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Rachel Moore
Works at King's College London
Attended University College London
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Embryonic development requires extensive growth, shape change and cell migration. The longest example of cell migration, in both duration and distance, is of enteric neural crest cells. They start close to the spinal cord and travel through the body to the stomach, then along the entire intestine. They become nerve cells and form the enteric nervous system that, among other things, controls the movement of food along the gut during digestion.

Why do we care?
In Hirschsprung’s disease, which occurs at 1/5000 live births, the cells don’t make it to the end of the intestine. This means that there is a section at the end of the intestine without nerve cells, so food can’t get pushed all the way along and out of the intestine. This is a serious disease that can be fatal if untreated, so it is important to understand how it occurs in order to prevent it.

What do we already know about enteric neural crest cell migration?
1. There is no fixed migration direction: Colonisation of the gut always occurs in one direction. However, when cells are implanted into the middle of the gut, they migrate in both directions. This suggests that the normal direction of migration is not due to something within the neural crest cells or the gut, but simply because the cells always start at the stomach-end of the gut and only have one way to can go.
2. There is a maximum density of cells: No matter the initial number of cells, the density of always ends up the same. This implies that cells keep proliferating until the maximum density is reached.
3. A certain population size is required: When cells at the front of the migrating population are separated from those behind them, their rate of migration is reduced. This suggests that the cells are “pushed” from behind by other cells. If so, an adequate population size is required for the leading cells to maintain the right speed to get to the end of the gut.

What does this study investigate?
Simpson and colleagues wanted to find out how these cells travel such a long distance. They suggest four potential models:
1. Leapfrog: Leading cells stop migrating when they find a good spot and those following overtake them. They in turn stop migrating when they come to an empty section of the gut, and so on.
2. Mixing expansion: All neural crest cells proliferate and migrate forwards, swapping neighbours as they go. Any cell can end up and the front or the back of the population.
3. Shunting expansion: All cells proliferate and move forward, but they tend to keep the same neighbours. Cells that start at the front stay at the front.
4. Frontal expansion: Leading cells keep proliferating and moving forward, leaving a trail of immobile cells behind them.

Their study also investigates whether a mathematical simulation can help to answer their question. Other studies have already discovered many factors that are important in enteric neural crest migration - genetics, molecular interactions, cell movement, cell-cell interactions, and so on. The next hurdle is to combine individual bits of information from the genetic, molecular, cellular and tissue levels to understand how the entire system works. To do this, the authors create a mathematical simulation and compare it to their experimental results.

Can the mathematical simulation make accurate predictions?
They created a simulation that mimics “normal” neural crest migration and test it by asking it what happens when cells were put in the middle of the gut. We already know that the cells will migrate in both directions, and this is also what the mathematical simulation predicts. So far, so good.

Do cells from the front migrate when they’re put at the back? Can cells from the back colonise the gut?
Next they start testing their models. The mathematical simulation suggests that cells put at the back of the population will not be able to migrate, presumably because other cells are in the way, and will also not be able to proliferate, because cell density is already at capacity. The experiment gave the same results.
This begins to cast doubt on the leapfrog, mixing expansion and shunting expansion models, all of which predict that cells at the back can move forwards. To investigate further, cells from the back were moved to the front of the cell population. These cells were able to move forward a huge distance - much further than cells put at the back of the population. It seems that cells from the back have a similar migratory potential to those at the front and this suggests that cells at the back and the front are identical - they simply end up in a certain position by chance. From these results, the researchers conclude that the frontal expansion model is the one that best explains the mechanism by which neural crest cells colonise the gut.

What keeps cells in their place?
Finally, they test the importance of proliferation by putting donor cells at the front that were unable to proliferate. They suggest two possible outcomes for this experiment - these cells might be pushed forward by the cells behind them; or, they might get in the way of those behind them. Mathematical simulations suggest that, if leading cells aren’t able to proliferate and increase cell density, some other cells will eventually be able to overtake them and colonise the gut. The experiments completely agree with the mathematical simulation, providing further evidence that the frontal expansion model is correct - or, at least, is the best model we have for the moment.


#developmentalbiology #neuroscience #cellbiology


REFERENCES
Simpson, M. J., Zhang, D. C., Mariani, M., Landman, K. A. and Newgreen, D. F. (2007) Cell proliferation drives neural crest cell invasion of the intestine. Developmental Biology 302:553-568
http://www.sciencedirect.com/science/article/pii/S0012160606013054
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I finally got a chance to read this new paper last week. Rather than reporting on their experiments, Jeremy Green and James Sharpe discuss a controversy in their field of developmental biology. They present the historical context and current thinking, then propose a hypothesis that brings together the alternatives to explain some well-known situations in embryonic development. I haven’t summarised this paper because I think it is quite accessible as it is. Give it a go, and I'm happy to (try to!) answer any questions.

Combining reaction-diffusion and positional information

A fundamental question in developmental biology is how all of the various structures of an organism are formed. During embryonic development, a clump of cells somehow manage to organise themselves into an organism consisting of many different cell types (skin cells, kidney cells, nerve cells, muscle cells …), with all of them in the right place and in the correct proportions. This paper discusses the relationship between two major ideas that have both been put forward to try to explain this: reaction-diffusion, suggested by Alan Turing of Enigma fame in his final paper, and positional information, proposed by Lewis Wolpert about 20 years later.

#AlanTuring #LewisWolpert #developmentalbiology #openaccess

http://dev.biologists.org/content/142/7/1203.full
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Rachel Moore

• Biology  - 
 
I finally got a chance to read this new paper last week. Rather than reporting on their experiments, Jeremy Green and James Sharpe discuss a controversy in their field of developmental biology. They present the historical context and current thinking, then propose a hypothesis that brings together the alternatives to explain some well-known situations in embryonic development. I haven’t summarised this paper because I think it is quite accessible as it is. Give it a go, and I'm happy to (try to!) answer any questions.

Combining reaction-diffusion and positional information

A fundamental question in developmental biology is how all of the various structures of an organism are formed. During embryonic development, a clump of cells somehow manage to organise themselves into an organism consisting of many different cell types (skin cells, kidney cells, nerve cells, muscle cells …), with all of them in the right place and in the correct proportions. This paper discusses the relationship between two major ideas that have both been put forward to try to explain this: reaction-diffusion, suggested by Alan Turing of Enigma fame in his final paper, and positional information, proposed by Lewis Wolpert about 20 years later.

#AlanTuring #LewisWolpert #developmentalbiology #openaccess

http://dev.biologists.org/content/142/7/1203.full
 Next Section Abstract One of the most fundamental questions in biology is that of biological pattern: how do the structures and shapes of organisms arise? Undoubtedly, the two most influential ideas in this area are those of Alan Turing's ‘reaction-diffusion’ and Lewis Wolpert's ‘positional information’. Much has been written about these two concepts but some confusion still remains, in particular about the relationship between them. Here, we ad...
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3 comments
 
I was going to say the same thing. I, too, found it fascinating! Thank you for sharing, +Rachel Moore!
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Rachel Moore

• Neurobiology (erstwhile Psych)  - 
 
Note: I've tried really hard to upload example movies, but it just doesn't want to! Follow the link provided in 'References' to find many movies and of course a lot more information as well.

Nerve cells, called neurons, have processes extending from their central cell body. Typically, they have several short dendrites, which receive information, and one long axon, which sends information to other cells.

How do neurons form these structures?
In the 1980’s, Dotti and colleagues cultured neurons in a dish, in vitro. The cells were initially round (Stage 1), then extended and retracted many small protrusions in all directions (Stage 2). In Stage 3, one protrusion suddenly grew more quickly and longer than the others, becoming the axon and making the cell asymmetrical or polarised. The other processes then become dendrites.

These observations show that neurons can polarise randomly with no external cues. However, we know that axons of mature neurons within an organism are always oriented in a certain direction. For example, some types of neurons always have their axon directed towards the basal lamina, a layer of proteins that lies along one side of the layer of neurons. Interestingly, neurons send axons towards or away from certain proteins in vitro.

How do neurons grow their axon and dendrites from correct sites, within the context of a growing, 3D embryo?
Randlett and colleagues looked at neuronal polarisation in developing zebrafish embryos. Zebrafish embryos are transparent, which makes it possible to observe individual cells during development. In vitro a fluorescent protein, Kif1-YFP, goes around the cell body and in and out of many protrusions during Stages 1 and 2, then in Stage 3 moves to and stays in the protrusion that becomes the axon. However, in the embryo, Kif1-YFP localised to the side of the neuron closest to the basal lamina BEFORE it extended an axon. In fact, these neurons didn’t really have a “Stage 2” – they just extended one protrusion, the axon, towards the basal lamina. This is shown in the movie below.

One protein in the basal lamina is laminin. When laminin was removed, the neurons extended lots of small processes, reminiscent of Stage 2 in vitro. Kif1-YFP moved around until it eventually accumulated in the process that became the axon. However, when small beads covered in laminin were placed next to neurons, either in vivo or in vitro, processes that touched the bead turned into axons. Importantly beads without laminin had no effect, showing that it is laminin that is important rather than the bead.

So, laminin directs neuronal polarisation?
Well … yes and no. We already knew that laminin could direct neuronal polarity in vitro, so it’s nice to see that it also plays a role in vivo. Perhaps laminin provides a cue that stabilises processes and tells them to become axons, making the neuron go straight to Stage 3 before it has a chance to go through Stage 2? Randlett and colleagues suggest that Stage 2 represents the behaviour of cells without relevant cues.

But there must be more to it than that. Even without laminin, Kif1-YFP still stayed close to the basal lamina side of the neuron during it’s “Stage 2” phase. Also, although axons without a laminin cue were not extended exactly next to the basal lamina, as is the case normally, they were only very rarely seen on the opposite side of the cell. This suggests that there are other cues that help neurons polarise correctly as well.

Any ideas what these might be?
Maybe there is something on the other side of the neurons that “pushes” axon extension away? Alternatively, maybe the neurons have some sort of intrinsic polarity, that does not rely on extrinsic cues? Before they become neurons, neuronal precursors have two very distinct ends. Indeed, Randlett and colleagues saw Kif1-YFP on only one end in neuronal precursors. Perhaps the polarity of neuronal precursors is maintained, and is somehow “inherited” by neurons.

At any rate, we are slowly starting to understand an important part of developmental biology, which is how neurons develop, how they manage to make the right connections, and so how they form a functioning nervous system.

#neuroscience #cellbiology #development     



REFERENCES
Dotti, C.G., Sullivan, C.A. and Banker, G.A. (1988) The establishment of polarity by hippocampal neurons in culture. Journal of Neuroscience 8:1454
http://www.jneurosci.org/content/8/4/1454.long

Randlett, O., Poggi, L., Zolessi, F.R. and Harris, W.A. (2011) The oriented emergence of axons from retinal ganglion cells is directed by laminin contact in vivo. Neuron 70:266
http://www.cell.com/neuron/fulltext/S0896-6273%2811%2900253-4
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mind blowing. nice
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Rachel Moore

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Unknown brain cell types discovery

Physicians and technicians depend on histological classifications to assess patients’ health and classify pathologies accurately. A recent advanced brain mapping study brought together single cells genetic analysis and histology to help identifying new brain cell types. Researchers from the Karolinska Institutet in Sweden mapped cerebral cortical cell types and the genes that are active in them. The study was published in the Science journal and unveils the discovery of new cells types using the mouse brain as a model. The analyses of more than 3000 cells individually allowed the identification of 47 different new cell types. Based on this study doctors will be able to assess patient's samples with more accuracy. The used analytical method provided a new tool to study brain cells and will help scientists to understand better how brain cells respond to injury and disease. 

Source: EurekAlert! Science News - http://ow.ly/Jr5vt

Original Study: Science – Cell types in the mouse cortex and hippocampus revealed by single-cell RNA-seq – http://ow.ly/Jsm8t 

#brain #cortex #hypocampus #celltypes #RNAseq #histology #singlecellsgeneticanalysis
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Rachel Moore

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Blog post from MindHacks has a brief review of a free online neuroscience course from +HarvardUni.

Register before mid-December - http://www.mcb80x.org/
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Rachel Moore

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How have I possibly not seen this site until now? It's full of infographics and includes all sources / data that was used to create them.

Here's one of the latest:
http://www.informationisbeautiful.net/visualizations/common-mythconceptions-worlds-most-contagious-falsehoods/

#informationisbeautiful  
We only use 10% of our brain. We evolved from chimps. Dairy foods increase mucous. Pfffff! These and 45 other myths & misconceptions debunked. Solidly.
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Rachel Moore

• Biology  - 
 
Embryonic development requires extensive growth, shape change and cell migration. The longest example of cell migration, in both duration and distance, is of enteric neural crest cells. They start close to the spinal cord and travel through the body to the stomach, then along the entire intestine. They become nerve cells and form the enteric nervous system that, among other things, controls the movement of food along the gut during digestion.

Why do we care?
In Hirschsprung’s disease, which occurs at 1/5000 live births, the cells don’t make it to the end of the intestine. This means that there is a section at the end of the intestine without nerve cells, so food can’t get pushed all the way along and out of the intestine. This is a serious disease that can be fatal if untreated, so it is important to understand how it occurs in order to prevent it.

What do we already know about enteric neural crest cell migration?
1. There is no fixed migration direction: Colonisation of the gut always occurs in one direction. However, when cells are implanted into the middle of the gut, they migrate in both directions. This suggests that the normal direction of migration is not due to something within the neural crest cells or the gut, but simply because the cells always start at the stomach-end of the gut and only have one way to can go.
2. There is a maximum density of cells: No matter the initial number of cells, the density of always ends up the same. This implies that cells keep proliferating until the maximum density is reached.
3. A certain population size is required: When cells at the front of the migrating population are separated from those behind them, their rate of migration is reduced. This suggests that the cells are “pushed” from behind by other cells. If so, an adequate population size is required for the leading cells to maintain the right speed to get to the end of the gut.

What does this study investigate?
Simpson and colleagues wanted to find out how these cells travel such a long distance. They suggest four potential models:
1. Leapfrog: Leading cells stop migrating when they find a good spot and those following overtake them. They in turn stop migrating when they come to an empty section of the gut, and so on.
2. Mixing expansion: All neural crest cells proliferate and migrate forwards, swapping neighbours as they go. Any cell can end up and the front or the back of the population.
3. Shunting expansion: All cells proliferate and move forward, but they tend to keep the same neighbours. Cells that start at the front stay at the front.
4. Frontal expansion: Leading cells keep proliferating and moving forward, leaving a trail of immobile cells behind them.

Their study also investigates whether a mathematical simulation can help to answer their question. Other studies have already discovered many factors that are important in enteric neural crest migration - genetics, molecular interactions, cell movement, cell-cell interactions, and so on. The next hurdle is to combine individual bits of information from the genetic, molecular, cellular and tissue levels to understand how the entire system works. To do this, the authors create a mathematical simulation and compare it to their experimental results.

Can the mathematical simulation make accurate predictions?
They created a simulation that mimics “normal” neural crest migration and test it by asking it what happens when cells were put in the middle of the gut. We already know that the cells will migrate in both directions, and this is also what the mathematical simulation predicts. So far, so good.

Do cells from the front migrate when they’re put at the back? Can cells from the back colonise the gut?
Next they start testing their models. The mathematical simulation suggests that cells put at the back of the population will not be able to migrate, presumably because other cells are in the way, and will also not be able to proliferate, because cell density is already at capacity. The experiment gave the same results.
This begins to cast doubt on the leapfrog, mixing expansion and shunting expansion models, all of which predict that cells at the back can move forwards. To investigate further, cells from the back were moved to the front of the cell population. These cells were able to move forward a huge distance - much further than cells put at the back of the population. It seems that cells from the back have a similar migratory potential to those at the front and this suggests that cells at the back and the front are identical - they simply end up in a certain position by chance. From these results, the researchers conclude that the frontal expansion model is the one that best explains the mechanism by which neural crest cells colonise the gut.

What keeps cells in their place?
Finally, they test the importance of proliferation by putting donor cells at the front that were unable to proliferate. They suggest two possible outcomes for this experiment - these cells might be pushed forward by the cells behind them; or, they might get in the way of those behind them. Mathematical simulations suggest that, if leading cells aren’t able to proliferate and increase cell density, some other cells will eventually be able to overtake them and colonise the gut. The experiments completely agree with the mathematical simulation, providing further evidence that the frontal expansion model is correct - or, at least, is the best model we have for the moment.


#developmentalbiology #neuroscience #cellbiology


REFERENCE:
Simpson, M. J., Zhang, D. C., Mariani, M., Landman, K. A. and Newgreen, D. F. (2007) Cell proliferation drives neural crest cell invasion of the intestine. Developmental Biology 302:553-568
http://www.sciencedirect.com/science/article/pii/S0012160606013054
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Thanks for the kind words +Cliff Bramlett and +Gary Ray R! Glad you both enjoyed it.
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Rachel Moore

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Cut Paper Bacterium

Artist Rogan Brown recently completed work on this new cut paper sculpture titled Cut Microbe. 

Four months in the making, the piece is a continuation of Brown’s exploration of the human biome and was inspired by the form of salmonella and ecoli bacteria (this 44″ sculpture is about half a million times bigger than the real thing). The sculpture will be on view this May as part of a commission by the Eden Project in the UK. 

more: http://www.thisiscolossal.com/2015/03/a-sprawling-cut-paper-bacterium-by-rogan-brown/
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Note: I've tried really hard to upload example movies, but it just doesn't want to! Follow the link provided in 'References' to find many movies and of course a lot more information as well.

Nerve cells, called neurons, have processes extending from their central cell body. Typically, they have several short dendrites, which receive information, and one long axon, which sends information to other cells.

How do neurons form these structures?
In the 1980’s, Dotti and colleagues cultured neurons in a dish, in vitro. The cells were initially round (Stage 1), then extended and retracted many small protrusions in all directions (Stage 2). In Stage 3, one protrusion suddenly grew more quickly and longer than the others, becoming the axon and making the cell asymmetrical or polarised. The other processes then become dendrites.

These observations show that neurons can polarise randomly with no external cues. However, we know that axons of mature neurons within an organism are always oriented in a certain direction. For example, some types of neurons always have their axon directed towards the basal lamina, a layer of proteins that lies along one side of the layer of neurons. Interestingly, neurons send axons towards or away from certain proteins in vitro.

How do neurons grow their axon and dendrites from correct sites, within the context of a growing, 3D embryo?
Randlett and colleagues looked at neuronal polarisation in developing zebrafish embryos. Zebrafish embryos are transparent, which makes it possible to observe individual cells during development. In vitro a fluorescent protein, Kif1-YFP, goes around the cell body and in and out of many protrusions during Stages 1 and 2, then in Stage 3 moves to and stays in the protrusion that becomes the axon. However, in the embryo, Kif1-YFP localised to the side of the neuron closest to the basal lamina BEFORE it extended an axon. In fact, these neurons didn’t really have a “Stage 2” – they just extended one protrusion, the axon, towards the basal lamina. This is shown in the movie below.

One protein in the basal lamina is laminin. When laminin was removed, the neurons extended lots of small processes, reminiscent of Stage 2 in vitro. Kif1-YFP moved around until it eventually accumulated in the process that became the axon. However, when small beads covered in laminin were placed next to neurons, either in vivo or in vitro, processes that touched the bead turned into axons. Importantly beads without laminin had no effect, showing that it is laminin that is important rather than the bead.

So, laminin directs neuronal polarisation?
Well … yes and no. We already knew that laminin could direct neuronal polarity in vitro, so it’s nice to see that it also plays a role in vivo. Perhaps laminin provides a cue that stabilises processes and tells them to become axons, making the neuron go straight to Stage 3 before it has a chance to go through Stage 2? Randlett and colleagues suggest that Stage 2 represents the behaviour of cells without relevant cues.

But there must be more to it than that. Even without laminin, Kif1-YFP still stayed close to the basal lamina side of the neuron during it’s “Stage 2” phase. Also, although axons without a laminin cue were not extended exactly next to the basal lamina, as is the case normally, they were only very rarely seen on the opposite side of the cell. This suggests that there are other cues that help neurons polarise correctly as well.

Any ideas what these might be?
Maybe there is something on the other side of the neurons that “pushes” axon extension away? Alternatively, maybe the neurons have some sort of intrinsic polarity, that does not rely on extrinsic cues? Before they become neurons, neuronal precursors have two very distinct ends. Indeed, Randlett and colleagues saw Kif1-YFP on only one end in neuronal precursors. Perhaps the polarity of neuronal precursors is maintained, and is somehow “inherited” by neurons.

At any rate, we are slowly starting to understand an important part of developmental biology, which is how neurons develop, how they manage to make the right connections, and so how they form a functioning nervous system.

  #neuroscience #cellbiology #development  



REFERENCES
Dotti, C.G., Sullivan, C.A. and Banker, G.A. (1988) The establishment of polarity by hippocampal neurons in culture. Journal of Neuroscience 8:1454
http://www.jneurosci.org/content/8/4/1454.long

Randlett, O., Poggi, L., Zolessi, F.R. and Harris, W.A. (2011) The oriented emergence of axons from retinal ganglion cells is directed by laminin contact in vivo. Neuron 70:266
http://www.cell.com/neuron/fulltext/S0896-6273%2811%2900253-4
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Thanks for looking this up. We have several labs studying axon guidance at my institution, and I hear about semaphorins, netrins, Slit/Robo -it's quite challenging to keep up! 
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Rachel Moore

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"How does the nervous system ignore touch inputs coming from our own movements (e.g. when we touch something) while still robustly responding to ones that arise from external sources (e.g. when something touches us)?"
Unlike the sense of vision, which is perceived only by light-sensitive photoreceptors in our eyes, the mechanoreceptors that respond to light touch are located in sensory neurons all over the body....
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Where should the balance lie?
 
In the spirit of scientific peer review, my post for +ScienceSunday today is a bit of a critique of an article I read. I'm curious to see what people think not just of the article but also of public figures speaking out in the name of science: are they doing science a favor? do you think it's fair that they "sensationalize" it (some more, some less) so that the message reaches out to more people and becomes more accessible to people who don't have a scientific background? To what extent do we need "translators" of the scientific content given that often us scientists sound too technical to be understood? And why is it so, why are we so handicapped when it comes to communicating not just what we do but also our enthusiasm and the importance of teaching our children a rigorous way of thinking? 

Sorry, I went off a tangent, but anyways, with thanks to the awesome team +Allison Sekuler , +Rajini Rao , +Buddhini Samarasinghe , and +Robby Bowles 
I came across an article on the Popular Science website, which, turns out, is the excerpt of a new book on evolution by Science Guy Bill Nye. From the reviews I gather that Bill Nye is an excellent writer and, being also an entertainer, he knows how to not only expose well but also infuse some ...
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Have them in circles
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Education
  • University College London
    PhD, Cell and Developemental Biology
  • University of Melbourne
    Bachelor of Biomedical Science (Honours), Diploma of Modern Languages (German)
Story
Introduction
How do you make a multi-cellular organism out of a single cell?  I'm interested in how cells communicate with each other during development.  Currently looking at neurogenesis in zebrafish.
Work
Occupation
Scientist
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  • King's College London
    Research Associate, 2014 - present
Rachel Moore's +1's are the things they like, agree with, or want to recommend.
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