Last year we were approached by Andreas Prokop of The University of Manchester (who is also Communications Officer of the British Society for Developmental Biology), with an offer to write a paper on our experiences of running the Node and using social media to build scientific networks. We – that is Aidan Maartens (the Node’s Community Manager), Catarina Vicente (who previously held the post) and Katherine Brown (Development’s Executive Editor) – accepted, seeing it as a great opportunity to promote our work as well as explore what we have learned after six years. The paper is part of an exciting upcoming Special Issue of Seminars in Cell & Developmental Biology on science communication, and features input from individuals and organisations who use social media 

The following excerpts give a taste of where we came from in the article, and you can find a link to it below.

Launching the Node

Established in 1953 and initially known as the Journal of Embryology and Experimental Morphology, Development (www.dev.biologists.com) is a leading research journal in developmental biology. Run by the not-for-profit publisher The Company of Biologists, whose mission is to support and inspire the biological community, it has a specific remit to support the needs of developmental biologists. In 2009, a survey conducted by the journal highlighted the idea that Development − seen as a community journal − should be doing more for the community. Specifically, the survey identified a desire for an environment where members of this and related fields (most notably stem cell biology, but also other intersecting fields such as cell biology, evolution and genetics) could gather and interact online, bypassing the need for each internet-savvy researcher to build their own network from scratch. Development responded in 2010 by establishing an online hub called the Node. The site’s name reflects its aim: from a technical perspective, a node is simply a connection point, while developmental biologists know the node as an important group of cells that instruct and organise the activity of others in the early embryo. The Node was hence conceived as an online connection point for developmental biologists. It would provide a place where ideas could be discussed and exchanged by the whole community, without the restrictions of more formal publications, and would encourage an informal style and varied content, as well as dedicated pages for job opportunities and events useful for community members. Importantly, the Node would be open to anyone interested in contributing and would be easy to use. Thus, to some extent, the Node could be considered an online (and hence more flexible and accessible) version of a scientific newsletter − an informal form of communication aimed at a defined group of researchers with a remit to facilitate exchange of ideas and provide information on useful resources.

The Node was conceived as an online connection point for developmental biologists

6 years on

The digital age has opened the doors to a brave new world of communication outside traditional restrictions of geography, funding and editorial control. While the scientific community in general has not necessarily been quick to adopt and exploit all the opportunities now available, these technologies are changing the way we communicate. The Node, born out of a desire among the developmental biology community for an online communication hub, exemplifies both the opportunities and the challenges of community building online. Perhaps the biggest lesson we have learned in the 6 years of operating the Node is that the initial concept of a self-sustaining community site was unrealistic: the Node relies on ongoing financial, technical and strategic support from The Company of Biologists. However, we have also learned that this support is recognised and appreciated: most members of the developmental biology community are now aware of the Node, even if they don’t actively participate in it, and value its utility as an online hub for the field. Social media, particularly Twitter, have helped us reach a wider audience, and better gather and disseminate information. The original vision of the Node – as your online coffee break, a place to catch up on the latest news from the field − has been realised, although we continue to develop and grow. Currently, significant efforts are focussed on improving the resources section of the site, to help with teaching, advocacy and outreach activities, as well as on growing our reader- and authorship in particular geographic and scientific areas where we are less well represented than we would like. We are also exploring formats that can better facilitate online discussion.

The Node exemplifies both the opportunities and the challenges of community building online

You can read the full paper freely here:

The Node and beyond–using social media in cell and developmental biology

Catarina Vicente, Aidan Maartens, Katherine Brown

Seminars in Cell & Developmental Biology

https://doi.org/10.1016/j.semcdb.2017.05.009

(4 votes)

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POSTDOCTORAL POSITION is available to study different aspects of lymphatic vasculature development and metabolism in health and disease. Some of the projects include the characterization of the cellular and molecular mechanisms controlling the development of the lymphatic vasculature, endothelial cell plasticity and reprogramming, as well as different aspects related to lymphatic function and metabolism. Highly motivated individuals who recently obtained a PhD. or MD degree and have a strong background in mammalian vascular, molecular and developmental biology are encouraged to apply. Interested individuals should send their curriculum vitae, a brief description of their research interests, and the names of three references to:

Guillermo Oliver, Ph.D

Thomas D Spies Professor of Lymphatic Metabolism

Director Center for Vascular and Developmental Biology

Northwestern University Feinberg School of Medicine

303 East Superior Street, 10-107

Chicago, Illinois 60611

Email: guillermo.oliver@northwestern.edu

http://labs.feinberg.northwestern.edu/oliver/

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A Postdoctoral Research Associate position is available in the Conduit lab to study the role of the nuclear envelope in centrosome assembly. Our lab studies how microtubule formation is regulated in cells, including how microtubule organising centres (MTOCs) are assembled. The post-holder will use Drosophila melanogaster to follow up on our recent discover that the nuclear envelope may help regulate centrosome assembly. They will use CRISPR/HDR to generate a series of new fly strains, and then use advanced live-cell fluorescence imaging, including super-resolution imaging, and biochemistry to establish how the nuclear envelope helps regulate centrosome assembly.

The appointment will be for a period of up to three years starting 2nd October 2017, or as soon as possible thereafter.

Candidates are expected to have (or soon have) a PhD in cell/developmental biology and have experience in fluorescent microscopy. Prior experience in Drosophila, centrosome biology, molecular biology and/or basic biochemistry would be an advantage, but not essential.

Applications should include a C.V. and a brief statement of your scientific background and why you would like to join the lab.

To apply, please follow this link: http://www.jobs.cam.ac.uk/job/13999/

Informal enquiries are welcomed and can be addressed to Dr. Paul Conduit ptc29@cam.ac.uk

Please see the lab website for more information on our research http://conduitlab.zoo.cam.ac.uk

PDRA_job_advert_2017

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Job Details

Fully funded postdoctoral positions are presently available in the Conlon Lab whose studies focus on identifying the molecular networks that are essential for early heart development and how alterations in these networks lead to congenital heart disease. For these studies, we use a highly integrated approach that incorporates developmental, genetic, proteomic, biochemical and molecular based studies in mouse, Xenopus and stem cells.

Recent advances and projects of interest in the Conlon lab include studies that define the cellular and molecular events that lead to cardiac septation, those that explore cardiac interaction networks as determinants of transcriptional specificity, the mechanism and function of cardiac transcriptional repression networks and, the regulatory networks of cardiac morphogenesis.

http://www.unc.edu/~fconlon/

Twitter: @fconlon

Job Requirements

Candidates should have recently obtained or be about to obtain a Ph.D. or M.D. in a field of biological science and should have a strong publication record. Outstanding and highly motivated candidates should apply by email to Dr. Frank L. Conlon and include a CV/resume, three references and description of your specific interest in our research programs.

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Daily life changes when you set foot in Woods Hole. There is a beauty in your surroundings and energy in the air that invigorates you. The days are long (8am to 2 or 3 am most days!) and we have a full schedule but we are all so excited to be here – to learn – to question – to move the field forward.

A typical day in the course starts with morning lecture at 9am. The lecture is broken down into two parts, the first part is general information about the model system we are working with and the second is about the current research project in the speaker’s lab. After lecture we head to the ‘Sweat Box’ where the students ask the speaker questions. This includes grilling them about their research, it was said this session is like a qualifying exam for the professors! We can also use this time to ask them about their career trajectory and for career advice. We then break for lunch; two students take the speaker to lunch where they get to talk more in depth about science and life.

After lunch we head to the lab, we get a ‘cookbook’ for each organism; this includes information on how to take care of them and many protocols. In this ‘cookbook’ there are instructions on how to fertilize the egg, manipulate the embryo and the organism as well as a list of reagents and tools that are available to us. We then brainstorm ideas in groups and have full access to the teaching assistants, professors and course directors to plan and execute our experiments.

We break in the early evening to take a run, shoot some hoops or practice softball for the annual softball match (watch out physio) and eat dinner. Two students also get to take the speaker out to dinner at a local Woods Hole restaurant during this time. Then it’s back to the lab to continue our experiments into the wee hours of the morning!

How do we survive this schedule for six weeks? We drink a lot of coffee!

Follow the course here on the blog and on twitter #embryo2017

(1 votes)

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A postdoctoral position is available to study the extrinsic modulation of intestinal proliferation in the research group of Golnar Kolahgar at the Department of Physiology, Development and Neuroscience at the University of Cambridge. The candidate is expected to hold a PhD in cellular, molecular or developmental biology.

Our goal is to identify the components of the extracellular space that contribute to maintaining and remodelling the adult intestine in response to various physiological conditions. We use the genetically tractable Drosophila gut as a paradigm to investigate cell fate decisions in vivo (e.g. Kolahgar et al, Dev Cell, 2015; Suijkerbuijk et al, Curr. Biol, 2016). The aim of this project is to explore how integrin signalling promotes intestinal stem cell proliferation and contributes to gut plasticity, using a combination of Drosophila genetics, lineage tracing and clonal analysis, confocal imaging and whole genome sequencing, thus experience with one or several of these techniques is required.

The post is funded for an initial period of 3 years.

For more information and to apply, follow this link: http://www.jobs.cam.ac.uk/job/13950/

Informal enquiries to Golnar Kolahgar (gk262 [at] cam.ac.uk)

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Development of the placental vasculature – known as the labyrinth – is critical for foetal development. Today’s paper comes from the most recent issue of Development and addresses the signalling events involved in placental vascular maturation. We caught up with lead author Lijun Chi and her PI Paul Delgado-Olguin of the Hospital for Sick Children and University of Toronto.

Can you give us your scientific biography and the main questions your lab is trying to answer?

PD-O As a Ph.D. student at the Universidad Nacional Autónoma de México (UNAM) under supervision of Dr. Ramón Coral Vázquez and Dr. Félix Recillas Targa, I investigated the transcriptional regulation of genes expressed in skeletal muscle and whose mutations cause muscular dystrophies. My reading during my Ph.D. studies led me to numerous landmark papers from Eric Olson’s lab on skeletal muscle gene regulation. I soon discovered Dr. Olson’s and Dr. Deepak Srivastava’s seminal work on the transcriptional pathways controlling heart development, a process that I always found fascinating. Working at Dr. Recilla’s lab, I became very interested in the function of chromatin modifiers in gene control, which led me to mine the scientific literature to learn about the function of chromatin structure regulators in cardiac gene control and development. This made me realize how little was known on the subject at the time, and brought me across a pioneering paper from Dr. Benoit Bruneau’s lab describing an essential function of Baf60c, a subunit the SWI/SNF chromatin remodelling complex, in heart development. This helped me decide what I wanted to do as a postdoc.

I obtained my Ph.D. degree in June 2005, and by August I was in Dr. Bruneau’s laboratory ready to start my postdoctoral research. In Dr. Bruneau’s lab I investigated the function of the histone methyltransferase Ezh2 in the heart. This enzyme tri-methylates the lysine 27 of histone H3 to repress gene expression, and its global deletion causes lethality early in mouse development. Surprisingly, we found that deletion of Ezh2 in cardiac progenitor cells, despite altering embryonic gene expression, did not alter heart development, and mutant mice had normally structured hearts. However, adult mutants developed heart disease. This raised the possibility that epigenetic alterations in differentiating cardiovascular progenitor cells early in development might program adult heart disease susceptibility. To address this possibility, my lab at The Hospital for Sick Children (SickKids) has been studying the function of several histone modifiers in cardiac and vascular development, and in regulating adult cardiovascular system function since 2012. Because the placental vasculature is required for proper embryo development, and its malfunction can affect heart development and program adult disease in the offspring, my lab is also interested in uncovering the mechanisms controlling its development. My lab will continue to focus on uncovering the mechanisms controlling cardiovascular development and programming postnatal disease during embryogenesis.

And what is Toronto like to do science in?

PD-O Toronto is a great place to do science. It is home for numerous world-class scientists, research institutes, numerous hospitals with very strong research programs, and the University of Toronto, which has an outstanding research curriculum. These attributes make Toronto and ideal place to develop multidisciplinary research of the highest quality. For example, my lab investigates fundamental biological processes, and being at SickKids and in Toronto’s rich scientific environment allowed establishment of key collaboration with clinician scientists in neighbouring institutions, which has facilitated me to explore the translation potential of my lab’s research.

Lijun, how did you come to join the Delgado-Olguin lab?

I obtained my PhD. at the University of Oulu, Finland under the supervision of Professor Seppo Vainio. My PhD thesis, published in 2007, describes the role of Sprouty2 in development of the urogenital system. I then pursued a postdoctoral fellowship in Dr. Norman Rosenblum’s laboratory at SickKids in Toronto, Canada. During my fellowship I investigated the function of the cilia protein Kif3a, whose deficiency causes polycystic kidney in human and mouse models. After finishing my fellowship in 2011, I wanted to learn about cardiovascular development, and I knew Paul was just about to Join SickKids. Working at the Delgado-Olguin lab has given me the opportunity to work in exciting projects to understand the basis of cardiovascular development and disease.

What was known about signalling pathways controlling placental vascular maturation before you started this work?

PD-O Because of its relevance in embryogenesis and in postnatal health, I was surprised to find out how little we knew about pathways controlling placental vascular maturation before we started our work. Perhaps the most informative report on the subject is from Knox & Barker (2008), who performed global gene expression analyses on the embryonic portion of mice placental vasculature, known as the labyrinth, at consecutive days of development. This analysis revealed a sharp molecular transition defining the developmental and the maturation phases of the placenta. In this transition, over 700 genes change their expression from embryonic day 12.0 to E13.5, and functions associated with these genes provided a general idea of some of the processes occurring in each phase. For instance, genes that are expressed in the developmental phase are involved in growth, metabolic processes, DNA and RNA processing, and cell cycle regulation. While genes active in the maturation phase are involved in pregnancy and reproduction. However, these studies were done on whole labyrinth, and thus tell us little on the pathways controlling this transition in specific cell types. To the best of my knowledge, our work is the first one to address the regulation of the transition from development to maturation in placental vascular maturation, and to define pathways active in endothelial cells regulating this process.

Can you give us key results of the paper in a paragraph?

PD-O We found that the histone methyl transferase G9a activates the Notch pathway in endothelial cells to promote maturation of the placental vasculature. We inactivated the histone methyltransferase G9a in endothelial progenitors and their derivatives, and found that mutant embryos died with placental defects. Closer examination revealed that the gross morphology of the placentae from mutant embryos appeared normal at E12.5, but had a smaller vascularized area at E13.5. Because the transition from the developmental to the maturation phase of the placenta occurs precisely between these stages, this raised a possible function for G9a as a regulator placental vascular maturation. Analysis of cell proliferation revealed that growth of the labyrinth is coordinated with decreased growth of the spongiotrophoblast during the development to maturation transition, and that this balance is lost in G9a mutant placentae. To uncover regulatory pathways we performed global gene expression analysis, which revealed that effectors of the Notch pathway were downregulated in G9a mutant placental endothelial cells. We then introduced a transgene to activate the Notch pathway in G9a mutants, and we found that the placental morphology was rescued! This opened the possibility that a G9a-Notch axis might be disrupted in placental diseases with vascular maturation defects. Indeed, we found that G9a, and Notch regulators were downregulated in human placentae from pregnancies affected with intra uterine growth restriction.

How might your work inform efforts to diagnose or even treat placental defects during pregnancy?

PD-O These are very exciting possibilities. Intra uterine growth abnormalities are diagnosed only when the foetus is smaller than expected for the gestational age or when the placenta is already malfunctioning. The ability to identify preclinical placental insufficiency is limited because we know very little about the regulation of placental vascular development, and on the events that precede placental malfunction. We found that imbalanced growth of the labyrinth vs the spongiotrophoblast precedes the appearance of gross morphological abnormalities in G9a mutant placentae. Based on these results, we think that being able to define the growth ratio of these placental cell types, and detect imbalances might offer a way of identifying foetuses at risk of defective intrauterine growth. In terms of prevention or treatment, our findings open the possibility that activating the Notch pathway might be investigated as a means to promote placental vascular maturation. Our mouse model, combined with availability of pharmacologic compounds that activate the Notch pathway, will allow us to further investigate these possibilities.

When doing the research, did you have any particular result or eureka moment that has stuck with you?

LC In the initial stage of the research, we were mainly focused on identifying cardiac defects in G9a mutants. However, I noticed that mutants had placentae with reduced vascularization. I decided to analyze embryos at consecutive developmental stages and I found that the vascular defect was obvious only at E13.5 and onwards. When I realized that the transition from the developmental to the maturation phase occurs precisely from E12.5 to E13.5, I hypothesized that G9a might regulate this transition. Given that the regulation of placental vascular maturation is very poorly understood, we decided to investigate further and test the hypothesis.

What about the flipside: any moments of frustration or despair?

LC As often happens with genome wide gene expression data, it was difficult to identify potentially relevant targets downstream of G9a from our RNAseq results. Fortunately, we found published reports demonstrating the involvement of the Notch signalling pathway in vascular maturation in the retina. We also found a report showing downregulation of some Notch regulators in placentae from pregnancies affected by intrauterine growth restriction. These reports encouraged me to confirm downregulation of Notch effectors in G9a mutant placental endothelial cells, and later on to test the effect of activating the Notch pathway in G9a mutant endothelial cells. These experiments were nerve wracking, because if the vascular phenotype were not to be corrected at least partially, I would have had to keep trying to identify functionally relevant G9a targets.

What are your career plans following this work?

LC With the completion of this current study, I am planning to test whether pharmacologically activating the Notch pathway in the G9a mutant placental vasculature promotes the maturation process and ameliorates or prevents placental defects. This might open the door to new experiments to try to promote vascular maturation in other models of intrauterine growth restriction.

And what next for the Delgado-Olguin lab?

PD-O We will delve deeper into the mechanisms by which G9a controls placental vascular maturation and the effects of activating Notch signalling in the placental vasculature. There are outstanding questions from our work. Particularly intriguing is how G9a activates the Notch pathway, as it is predominantly known as a transcriptional repressor, while its function as a transcriptional activator is less understood. Dissecting the mechanisms of action of G9a in placental endothelium will likely reveal additional regulatory pathways and potential approaches to promote vascular maturation. More broadly, our lab will continue to investigate the mechanisms by which postnatal cardiovascular disease is programmed during embryogenesis.

Finally, what do you two like to do in Toronto when you are not in the lab?

PD-O I enjoy hiking the many trails and parks in the city with my family and dogs, visiting museums, and fishing. Also, being an avid foodie, living in a city where there is food from all over the world available close by is a great bonus!

LC During my spare time, I am a passionate reader who enjoys a diversity of novels. I am also a skilful cook who loves exploring different recipes and trying out new styles. To stay physically well rounded, swimming is one of my weekly activities.

(5 votes)

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Today marks Day 3 of the Embryology: Concepts & Techniques in Modern Developmental Biology course (http://www.mbl.edu/education/courses/embryology/) at the Marine Biological Laboratories in Woods Hole, MA (http://www.mbl.edu/).

24 students along with faculty, teaching assistants and course assistants arrived over the weekend to embark on a life changing summer experience. Since my days in undergraduate research in cell biology, I always heard fascinating stories about the science and life at Woods Hole. I knew it was an experience that I wanted to take part in during my training. The MBL at Woods Hole is a mecca of research, creativity, ingenuity and curiosity it gives everyone who sets foot on its campus the opportunity to learn new concepts and techniques. This course and the community here allow you to test your cool and creative hypotheses and push you out of your comfort zone. It’s an experience that empowers scientific adventure and will leave you wanting to come back year after year.

In the first days here as a student in one of the longest standing classes at the MBL I have been welcomed into an amazing group of scientists. My fellow students and I had the opportunity to share our research with our peers and some of the course faculty during an informal poster session over pizza, listened to amazing lectures on echinoderm development, and started to learn how to make the tools and run the microscopes that will enable us to conduct our experiments.

I can’t wait to see what we learn and discover this summer!

Follow the course here on the blog and on twitter #embryo2017.

(5 votes)

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One of the research topics in Michel Milinkovitch’s laboratory (https://www.lanevol.org) at the University of Geneva (Switzerland) is to understand how squamates (lizards and snakes) generate such a tremendous variety of colours and colour patterns.

Colours

The colour of a lizard’s patch of skin is generally the result of the combination among structural and pigmentary elements found in various types of chromatophores^(1-5). Pigmentary colours are produced by brown/black melanins in melanophores, as well as by yellow and red pteridines/carotenoids in xanthophores and erythrophores, respectively. On the other hand, structural colours are produced by light interference in iridophore cells containing layers of guanine nanocrystals⁽⁵⁾: the wavelengths specifically reflected by these periodic structures is a function of the mean distance between successive layers of guanine nanocrystals — the longer the distance, the longer the wavelengths that are reflected. For example, many species of reptiles and amphibians are green despite that their skin does not contain any green pigment! They produce their chlorophyll-matching colour in a more sophisticated way⁽⁴⁾: a layer of iridophores selectively reflects most of the incoming green and blue wavelengths but a layer of yellow pigments absorbs blue. As all other wavelengths of the visible range (yellows, oranges, and reds) go through the skin (and are absorbed by deeper tissues), the only colour that bounces back from the skin is pure bright green⁽⁴⁾, as in day geckos (Fig. 1a).

The Milinkovitch lab also discovered that chameleons change colour by manipulating structural colours rather than by dispersion/aggregation of pigment-containing organelles within chromatophores. Indeed, combining microscopy, videography, RGB photometry and photonic band-gap modelling, they showed that chameleons shift colour through active tuning of a 3D lattice of guanine nanocrystals within a superficial layer of dermal iridophores⁽⁵⁾. In other words, chameleons manipulate light interference by changing the distance among their nanocrystals of guanine. Take an adult male panther chameleon. In its cryptic state, it is green for the same reason as the Phelsuma lizards: its dermal iridophores reflect green and blue, and the latter is being absorbed by a yellow pigment. But if another mature male enters its territory, the two animals increase the distance between the nanocrystals within their iridophores … such that they both turn yellow or orange or red to become as visible as possible and impress each other (Fig. 1b and link to YouTube videos). This usually suffices for one of the two males to give up…otherwise they will start a physical fight.

These studies provided some new answers but also opened many new questions. How do iridophores generate and spatially organise nanocrystals? What is the cellular mechanism involved in the tuning of the distance among nanocrystals in iridophores of chameleons when they change colour? Milinkovitch is now teaming up with biochemists/cell biologists such as Marcos Gonzalez-Gaitan for investigating these questions.

Colour change in chameleons YouTube playlist.

Colour Patterns

Animals display colours, but they often additionally exhibit colour patterns, i.e., symmetry-breaking regularities (stripes, spots, tessellations, meanders, and labyrinths) that result from short-range and long-range interactions among chromatophores^(6-11). At the macroscopic scale, these dynamical processes obey reaction-diffusion (RD) equations discovered by the mathematician Alan Turing^(12-14). Strikingly, the formation of skin colour in the ocellated lizard (Timon lepidus) seems to conflict with this RD framework as skin scales, rather than individual chromatophore cells, establish the pattern. Indeed, the brown juvenile lizard gradually transforms its skin colour as it ages to reach an intricate adult labyrinthine pattern where each scale is either green or black (Fig. 2).

But why would the pattern form at the level of scales, rather than at the level of biological cells? This is the questions that the Milinkovitch team solved recently, as reported recently in the journal Nature⁽¹⁵⁾.

To tackle this question, two PhD students, Liana Manukyan (computer scientist) and Sophie Montandon (developmental biologist), followed individual lizards during three to four years of their development from hatchlings crawling out of the egg to fully mature animals. For multiple time points, they reconstructed the geometry and colour of the network of scales on three animals by using R²OBBIE-3D (YouTube playlist), a very high resolution robotic system⁽¹⁶⁾ developed previously in the Milinkovitch laboratory by a physicist PhD student: Antonio Martins.

R²OBBIE-3D YouTube playlist

R²OBBIE-3D allows to reconstruct the 3D geometry and colour texture of objects up to 1.5 meters with a resolution of … 15 microns ! The Swiss team then set up a software pipeline that allowed them to automatically detect scales on each animal at each time point and match these networks. This was not a trivial task because the size of the animal, the positions of its body parts, and its skin pattern all change from scan to scan. Fortunately, the number of scales is invariant for a given individual throughout its life. This analysis indicated that the brown juvenile scales change to green or black then, surprisingly, continue flipping colour (between green and black) during the life of the animal (Fig. 3).

This very strange observation prompted Milinkovitch to suggest that the skin scale network forms a so-called ‘Cellular Automaton’. This esoteric computing system was invented in 1948 by the mathematician John von Neumann. Cellular automata are lattices of elements in which each element changes its state (here, its colour, green or black) depending on the states of neighbouring elements. The elements are called cells but are not meant to represent biological cells; in the case of the lizards, they correspond to individual skin scales. These abstract automata were extensively used to investigate computing systems and to model natural phenomena, but the Geneva team discovered what seems to be the first case of a genuine 2D automaton appearing in a living organism. Analyses of the four years of colour change allowed to confirm Milinkovitch’s hypothesis: the scales were indeed flipping colour depending of the colours of their neighbour scales. Computer simulations implementing the discovered mathematical rule generated colour patterns that could not be distinguished from the patterns of real lizards.

How could the interactions among pigment cells, described by Turing equations, generate a von Neumann automaton exactly superposed to the skin scales? The skin of a lizard is not flat: it is very thin between scales and much thicker at the center of them. Given that Turing’s mechanisms involves movements of cells, or the diffusion of signals produced by cells, Milinkovitch understood that this variation of skin thickness could impact on the Turing’s mechanism. Liana Manukyan, but also Anamarija Fofonjka, a third PhD student in Milinkovitch’s team, then performed computer simulations and saw a cellular automaton behaviour emerge, demonstrating that the development of Cellular Automata as computational systems is not just an abstract concept developed by John von Neumann, but also corresponds to a natural process generated by biological evolution.

However, the automaton behaviour was imperfect as the mathematics behind Turing’s mechanism and von Neumann automaton are very different. Milinkovitch called in Stanislav Smirnov, Professor of mathematics at the University of Geneva. Stanislav was awarded in 2010 the Fields Medal (the equivalent of the Nobel Price in Mathematics). Before long, Smirnov derived a so-called discretisation of Turing’s equations that would constitute a formal link with von Neumann’s automaton. Anamarija Fofonjka implemented Smirnov new equations in computer simulations, obtaining a system that had become un-differentiable from a von Neumann automaton (Fig. 4). The highly multidisciplinary team of researchers had closed the loop in this amazing journey, from biology to physics to mathematics.

Bibliography

1. T. Kuriyama, K. Miyaji, M. Sugimoto, M. Hasegawa, Zoological Science 23, 793-799 (2006).

2. J. Cote, S. Meylan, J. Clobert, Y. Voituron, J Exp Biol 213, 2116-2124 (2010).

3. S. L. Weiss, K. Foerster, J. Hudon, Comp Biochem Physiol B Biochem Mol Biol 161, 117-123 (2012).

4. S. V. Saenko, J. Teyssier, D. van der Marel, M. C. Milinkovitch, BMC biology 11, 105 (2013).

5. J. Teyssier, S. V. Saenko, D. van der Marel, M. C. Milinkovitch, Nature communications 6, 6368 (2015).

6. M. Inaba, H. Yamanaka, S. Kondo, Science 335, 677 (2012).

7. H. G. Frohnhofer, J. Krauss, H. M. Maischein, C. Nusslein-Volhard, Development 140, 2997-3007 (2013).

8. H. Hamada, M. Watanabe, H. E. Lau, T. Nishida, T. Hasegawa, D. M. Parichy, S. Kondo, Development 141, 318-324 (2014).

9. U. Irion, H. G. Frohnhofer, J. Krauss, T. C. Champollion, H. M. Maischein, S. Geiger-Rudolph, C. Weiler, C. Nusslein-Volhard, Elife 3, (2014).

10. A. Fadeev, J. Krauss, H. G. Frohnhofer, U. Irion, C. Nusslein-Volhard, Elife 4, (2015).

11. D. S. Eom, D. M. Parichy, Science 355, 1317-1319 (2017).

12. A. M. Turing, Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences 237, 37-72 (1952).

13. A. Gierer, H. Meinhardt, Kybernetik 12, 30-39 (1972).

14. S. Kondo, T. Miura, Science 329, 1616-1620 (2010).

15.L. Manukyan, S. A. Montandon, A. Fofonjka, S. Smirnov, M. C. Milinkovitch, Nature 544, 173-179 (2017).

16. A. F. Martins, M. Bessant, L. Manukyan, M. C. Milinkovitch, PloS one 10, e0126740 (2015).

(3 votes)

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