tissue in the endometrium,
pregnancy wouldn't happen. And so, these
are mammal-specific transposons. And
over over the kind of next 15 years or
so, people have been looking at
transposons as gene regulatory elements.
And there's a couple of different
reasons I think why the placenta has
come to the fore. One of which is a bit
contentious. It's the fact that
placental
genomes tend to be quite permissive for
gene regulation. That their epigenetics
is a bit different to other tissues.
And so, potentially regions of
transposons are open for kind of
regulatory molecules to bind. And so,
it's potentially thought that it's quite
a prominent place for transposons to be
active. I don't know really whether
that's true. There might be some
ascertainment bias. There's certainly a
lot of research showing that transposons
are active as regulatory elements in
many tissues, in liver, in the pancreas.
And it and in disease, in cancers.
But the other I think more interesting
part of the placenta is that it's very
quickly evolving. So, placentation is
very different even within primates,
certainly amongst mammals. Placental
structure in different mammals is wildly
different
in a different way to other organs, for
example. Sort of a liver looks like a
liver in a mouse and in a human and in a
sheep, but a placenta is completely
different in sheep. And so, it's thought
that these transposons
are sources of species-specific
regulation.
Because the kind of cohort of
transposons that you have in your genome
is very particular. So, primates have
different transposons than sheep. And
so, it's thought that the differences
between sheep and primates, for example,
comes from these transposable elements.
There's a few different reasons why when
you think about transposons and
retrotransposons in biology that the
placenta pops up as an organ of
interest. And and one is sort of linked
to the idea of transposons being genes,
which is certainly a rare case. So, most
of them are
are not. But there's a really exciting
and cool well
for the placenta biologists and
transposon biologists of the world, a
really exciting and cool example of a
protein which is derived from a virus.
So, viruses have these genes within
them, and there's an envelope gene. And
the envelope gene allows the virus to
bind with the cell membrane and insert
viral particles into that cell and then
resulting in the infection process. So,
it's really key for the virus, this
envelope protein.
And so, this envelope protein has been
inserted in hosts. And over millennia,
the kind of evolution of eutherian
mammals happened in concert with an
envelope-derived protein which we now
which we know is syncytin.
And this protein is a human protein now,
but it it was from a virus. And
we domesticated the sequence. And this
syncytin sequence is present probably in
all placental mammals and even in some
non-mammals. So, there's a lizard called
a mobile lizard that has a decidual
placenta, and this has a syncytin gene.
And these proteins are required for the
fusion of cells that happen in the outer
part of the placenta that interfaces
directly with maternal blood. So, rather
than having kind of individual cells
with membranes, you have this continuous
layer
of this multinucleated tissue called a
syncytium.
And it's really important for the
placenta. If you don't have this, you
don't have a pregnancy. And this gene
was stolen from a virus. It's a really
nice example of convergent evolution
because the viruses that these envelope
proteins were derived from in different
mammals are different viruses. So, these
viruses inserted their bits of genome
into these different species at
different points into their common
ancestors, and they became their
envelope proteins in these different
species. So, it's happened over and over
again in mammals.
What are some of the specific genes that
we have identified that then go on to
cause some of these pregnancy
complications? There's one protein
called FLT1 that was correlated with
preeclampsia, for example. And so,
actually identifying
interesting genes that might be good to
look at to sort of investigate pregnancy
in itself is quite hard. But in the work
I carried out previously in Miguel
Branco's lab at Queen Mary's,
we took a kind of backwards approach
where we looked at transposons that were
active as regulatory sequences in human
placenta and then looked at which genes
they might regulate based
on their location. So, generally if a
gene is close to a transposon, it may
well be that that transposon can
regulate that gene.
And we looked genome-wide in
in human placenta and and in trophoblast
stem cells that I mentioned earlier.
And we found
around 1,500 or so transposon copies
throughout the genome that look like
they might regulate genes.
And we then kind of picked that apart by
looking through those lists of genes
that were close to these regions and
which ones were really important in the
placenta. Were they expressed there?
Were they functional there?
And removed the sequence of those
transposons that were near those genes
and then had a look what happened. Did
it change the gene expression? And we
did find some really nice examples of
genes that their expression went down
when we removed that transposon.
And some of these genes include things
like pregnancy-specific glycoproteins,
which is super important in in
pregnancy. There's lots of copies of
them. There's this sort of bunch of them
all all together in one locus on
chromosome 19, and they're involved in
immune function and in vascular function
during placental development. And
they're super highly expressed. So,
they're one of the most highly expressed
molecules you'll find in maternal blood
during pregnancy.
So, we showed that a transposon
regulates the expression of these. And
other groups have shown have shown this,
too. And one really exciting one was a
gene called endoglin, which is
functionally linked to FLT1, which I
mentioned earlier, which has been
definitively linked to preeclampsia. And
endoglin is found to be overexpressed in
preeclampsia. So, the thing about that
is it's a correlation, right? You have a
preeclamptic pregnancy, and you see
increased endoglin. You don't know
whether that's a cause or an effect. And
but certainly those
the expression of endoglin in in
preeclampsia is linked. And we there was
a really nice
transposon within endoglin that we
removed. And this transposon is only in
old world monkeys. So, it's quite a
recent insertion. And when we took that
away, endoglin expression went down,
showing that that region does regulate
endoglin. And it reduced the amount of
protein as well that that this region
was making. So, it was a really nice
example of showing that that these
transposons can regulate genes that are
important in the placenta. So, endoglin,
whilst it's only been linked to
preeclampsia, when you look at its
function, it makes a lot of sense, you
know, it regulates vascular development.
And so, there's
sort of a nice story you can make about
blood vessel remodeling and and the
involvement of endoglin. But that's
something that we're studying to to pull
that apart and see whether this is
really involved.
And and part of that will be looking in
these placentas as well. So, we we want
to get these real samples of placentas
from women and actually look at what's
going on there
um rather than taking a just an overview
of like oh which genes look interesting.
We want to know which genes actually are
changing in in these placentas that we
can look at and and test. [music]
So, we're in your lab, well, we're in
your office technically across the
corridor from your lab in
Guy's Hospital just across from the
shard and you gave me a quick tour
around your lab before we started
recording today and I think it is
got to be top three best lab views in
London.
>> [laughter]
>> Some mega view outside of the lab.
But, what is the actual How do How do
you investigate this? Because there's
obviously genetic elements and then
there are cellular elements and it it's
covers huge range of investigative
biology. So, what does the actual
research process look like? We have a
couple of uh different approaches. So,
on one hand, we have um a very special
model
stem cell which is called a human
trophoblast stem cell line which we
derived in Japan um in 2018
and they grow fairly indefinitely. You
can give them you give them a particular
cocktail of of uh growth factors and
inhibitors and they'll grow happily and
they are epithelial cells that are
specific to the placenta. So,
trophoblast is is a placenta specific
cell.
And um we use those as a model. So, we
grow them in a in a particular room in a
special hood so that they don't get
infections and you can interfere with
them in a way that you can't in you
know, within a person, especially not
within a pregnant person.
So, we do things like we can knock genes
out or in our case we would knock out
transposons from the genome of these
cells and then look at what the effect
downstream is on the way the cells grow,
the way that they can change into the
different tissues of the placenta. So,
there's a couple of different cell
types. So, there's this invasive cell
type I spoke about where these cells
actually invade maternal vessels and
then there's another cell type which
forms this fused tissue at the edge of
the placenta that provides some immune
protection to the fetus. So, these cells
make these differentiated tissues
generally routinely, but then the hope
is that if we knock out a special gene
or a special region, they won't do that
anymore and that gives us a really
strong indication of function of of the
kind of interference that we that we did
there. And so, we use those a lot, but
the other thing that we do which is much
more difficult in in one way
just simply because of we're not relying
on ourselves. We have to rely on other
people that have collected pieces of
placenta.
And so, we're working with different
teams um both at King's and in Cambridge
and at UCL who have painstakingly
collected placentas from women giving
birth over, you know, the last 20 years
or so collecting placenta at birth and
then freezing it down and storing that
with the information from the
pregnancies of these women. So, some of
these samples of placenta are from
normal pregnancies and some are from
pregnancies with some form of
complication. So, perhaps preeclampsia
or growth restriction or preterm birth.
And the idea behind our research is to
try to look at differences in the way
that transposons are active in placenta
from normal pregnancies and those with
these complications. And so, one of my
postdocs, Anna, who you met, she's
trying to extract a particular component
of the cell called chromatin which is a
a mixture of DNA and different proteins
that regulate that DNA, extract that
from these placental cells and then look
at it and look at our transposons in
these in these samples and then try and
correlate differences in these two
placentas. And and then when we find
correlations, the plan will be to then
use those trophoblast stem cell lines to
test those correlations.
This is a a research group that I
mentioned at the start has been funded
by the Wellcome Trust, this grant. So,
what it's it's obviously hard to
gauge how a research project is going to
go and you don't want to have too much
of an idea of it and then steer it in
that direction. But, what would be the
forward look in this area? What
direction do you think it's moving in
and what would the next steps if it all
goes to plan? What would that be? If it
all goes to plan big yeah, that's a big
>> [laughter]
>> big factor. So, if everything goes to
plan, there'll be a lovely transposon at
the at the core of pregnancy
complications that if we can interfere
with that in the placenta, we can fix
pregnancy complications. That's, you
know, a very bold Mhm. um view, but I
think what we're trying to get to is is
is part of that. So, um
the idea that transposons are really
important in placental development, in
its regulation
um in a very species specific way. So,
this very invasive phenotype of of human
and great ape placentas and the idea
that transposons might actually
be the part of our genome that regulates
that. And so, pregnancy complications
are are not perhaps human specific. I
think there's some evidence of
preeclampsia-like phenotypes in in
chimps and in gorillas.
Um and so, the idea being that
potentially these complications are
caused by a problem with that really
invasive phenotype. So, perhaps those
cells aren't invasive enough. And the
idea is that these transposons are
actually what regulates that invasive
phenotype. And so, if we can drill down
into which transposons are contributing
to the way that these cells behave and
perhaps in the pregnancies that we have
samples from see different transposons
and regions that regulate
genes in the placenta that go wrong in
pregnancy complications,
the idea is that potentially those
pregnancy complications might be caused
by by a a dysregulation of transposons.
And so, the the plan would be to
identify those and then from there
different research avenues open up with
looking at these different uh regions
and potentially because this is the
placenta, it's a temporary organ. Mhm.
And so, it opens itself up to treatment
in the way that a lot of other things
don't because if you change something in
the placenta after delivery, it's gone.
You're not changing the mother
fundamentally. Um and so, perhaps, you
know, we could use an epigenetic drug to
upregulate this transposon in the
placenta and change the course of that
pregnancy. I think it's very, you know,
that sounds mad and it is a bit because
the the development of placenta happens
very early on. Um and so, that would
this is something looking at perhaps
infertility is a is potentially a more
accessible way of of getting at how we
might change the placenta. So, if you
have somebody who's perhaps having um
IVF,
the first stage the first
differentiation of that embryo is to
form what's called a trophectoderm which
is the outer part of uh the blastocyst
which is the embryo that gets
re-implanted back into these women. And
that becomes the placenta. And if you
have, say, a history of infertility or
pregnancy complications that's derived
from the placenta, you might be able to
fix those embryos and when you implant
them, they will develop properly.
Would this then be if if this was
to to go
in the direction where you can identify
a specific transposon and you know, it's
it's all
packaged very neatly and and easy to
then identify.
Would that then in a
a natural pregnancy situation, there's a
lot of genetic testing that can you can
opt in or you can opt out um and there's
it's obviously a very sensitive issue
compared to some other pathologies.
But, [sighs]
is that then something that would fall
into that genetic testing element?
>> one thing would be screening. So, if you
So, one of the lovely things now is the
non-invasive prenatal testing that you
can do. So, the clinician takes a sample
of your blood and then tells you right,
you're more or less at risk of various
fetal defects. So, that's the kind of
primary goal now is to is to look at the
baby, but perhaps in that we could
include the placenta as as part of that
pregnancy as an important part of that
pregnancy and say, well, you know, these
biomarkers in your blood
are showing you that this placenta isn't
developing that well and perhaps there
might be a follow-up drug or uh keep a
special eye on that
uh mother in terms of the the kind of
blood flow
to the baby because the placenta is is
what mediates that blood flow. And so,
when you go in and have ultrasounds, you
have Doppler flow and it shows you how
the blood vessels have developed and
whether that's working properly and the
placenta is integral to that. And so, if
you can look at a biomarker early in
pregnancy and and highlight potentially
women who are at risk of the placenta
not developing properly, that would be
useful. Whether that would relate
directly to these, you know, these
transposable elements, potentially.
They're genetic elements. Their genetics
will impact their function and so, you
know, the idea that they could be a
biomarker is is valid. I think
transposons certainly could form part of
a genetic test in the same way that
genes can and particular biomarkers
because their function is integrally
tied to their sequence um in perhaps a
different way. Their sequence dictates
what molecules can bind to them and then
the downstream regulation from that
rather than a gene which has a specific
sequence that encodes a protein. So, it
it's important in different ways, but
can certainly be part of a, you know,
genetic screen potentially
in the future.
Looking way, way further into the
future,
you mentioned how obviously COVID-19 was
a big virus that was flying around
relatively recently, and it will have
been instances like that where now
ancient transposons have been integrated
into our genome.
How far in the future do you think it
would have to be for
>> [laughter]
>> It's a horrible question.
Um,
how [snorts] what are the timescales
with
viruses becoming incorporated, and
because you also mentioned that it it
can be hard to tell
when things are specific to a person and
when they're fully
in the in the gene line. So, how
long would it have to take for COVID to
be one of those ancient transposons, or
is it just not possible to work that
out?
So, that's a great question, and it
depends on the on the sequence on the
virus.
So, which is a big cop out.
So, the timescales we're talking in
terms of the kind of more ancient
viruses are, you know, the differences
between say human and chimpanzees, our
common ancestor, between 6 and 9 million
years ago the divergence happened. And
so, the viruses that infected the our
common ancestor
6 million years ago are the ones that
we're potentially interested in. It's
sort of hundreds of thousands of years
that it takes, I think, for us to be
able to see that these virus sequences
are say human specific, for example, and
they are mostly sort of repressed and
hidden. When we talk about function of
these virus derived sequences,
often because transposons jump, because
they move, they're really dangerous. And
so, your genome silences them. It uses
molecules called epigenetic molecules
like DNA methylation, for example,
to silence these these loci. And so,
they cannot jump, they can't move, and
they also can't regulate genes. And so,
these sort of more modern virus
sequences
are likely to not be contributing to
gene regulation in that way because
they're dangerous.
And over millennia, these sequences
change. So, they get mutations, they
recombine, and they become much less
dangerous. And so, that's when they
start to be useful to to the genome.
When I say it depends on the virus, I
think it's important to know that
I I So, I certainly don't know
of the viruses that infect you
throughout your lifetime, how many of
them kind of get DNA into your germline.
Very few. Um, and for the sequence to
stick around and propagate, it needs to
have particular these LTRs need to have
specific sequences that are expressed in
the tissue where they are
for them to jump. And for So, for
something to to stick around in your
germline, it has to be open in your
germline and to jump around. And I think
that's that's quite rare. I couldn't put
a number on it.
Um, and then for that to spread
and [music]
not be lost and be fixed, it all takes a
a long time. [music] So, it's not going
to be coming up in the Frost Research
Lab.
COVID-19
>> [music]
>> transposon linked to pregnancy
complications. Unlikely, right?
Unlikely. [laughter] Yeah, maybe come
back in in like 100,000 years and we can
have a chat.
>> Sure.
>> [music]
>> It seems as though
in this topic more than others, maybe,
everything being connected is really
more true than ever, but it's a really
exciting area of research, and hopefully
the rest of your
grant [music] means you can find that
single transposon and will change the
future of placental biology. But, Jenny,
thank you so much for having me
in your office/lab, and thanks for
coming on the podcast. Thank you for
coming.
That's it for this month from the RI
Science Podcast. Thanks, as [music]
always, for tuning in.
In other RI news, we've just [music]
launched our summer program here at the
Royal Institution. So, head to our
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>> [music]