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Cell signalling in development: Notch signalling and establishment of the embryonic body plan £7.49
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Cell signalling in development: Notch signalling and establishment of the embryonic body plan

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Cell signalling in development: Notch signalling and establishment of the embryonic body plan

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  • February 18, 2021
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  • 2020/2021
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Kim Dale : a researcher in the division of Cell and developmental biology at the School of Life Sciences.

And this is the first of a series of lectures in which I'll be describing the research that we've been doing in my
lab to look at the signaling pathways that coordinate tissue and organ development during body plan formation
in the developing vertebra embryos.

Here is a list of primary research papers under review at the bottom, highlighting some of this work that I'll be
touching on today.

Like any developmental biologists, that holy grail of the research that my lab has been doing for some years
now is to try to understand how it is we go from a single fertilized egg, which is how we all start out
schematized here on the left side of the slide. And how we go from that single fertilized egg, this exquisitely
patterned organism on the right, where everything develops at the right time and in the right place. So the
reason that this is such a complicated sort of set of processes to try and understand is that what we have to do
is to go from this one cell into 200 different types of cells. That will then give rise to all of the tissues and all the
organs of the body. So we're trying to understand the molecular mechanisms that underlie the cell
communication systems that allow cells to talk to one another and build tissues and build organs. And that's
hugely important for our understanding of body plan formation in the human. But in addition, those signaling
pathways in communication systems are the same ones which if they go wrong, then underlie a whole host of
different developmental diseases, as well as diseases that occur in the adult.

the more we understand about the molecular biology of development, the better our understanding will be
about the molecular biology underlying disease. So in order to understand this human body plan information, I
don't use the human as a model system for obvious ethical reasons. So in my lab we use the chick and mouse
as a model systems. And the signaling pathway that I will focus on predominantly in my talk is that of the Notch
pathway. So the notch pathway is a cell communication system and the receiving cell when responding to
Notch signaling, can respond in a number of different ways. That cell might choose to proliferate, differentiate,
undergoes sulfate decision, perhaps die or indeed survive. And the reason for these multitude of different
responses is that cells are of course in different cell contexts and exposed to a multitude of other signals. So no
signaling pathway is acting on its own in isolation. And we'll see more about during my lectures. So then what
does this notch pathway look like? Well here we have a representative of the signaling cell and in the
membrane of fat cell to coach a fat cell, we see this little blue protein which represents the ligand, which part
of the Delta and Jacket family of proteins that are transmembrane proteins. And they interact with a
transmembrane receptor in the receiving cell. And that receptor protein is called a notch. So that ligand
receptor interaction. Once that happens, that leads to a pulling effect on this receptor, that exposes a cleavage
site, and that receptor then undergoes a number of different a cleavage events. The last one of which is
mediated by gamma secretase complex. And that then liberates the intracellular region of notch, that we call
the notch intracellular domain or NIS city. And that portion of the receptor is Ben translocated into the nucleus,
where it combines with a number of other transcription factor proteins in order to make the transcripts
transcription complex that activates expression of target genes in the absence of NICD. One of those core
transcription factors called CSL actually functions as a repressor of these target genes. So NICD forms a complex
with CSL that includes MAML and changes CSL from a repressor into an activator. So we can interfere with this
pathway in a number of different ways in order to try and understand its role in body plan formation during
early stages of development. So we can interfere with the pathway either by blocking the gamma-secretase
activity, such that even if you have ligand-receptor interaction, you're unable to release intracellular portion of
the receptor, and so you don't get activation of target genes. Alternatively, you can block the pathway
downstream of that ligand-receptor interaction at the, at the level of the transcription complex. For example,
by introducing dominant negative versions of either RB PJ kappa IS called CFL or MAML. One can activate the
pathway by introducing ectopic levels of this constitutively active form of the receptor, that's ligand
independent. And we'll see examples of these different types of manipulating the pathway through my talk.

So what I'll be doing in the next few recordings is to outline some little stories or vignettes showing the
different roles that notch plays during development. And I will highlight the role that notch plays in the
contribution profile of self-run using renewing progenitor cells, I will show a role of notch in regulating cell fate
choice within the neural epithelium to give rise to different types of neurons, as well as establish, showing the

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