In my visual communication classes students increasingly want to learn how to make graphical abstracts. Below I summarized a few key points
What are Graphical abstracts?
Graphical abstracts are increasingly common to explain biomedical concepts and research results. “Summary slides” have been for long been used in talks or lectures. Today, graphical abstracts are omnipresent a thumbnail previews in online publications, and are also used in posters, on lab websites, and in research grant applications.
The key element of every graphical abstract are pictograms-like visualizations or icons. With text and arrows, the pictograms are then arranged into a sequential narrative or ‘story’. A consistent color scheme and clear layout help to orienting the audiences. Below are a few quick suggestions to help you design a graphical abstract quickly.
One main message
Before starting the design process, spend a good amount of time brainstorming the key message to get across. I personally do this by doodling on paper and discussing with peers. Without a clear main message, it will be impossible to design a good graphical abstract.
Pictograms as visual elements
Pictograms have long been used in science and in the early 20th century, Otto Neurath and Gerd Arntz started to systemically designed icons for communicating data to broad audiences. The past decade saw an explosion of new pictograms such as emoticons in social media.
A new resource for pictograms is fontawesome, a unicode-based icon library that can be installed locally as a font. The font can then be used in e.g. PowerPoint or Illustrator to directly “write” pictograms. Alternatively, pictograms can be accessed online and downloaded (svg, png). A larger collection is available at the Nounproject. Here, designers can upload icons for re-use with attribution. Scientific pictograms for free re-use are collected at the EBI reactome icon library. This site allows upload of user-designed pictograms for sharing with the scientific community.
In a graphical abstract, the pictograms used should have a similar overall appearance. Ensure that colors, line widths, and level of detail are comparable in all used icons. Best practice would be to use pictograms from one designer or one source only. And: start your own personal collection, chances are you might need them again!
All pictograms used have similar overall appearance (color, size, design)Bad combination of pictogram, all pictograms have different appearance
Layout: Dimensions
Layout describes the organization of visual elements on the page. First, consider the dimensions of your page: a graphical abstract for a journal website most often is square, while rectangle stretching across the entire page might be a better use of space for a graphical abstract in a grant application with limited word number.
Dimensions for Graphical Abstracts: square is often required by journals and works well online. Rectangle is easier for slides, posters etc. Adapt dimension when including Graphical Abstract in text.
Layout: Reading direction
The layout should provide a clear entry into the graphical abstract and a clear end. Typically, we read from left to right, and top to bottom. The visual elements should be arranged along the chosen reading direction.
For depiction of linear processes, which have a clear beginning and end, organization from left to right is most suitable: time is usually shown as the independent variable on the x-axis f graphs. Linea processes may be procedures, such as a methodical pipeline, or cellular events such as cell division, embryo development, or disease progression. For depiction of cyclic events, for example daily, annual or metabolic processes, consider a circular layout; for static events, e.g. contrasting two scenarios or providing two levels of details for one scenario, consider two parallel or nested organization.
Different layouts for Graphical Abstracts that have a clear start and end.
Arrows
Arrows (and lines) have several roles in graphical abstracts. First, arrows reinforce a reading direction that is already visually defined by a layout, or point out an exception from the reading direction. Second, arrows often indicate motion: a molecule passes a membrane, a cell migrates into a tissue, animals flock to food source. And third, arrows are used for labeling structures or regions of interest. Here, the arrow may be replaced by a simple line. Depending on the arrow head, the meaning can also change to showing an inhibition or forking etc.
It is important to clearly signal to the audience the intention of an arrow and, if two types of arrows are used in parallel, to contrast them visually. Note how changing the context of an arrow can also change its perceived meaning.
Different arrow types and arrow usage in Graphical Abstracts
Text
Understanding of complex scenarios is easiest when text and visual are used in synergy (Mayer RE 2002; Hegarty, 1993). First, text is used to substitute for pictograms where these are no available (e.g. specific molecules: ‘acetylcholine’). Second, text also serves to label pictograms that are otherwise ambiguous (e.g. a circle for ‘cell’, ‘bacteria’, ‘nucleus’), Third, text also enforces the meaning of an arrow: an upward arrow could indicate ‘move up’, ‘increase’ or ‘good’, or a circular arrow could be day, year or life cycle. Last, text often provides further explanations. Here it is critical that the it remains short and without jargon and sparse abbreviations.
Colors
As in all visualizations, colors are used in graphical abstracts to highlight and contrast, to encode numerical data, or to show the natural appearance of a visualized object. It is key to use colors consistently. A change in color is perceived as a change in meaning. Also use color sparsely as color always draws attention of the audiences, and might eclipse the key take home message of the graphical abstract.
For picking harmonious colors schemes use e.g. http://paletton.com. Colors schemes can be based on adjacent colors to appear harmonious or on complementary colors to contrast scenarios.
Color can highlight, encode numbers, or show natural appearance in Graphical Abstracts. Careful with color choice when using a background color!
Making of… Tools!
Graphical abstracts can, like a poster, be prepared with vector-design software (Illustrator, Inkjet, CorelDraw) or software for preparing slides (Powerpoint, Keynote). In both cases, pictograms can be included as images (png, tiff) or .svg files. https://biorender.com/ allows a web-based, drag-and-drop design of slides with a harmonious overall layout and biomedically relevant pictograms. For an annual fee, users can export graphical abstracts/figures in publication quality resolution.
Finish by…
Design is an iterative process of adjusting and assessing. A common problem in graphical abstracts is an unclear reading directions (Hullman and Bach): assess if your graphical abstract support a visual hierarchy with text, lines, and arrows. Often, elements are not connected to the rest of the graphical abstract, which forces readers to guess. Confusing also arises from inconsistent visual style: are your pictograms similar in detail? Do arrow with the same meaning have same appearance? Are colors used sparsely and consistently?
As always, source feedback from colleagues, ask them to tell you back what they see!
Tversky B. Lines, Blobs, Crosses and Arrows: Diagrammatic Communication with Schematic Figures. In: M. Anderson, P. Cheng, and V. Haarslev (Eds.): Diagrams 2000, LNAI 1889, pp. 221-230, 2000. Springer-Verlag Berlin Heidelberg.
Hullman J and Bach B. Picturing Science: Design Patterns in Graphical Abstracts. In: P. Chapman et al. (Eds.): Diagrams 2018, LNAI 10871, pp. 183–200, 2018. https://doi.org/10.1007/978-3-319-91376-6_19
Hegarty, M., Just, M.A.: Constructing mental models of machines from text and diagrams. J. Mem. Lang. 32, 717–742 (1993)
Myosin is a major component of the sarcomeres of muscle, but its roles during muscle development are still relatively poorly understood. A new paper in Development investigates the function of a developmentally expressed myosin heavy chain isoform during mice myogenesis. We caught up with the paper’s four co-first authors, Megha Agarwal, Akashi Sharma, Pankaj Kumar and Amit Kumar, and their supervisor Sam Mathew (Associate Professor in the Regional Centre for Biotechnology in Faridabad, India) to find out more about the project.
Sam, Megha, Pankaj, Akashi and Amit (L to R).
Sam, can you give us your scientific biography and the questions your lab is trying to answer?
I did my Bachelor’s and Master’s degree in Zoology in Kerala, India, and then got my first experience in research working as a research assistant for a year in Bangalore, in a lab that used Drosophila to study circadian rhythms. Soon after, in 2001, I joined the graduate program in Genetics and Functional Genomics at the University of Cologne, Germany. I joined Maria Leptin’s lab for my graduate work, trying to characterize a genomic region involved in gastrulation in Drosophila. Maria’s mentorship style of giving students a free hand helped me develop ideas and grow as a scientist. I got interested in understanding developmental processes using genetic tools and, although it took a while, this work led to the identification of the role of the TNF-Receptor Associated Factor 4 (TRAF4) in Drosophila gastrulation. I continued with Maria for 2 years as a postdoctoral fellow to complete this work and then wanted to switch to a vertebrate model. Thus, I joined Gabrielle Kardon at the University of Utah, USA, where she was using mouse models to understand the role of connective tissue fibroblasts in skeletal muscle development and regeneration. Using mouse genetics, we showed that Tcf4 is a marker of connective tissue fibroblasts and that Tcf4+ connective tissue fibroblasts are important regulators of muscle development and differentiation, especially regulating maturation of muscle fibre type. This is where I came across myosin heavy chain-embryonic (MyHC-emb), which we used as a marker for developing myofibres. Delving into the literature, I found that not much was known about MyHC-emb function even though it was used routinely as a marker for terminally differentiated myofibres during development and for regenerating fibres in adults. This led to discussions with Gabrielle, who was generous enough to allow me to start generating a targeted mouse model, which is an important tool used in the current work.
We are pursuing three main research directions in my lab: first, we are trying to understand the specific functions of developmental myosin heavy chains (MyHCs) and how mutations in these MyHCs lead to congenital diseases. Second, we are interested in how skeletal muscle differentiation occurs during development and stem cell-mediated regeneration, and are trying to identify genes and regulatory sequences involved in this. Third, we are working on signalling pathways that are misregulated and lead to the formation of a cancer type called rhabdomyosarcoma, in which the tumour cells exhibit muscle-cell characteristics. We use Drosophila, mouse and cell culture models, and employ imaging, biochemical methods and genetic tools to address all of these questions.
How did the four of you come to work in Sam’s lab, and what questions drive your research?
MA I was very clear that I wanted to work on stem cells for my PhD. I had already worked on mesenchymal stem cells during my Master’s degree project and was fascinated by how smart these cells are. How stem cells serve as a maintenance and repair resource for the entire body is something that has interested me all along. After checking out a few labs, I decided to join Sam’s since it provided me with a great opportunity to study stem cells and their behaviour during animal development and adult tissue regeneration. Since this research topic is something close to my heart, it has been easy to keep myself motivated.
AS I joined as a project fellow in Sam’s lab in 2014 and within 4 months I started my PhD with him! From my college days, I was interested in the processes of embryonic development that make an entire organism from a single cell. While working with Sam as a project fellow, I got an opportunity to develop a deeper understanding of the developmental processes that lead to muscle formation. Different muscles in our body have distinct muscle fibre type composition; however, all fibres express MyHC-emb during embryonic development. I was intrigued and wanted to explore more about this MyHC isoform and decipher the functional importance of MyHC-emb.
PK Before joining Sam’s lab, I briefly worked on Leishmania, a parasitic protozoan that causes kala-azar (visceral leishmaniasis) in humans. I discovered how intriguing animal development is while preparing for my PhD fellowship exams. Therefore, I scouted around for labs working on animal development and joined Sam when he was in the early phase of setting up his lab at RCB. My research is driven by a quest to understand the complexities underlying gene regulation during animal development and tissue regeneration.
Cross-sections through the shank of postnatal day 0 wild-type (right) and Myh3 knockout (left) mice, showing MyHC-slow (red), laminin (green) and DAPI (blue).
AK I joined Sam’s lab with a deep interest in studying development, as it has always fascinated me. I worked extensively on fetal tissues during my doctoral training. Sam explained some of the observations he made on the myosins and how human muscle defects are recapitulated in myosin heavy chain knockout mouse models. This was exciting and I was keen to understand the role of myosins during development and regeneration.
How much was known about the role of the developmental MyHCs before your work?
MA, AS, PK, AK & SM Developmental MyHCs were discovered in the 1980s and although they were found to be expressed during development and regeneration, not much has been known about their function since then. A few studies on the regulation of their expression were carried out during the 1990s and early 2000s. Then in 2006, Michael Bamshad’s lab identified that mutations in the MYH3 gene, which codes for MyHC-emb, lead to Freeman–Sheldon and Sheldon–Hall congenital contracture syndromes, indicating that developmental MyHCs – and MyHC-emb specifically – have important functions. Surprisingly, animal models for studying and understanding the mechanisms underlying these syndromes were not pursued or were unsuccessful. This was in contrast to adult MyHCs, for which knockout mice for two isoforms were generated and characterized successfully in the 1990s by Leslie Leinwand’s lab. This provided us an opportunity to explore the roles played by developmental MHCs.
Can you give us the key results of the paper in a paragraph?
MA, AS, PK, AK & SM In this paper, we describe the role of MyHC-emb in skeletal muscle development. By generating and making use of conditional targeted and null mouse alleles for Myh3, we characterize the role of MyHC-emb during embryonic, fetal and neonatal myogenesis. There are four key findings that we describe in this paper. First, we find that MyHC-emb has dual cell-autonomous and non-cell-autonomous roles during muscle development. MyHC-emb is expressed in myofibres, and in a cell-autonomous manner regulates muscle fibre type, fibre number and fibre size. In a non-cell-autonomous manner it regulates the rate of differentiation of myogenic progenitors and myoblasts during embryonic and fetal myogenesis (cells in which it is not expressed). Second, we identify fibroblast growthfactor (FGF) as the secreted signal from myofibres that mediates the non-cell-autonomous effects of MyHC-emb on muscle progenitors and myoblasts. Third, we find that, although MyHC-emb is expressed in all myofibres during development, different muscles respond differently to MyHC-emb loss. Fourth, adult mice null for Myh3 exhibit scoliosis, a phenotype seen in individuals with Freeman–Sheldon Syndrome, a congenital muscle contracture syndrome in which MYH3 is mutated. Thus, this work highlights the role of developmental MyHCs during development and how their loss of function leads to abnormalities.
Why do you think MyHC-emb has distinct effects in different muscle types?
MA, AS, PK, AK & SM This was a surprising finding since, to our knowledge, MyHC-emb is expressed by all myofibres during development. We believe that the distinct effects loss of MyHC-emb has on different muscles is down to unique fibre-type composition and metabolic characteristics, which in turn are determined by the anatomical location and functional needs of the specific muscle. We think that these differences between muscles are reflected in the distinct effects we observe upon loss of MyHC-emb.
How do you think an intracellular component of the sarcomere could act non-autonomously?
MA, AS, PK, AK & SM This was a puzzle for us until we came across some publications showing that the FGF pathway mediates differentiation and maintenance of the stem cell pool. FGFR4, a receptor in the FGF pathway, is important in regulating the rate of differentiation of myogenic progenitors and myoblasts during development, which are the cell populations that were affected upon loss of MyHC-emb. This led to additional experiments to test whether FGF signalling mediates the non-cell-autonomous effects of MyHC-emb on myogenic progenitors and myoblasts, which was indeed found to be the case. How MyHC-emb within myofibres controls the levels of FGF secreted by myofibres is a question we have been trying to find answers for, but have not been successful. This could hint at some novel function of MyHC-emb, which might be independent of its role in the sarcomere. Interestingly, Leslie Leinwand’s lab reported in 2003 that MyHC-emb is one of three MyHCs that are expressed in non-myogenic cell types such as pulmonary myofibroblasts, indicating that MyHCs may have functions that are not restricted to skeletal muscle cells.
When doing the research, did you have any particular result or eureka moment that has stuck with you?
MA While deciphering the non-cell-autonomous effect of MyHC-emb on muscle progenitors, we hypothesized that it is mediated by FGFs. My eureka moment was when I successfully figured out, by mass spectrometric analysis, that secreted FGF levels are altered upon knockdown of MyHC-emb. This led us to the mechanism of how MyHC-emb regulates muscle differentiation non-cell-autonomously, confirming and validating our hypothesis.
AS One of our first in vivo experiments was to investigate the effect of loss of MyHC-emb on other MyHC isoforms. I was full of curiosity while performing the immunostaining for other MyHCs on Myh3 knockout samples. I think finding more MyHC-slow+ fibres in Myh3 knockout muscles was a result I can never forget.
PK Two moments actually, both related to when I was quantifying data: first when I found that the muscle progenitor numbers reduced significantly upon Myh3 knockout, and second when FGF supplementation led to a rescue of the progenitor numbers in vitro.
AK To me, corroborating the in vivo results from the Myh3 knockout mice using C2C12 myogenic cells in vitro was highly satisfying. The in vitro system proved really handy for the demonstration of the non-cell-autonomous effect of MyHC-emb.
And what about the flipside: any moments of frustration or despair?
MA I started working on this project about 5 years ago and there were several instances when I got frustrated. For a while, we had difficulty in explaining the MyHC-emb loss-of-function phenotype, especially the mechanism of how MyHC-emb regulates muscle stem cells. Although we followed several directions, most were unsuccessful until we came upon FGF signalling. I think many of these failed experiments formed the basis of this manuscript and I kept going because, as Steve Jobs said, I considered what I do to be great work!
AS Not really a specific moment, but in the early days of the project, we did not have an animal facility on campus and were reliant on the samples brought by Sam from the laboratory of our collaborator, Gabrielle Kardon, at the University of Utah. This meant that every sample was precious and there were times when I had to wait for several months to get samples for new experiments, which was frustrating.
PK I faced some frustrating moments with the muscle-fibre size quantification. This was mainly related to finding a reliable software application that would make these measurements accurately. These problems went away after we came across a software application called SMASH, which was developed precisely for muscle fibre measurements.
AK I remember that one of the challenging moments early on was to draw an understanding of the sequence of events affecting normal myogenesis in the absence of MyHC-emb, and to identify the mechanisms underlying them. This led to testing a lot of possibilities without success, which for a while was frustrating.
So what next for the four of you after this paper?
MA This PhD training with all its ups and downs has helped me decide that research is what I want to do. Although there might be difficulties in research, with constant effort one can definitely achieve good results. I am keen to switch fields and am on the lookout for a postdoctoral position in computational modelling and bioinformatics.
AS I am currently working on other projects and plan to complete my PhD soon. In addition to skeletal muscle, I am also interested in the cardiac and smooth muscle. I would like to pursue postdoctoral research in the development of any or all of these three muscles.
PK I am also working on another project in the lab, related to the regulation of myogenesis. I am trying to complete this work and will be looking for postdoctoral opportunities in developmental biology, with translational relevance.
AK I left the lab in 2016, when this paper had started to take shape. I am now a postdoctoral fellow at the University of California Los Angeles, working on haematopoietic stem cells and cancer from a gene regulation perspective.
Where will this work take the Mathew lab?
SM This work originated when I was working as a postdoctoral fellow and I remember starting work on the gene-targeting construct almost 10 years ago! There have been a few milestones along the way, such as successfully identifying the gene-targeted mice, initial characterization of the knockout mice, moving to India and becoming an independent investigator, getting the mice shipped to India and now getting the work published. Although it took a while to get this paper out, we should now be able to come out with more interesting results, especially with respect to MyHC-emb in muscle regeneration. We are also keen to understand the precise mechanisms that underlie the phenotypes seen in individuals with Freeman–Sheldon Syndrome. I think skeletal muscle development, regeneration and homeostasis are all research areas with immense translational significance and hope to continue making new discoveries in these fields.
Am I right in thinking there is an increasing amount of developmental biology going on in India at the moment? As someone who left India for your PhD and postdoc but then returned to set up your own lab, what has your experience been like?
SM Yes, I think it is true. Actually, there are a lot of relatively young investigators, working in diverse areas, who set up their labs in the past 10-15 years. In my opinion, this resulted from several new research institutes being set up and an increase in funding over this period. Coming back to developmental biology in India, we have a set of diverse researchers working on different model systems, who are doing well. We also have an Indian Society for Developmental Biology with an ever-increasing number of members.
Returning to India was a decision I made after being abroad for more than 12 years. Although it took some getting used to, it is a decision I am quite happy with. Since I joined a relatively new research institute, some amount of time was spent initially on ordering equipment and getting facilities up and running. Some of the flexible funding I received, especially from the Wellcome Trust DBT India Alliance, really helped run the project during the initial days, when I had to travel to Gabrielle’s lab to carry out the mouse work. I have been lucky to work with some really smart, talented and dedicated graduate students and postdoctoral fellows, and mentoring them has been a lot of fun.
There are many labs working on developmental biology today in India
Finally, let’s move outside the lab – what do you like to do in your spare time in Faridabad?
MA When I have free time, I like to work out in the gym. I also like to go out shopping with friends.
AS Our campus in Faridabad is a really beautiful place, and I like to spend my leisure time enjoying the beauty of nature around me, while reading books.
PK I like playing badminton, going out with friends and especially visiting my cousins to enjoy home-cooked food!
AK I remember how we used to go out together with the lab for lunch, and also remember a trip to the Himalayan mountains for hiking and fun. Currently, I am in Los Angeles, where I like to try out different cuisines and go on long drives over weekends.
SM I like spending time with family and friends in my spare time. I also like to travel; Faridabad is close to a lot of places with historical significance, which I try to visit.
The Biology Department of Boston College seeks to recruit a tenure-track faculty member with research and teaching interests in the area of Cell & Developmental Biology.
The ideal candidate is expected to establish a rigorous, externally funded research program that contributes to, or complements, current strengths in using in vivo model systems to answer fundamental questions in cell and developmental biology. The successful candidate will receive a highly competitive startup package including research and equipment funds and laboratory space, IT/computational support, grant preparation and management assistance, and access to shared resources and state-of-the-art core facilities including imaging/microscopy (including super-resolution microscopy), NexGen sequencing, flow-cytometry/FACS, NMR, and mass-spectrometry. Finally, all new faculty members receive active and dedicated mentoring to help ensure success at Boston College.
In alignment with the University’s goal of building a culturally diverse, equitable and inclusive academic community, we are seeking individuals who are committed to the advancement of historically underrepresented and marginalized communities in the sciences. In addition, the successful candidate must have a strong record of research productivity, and a desire to teach, advise and mentor graduate students and undergraduate students in the biosciences.
The Biology Department is home to a dynamic research community embedded in a highly ranked, liberal arts university campus located close to downtown Boston and Cambridge. The surrounding region constitutes a global research hub, comprising numerous universities, research institutes, biotechnology firms and pharmaceutical companies. The Biology Department hosts a graduate program in the biosciences; provides lecture and laboratory courses and research opportunities for undergraduates majoring in biology and biochemistry; and actively participates in the Gateway Scholar’s Program for underserved minorities and first-generation college students majoring in STEM fields at Boston College. Faculty and their research teams also have access to new facilities and interdisciplinary collaborations provided by The Schiller Institute for Integrated Science and Society.
Application Instructions
Candidates starting at any rank (Assistant Professor, Associate Professor, Professor) may apply. Applications must include a cover letter, a three-page statement of research accomplishments and goals, and a statement of teaching and mentoring philosophy (2-3 pages). Applicants at the Assistant Professor level should also provide contact information for three (3) references. All applications received by December 1, 2020 will be given full consideration.
The Edmond and Lily Safra Center for Brain Sciences (ELSC) builds upon Hebrew University‘s record of excellence and innovation in its multidisciplinary approach to brain sciences.
ELSC invites applications for postdoctoral fellows in the following fields: theoretical and computational neuroscience, systems neuroscience, molecular and cellular mechanisms, cognitive neuroscience, and neuronal circuits. Postdoctoral fellows receive a competitive stipend for a period of up to two years.
WE OFFER:
State-of-the-art laboratories
Distinguished faculty
Generous Postdoctoral scholarships
Enriched academic milieu
Established ties and frequent collaborations with world renowned labs
Opportunities to audit advanced courses
Rich student and postdoctoral environments
Postdoctoral support staff
Eligibility:
The candidate must be (or have been) a student in an accredited institution of higher education and whose PhD training and post-doctoral projects are in the field of Brain Sciences.
The candidate’s doctoral degree has been submitted in the current year of applying or will be approved by the following year.
Candidates Commitments:
A recipient of an ELSC Fellowship must commence his/her post doctoral training no later than 5 years after completion of the PhD.
A recipient of an ELSC Fellowship must provide written approval from the authority of PhD students in his/her institute, confirming that his/her PhD has been submitted before they begin their post-doctoral training. If PhD was not yet awarded, the candidate must provide approval of a PhD during the first academic year of the post doctoral studies
A letter from the host is mandatory in order to commence the post doctoral studies
A recipient of an ELSC Fellowship must begin the postdoc training within 6 months after receiving the acceptance letter
Terms of Fellowship:
The fellowship can be extended up to 2 years, given availability of funds and the scientific achievements of the candidate. ELSC is not committed to prolong the fellowship in advance.
Preference will be given to students who completed their PhD abroad
In this episode we bring you an in-depth interview with Dr Eric Green, director of the US National Human Genome Research Institute and one of the key instigators of the Human Genome Project, to talk about the past, present and future of human genomics.
Thirty years ago this month saw the birth of one of the most audacious research programmes in biology: The Human Genome Project, an ambitious plan to read the DNA sequence of the entire human genome. Ten years later, in June 2000 – after billions of dollars, countless hours of DNA sequencing, and a huge amount of effort from an international collaboration from 20 institutions in six countries – the first draft of the Human Genome was unveiled.
Dr Eric Green has seen the Human Genome Project through from its inception through to the published sequence and into what’s now the fully-fledged field of human genomics. Today, he’s the director of the US National Human Genome Research Institute, and a leading light in the world of genes, genomes and genome sequencing. I called him up to chat about the past, present and future of the human genome – starting by going all the way back to the beginning of the Human Genome Project.
Mustafa Güven gives a student’s perspective on Development’s recent virtual meeting: From Stem Cells to Human Development. Below the piece you’ll also find Mustafa’s Turkish translation of the report. For a ‘behind the scenes’ look at the meeting, go here.
As a fourth-year medical student from Van, Turkey, I have witnessed birth and death on the same day. It is interesting how the two most certain things in human life bring the most joy and sadness. But between birth and death, these two inevitable events, change and development never stop.
I am fascinated by how development can occur without any problems, where even minor troubles can be fatal. And here we are, alive and full of passion to understand development and the “troubles” better.
The meeting poster
Embryology was by far my favorite lesson in my years studying basic medicine. I would always sit in the front of class and listen to the lectures as if I was enchanted. I continued to learn more about development in the following years, and so it was a wonderful opportunity to attend the virtual “From Stem Cell to Human Development” meeting, hosted by the journal Development on 8-11 September. I wasn’t sure if my knowledge was sufficient to benefit from this meeting but I wanted to take my chances. Also, I was very nervous before the meeting because I had not attended a meeting where many great scientists that I read works of would be close enough to say ‘hi’ to, at least virtually. Thanks to the interactive environment of the platform used, I wasn’t nervous after the first day.
The Remo software used for the meeting
Although online conferences might not be as efficient as regular ones, I think they offer important opportunities. In normal times, I would not have been able to attend this congress, mainly because of economic reasons and also because of my studies. I also think that online meetings will become part of every conference, and the quality of them will improve over time. The platform used in this conference, called Remo, was already good quality. There were different floors and tables for different purposes as if it was a real conference building. Two floors were for poster sessions but unfortunately, I could only check out two posters. I have had time to explore more after the meeting finished. The only negative thing I can say is that, although I don’t know why, I had a little difficulty concentrating on pre-recorded talks. I wonder if this is something other people experience?
In each of the sessions I was like “wow, cool!”, but I still would like to highlight some of the talks that really stuck with me.
The meeting started with Wieland Huttner (Max Planck Institute of Molecular Cell Biology and Genetics, Germany) explaining his lab’s research on how the size of the brain, especially the neocortex, increased during evolution. They investigated the effects of the ARHGAP11B gene on basal progenitor cells, which are the driving force in neuronal proliferation, and conducted further experiments on marmosets and human cerebral organoids. The results were exciting: ARHGAP11B is necessary for neuronal proliferation and folding of the neocortex, and exerts its effects through metabolic pathways. I’m looking forward to see the possible clinical applications. I was also amazed by the lab’s extensive collaborations.
This conference was exciting in many ways. Listening to the pioneering scientists developing new methods was one of them. It is exciting because thanks to new methods, I hope we will see rapid developments in treatment in the near future. Samira Musah (Duke University, USA) was one of these researchers. She is working on a relatively little studied but nonetheless vitally important organ: the kidney. After giving shocking statistics about chronic kidney disease, she talked about her group’s research interests and the field’s current limitations. One of the main limitations to study kidney diseases is the lack of physiologically relevant models. Using induced pluripotent stem cells, her lab managed to establish iPSs derived-podocytes (special cells that play crucial roles in filtration). Another important topic they are working on is a currently popular one: the kidney tropism of COVID-19. I hope to read their papers on the subject soon.
Because of my background, I was more interested in the talks related to current clinical applications, which in turn I was able to understand more. In this regard, James Wells (Cincinnati Children’s Hospital, USA) gave a particularly interesting talk. His lab’s discoveries about endocrine cell development in the gastrointestinal tract were remarkable. He showed that the deletion of neurogenin-3 culminates in the loss of enteroendocrine cells of the pancreas and intestines. This loss can cause diabetes and malabsorption. What I found interesting is that they can induce neurogenin-3 and restore the function of these cells. They also discovered the roles of a peptide, PYY, using neurogenin-3 deficient organoids in enteroendocrine cell functions. He talked about how additional PYY can improve malabsorption parameters in mice. These results are very promising for severe malabsorption patients because they require parenteral nutrition for the rest of their lives.
Being able to re-watch the talks was very beneficial, as I could revise the parts that I didn’t understand at first. Also, I couldn’t attend each live session, so I could catch up later. After listening to the talks for the second time, I see that my knowledge wasn’t completely sufficient after all, but I am glad that I pushed myself. I had a chance to get to know amazing scientists and listen to the cutting edge of developmental biology. These all made me look at the future with more hope and enthusiasm, and I hope I can find a chance to attend this meeting again, but this time in person.
Bir Öğrencinin Bakış Açısından: From Stem Cells to Human Development (PDF)
Dördüncü sınıf tıp öğrencisi olarak aynı gün içerisinde doğuma ve ölüme şahit oldum. İnsan hayatında gerçekleşmesi en kesin bu iki olayın en çok neşe ve üzüntüyü getirmesi ilginçtir. Bu iki kaçınılmaz olay arasında değişim ve gelişim ise asla durmaz.
Bir insanın dünyaya gelme sürecinde küçük sorunların bile ölümle sonuçlanabilirken gelişimin sorunsuz bir şekilde tamamlanması beni şaşırtıyor. Biz ise işte burada, hayatta ve insan gelişimini ve “sorunları” daha iyi anlamak için tutkuyla dolu haldeyiz.
Embriyoloji, temel tıp yıllarında açık ara en sevdiğim ders oldu. Sınıfta her zaman en önde oturur ve büyülenmiş bir şekilde dersleri dinlerdim. İlerleyen yıllarda gelişimsel biyoloji hakkında daha çok şey öğrenmeye devam ettim ve 8-11 Eylül tarihlerinde Development Dergisi’nin ev sahipliğinde sanal olarak düzenlenen “From Stem Cells to Human Development” toplantısına katılma gibi harika bir şansım oldu. Bilgilerimin bu toplantıdan yararlanmaya yeterli olup olmadığından emin değildim ama her ne olursa olsun şansımı denemek istedim. Aynı zamanda, toplantıdan önce çok gergindim çünkü makalelerini okuduğum birçok büyük bilim insanının sanal olarak da olsa ‘merhaba’ diyecek kadar yakın olacağı bir toplantıya katılmamıştım. Kullanılan platformun interaktif ortamı sayesinde ilk günden sonra bu gerginlik geçmişti.
Çevrimiçi konferanslar her ne kadar normal konferanslar kadar verimli olmasa da önemli fırsatlar sunduklarını düşünüyorum. Normal zamanlarda bu kongreye hem ekonomik nedenlerden hem de ders dönemim başladığından dolayı katılamazdım. İlerleyen dönemlerde çevrimiçi toplantıların her konferansın bir parçası olacağını ve zamanla kalitesinin artacağını düşünüyorum. Bu konferansta kullanılan Remo adlı platform ise şimdiden çok güzeldi. Sanki gerçek bir konferans binasıymış gibi çeşitli amaçlar için farklı katlar ve masalar vardı. Poster sunumları için de iki kat ayrılmıştı ama maalesef sadece iki poster sunumunu canlı olarak dinleyebildim. Posterleri daha fazla keşfetmek için toplantı bittikten sonra zamanım oldu. Nedenini tam olarak bilmesem de önceden kaydedilmiş konuşmalara konsantre olmakta biraz güçlük çekmem online konferansla ilgili söyleyebileceğim tek olumsuz şey olabilir.
Her konuşmada kendi kendime “vay, çok havalı” dedim ancak bazı konuşmaları ayrıca vurgulamak ve sanal deneyimimi daha detaylı paylaşmak istiyorum.
İlk gün, Wieland Huttner’ın evrim sırasında beynin, özellikle de neokorteksin, boyutunun nasıl arttığına dair laboratuvarlarında yaptıkları araştırmalarını anlatmasıyla başladı. Nöronal proliferasyonda itici güç olan bazal progenitör hücrelerinde ARHGAP11B geninin etkilerini araştırdıklarını, ileri çalışmalar için bir maymun türü olan marmosetler ve insan beyin organoidleri üzerinde ileri deneyler yaptıklarını anlattı. Sonuçlar çok heyecan vericiydi: ARHGAP11B’nin, neokortekste sinir hücrelerinin artması ve neokorteksin katlanması için gerekli olduğunu ve metabolik yolaklar üzerinden etki ettiğini göstermişler. Olası klinik uygulamaları görmek için sabırsızlanıyorum. Laboratuvarlarının dünyanın dört bir yanıyla yaptıkları ortak çalışmalarına da hayran kaldım.
Bu konferans birçok yönden heyecan vericiydi. Yeni yöntemler geliştiren öncü bilim insanlarını dinlemek kesinlikle bunlardan biriydi. Heyecan verici çünkü geliştirilen yeni “yöntemler” sayesinde yakın gelecekte kliniğe yansıyacak hızlı gelişmeler göreceğimizi umuyorum.
Samira Musah da bu araştırmacılardan biriydi. Nispeten az çalışılmış ama yine de hayati önemi olan bir organ üzerinde çalışıyorlar: böbrek. Konuşmasında kronik böbrek hastalığı hakkında şok edici istatistikler verdikten sonra, grubunun araştırma ilgi alanlarından ve alanın mevcut sınırlamalarından bahsetti. Böbrek hastalıkları üzerine çalışmanın ana sınırlamalarından biri fizyolojik şartlara uygun çalışma modellerin olmamasıymış. Laboratuvarında, indüklenmiş pluripotent kök hücreleri (İPSC) kullanarak, podositleri (filtrasyonda önemli rol oynayan özel hücreler) oluşturmayı başardıklarını anlattı. Üzerinde çalıştıkları bir diğer önemli konu ise şu anda popüler olan bir konu: COVID-19’un böbrek tropizmi. Yakın zamanda çalışmalarını okumayı umuyorum.
Güncel klinik pratiklerini değiştirme potansiyeli olan konuşmalar hem tıp arka planımdan hem de bu konuşmaları daha iyi anlayabildiğimden dolayı daha çok ilgimi çekti. Bu bakımdan James Wells’in konuşması özellikle ilginçti. Laboratuvarının gastrointestinal sistemdeki endokrin hücre gelişimi hakkındaki keşifleri dikkat çekiciydi. Neurogenin-3 gen delesyonunun pankreas ve bağırsaklardaki enteroendokrin hücrelerinin kaybıyla sonuçlandığını göstermişler. Bu hücrelerin kaybı şeker hastalığına ve emilim bozukluklarına neden olabilmekte. Neurogenin-3’ü indükleyebilmeleri ve bu hücrelerin işlevini geri kazanabilmelerini göstermeleri en çok heyecan verici kısmıydı. Ayrıca enteroendokrin hücre fonksiyonlarında neurogenin-3 geninden yoksun organoidleri kullanarak bir peptit olan PYY’nin rollerini keşfetmişler. PYY’nin farelere dışardan verilerek malabsorpsiyonla, emilim bozukluğu, ilgili değerleri nasıl iyileştirebildiğinden bahsetti. Bu sonuçlar, ağır emilim bozukluğu olan hastalar için çok umut verici; çünkü hayatları boyunca damar yoluyla beslenmeye ihtiyaç duymaktalar.
Konuşmaların kaydedilmesi de büyük kolaylık sağladı. İlk dinlediğimde anlamadığım kısımların üzerinden geçebildiğim için sunumları tekrar izleyebilmek faydalı oldu. Bir de her canlı oturuma katılamadığım için kaçırdığım konuşmaları daha sonra dinleyebildim. Konuşmaları ikinci kez dinledikten sonra bilgimin tamamen yeterli olmadığını gördüm ancak kendimi zorladığım için mutluyum. Harika bilim insanlarını tanıma ve gelişimsel biyolojinin öncü çalışmalarını dinleme şansım oldu. Bunların hepsi geleceğe daha fazla umut ve şevkle bakmamı sağladı. Umarım bu toplantıya tekrar katılma, lakin bu sefer yüz yüze, şansı bulabilirim.
Recruiting 16 motivated students from around the world to join a fully-funded four year PhD programme in an international scientific environment at the Novo Nordisk Foundation Research Centers. Positions starting September 2021. Applicants of all nationalities may be awarded funding, provided they fulfill all of the eligibility criteria.
Programme Outline
The four-year programme is divided into a pre-doctoral year followed by three years of PhD training at one of the four Novo Nordisk Foundation Research Centers based at the University of Copenhagen or the Technical University of Denmark:
The pre-doctoral year includes short rotation projects, choice of a lab for the long-term (PhD) project, and common research-based courses. Approximately 15% of time during the pre-doctoral year is spent on courses, and the rest of the time on research. Awardees must pass an assessment at the end of the pre-doctoral year to qualify for the following three years of PhD education.
Supervisors and Research Areas
Applicants pre-select one of the four Novo Nordisk Foundation Research Centers in their application. Each Center conducts research in several connected research areas in biotechnology or biomedicine. CBMR investigates how the interaction between genes and environment affects human metabolism, CFB promotes a sustainable biobased chemical industry using specifically designed cell cultures (cell factories) to produce chemicals and pharmaceuticals, CPR works on integrative protein technologies, and DanStem investigates stem cell differentiation and the role of cancer stem cells in different types of cancer. See the programme website, application webpage, and Center websites (links above) for more information.
Potential supervisors and projects are listed on the programme website: Potential Supervisors
The research project will consist of studying how cells become different from one another, forming spatial patterns of different cell types in plant tissues such as the leaf epidermis and the shoot meristem. This will involve time-lapse microscopy, quantitative image analysis and mathematical modelling. This position is initially for 3 years and can start from January 2021, although the start date is flexible.
We are seeking a highly motivated candidate that is willing to combine computational and experimental work in plants. The ideal candidate would have a PhD in Quantitative Biology, Systems Biology, Biophysics or a related field. Applicants coming from Physics, Maths, Computer Science, Engineering background or related fields are also very welcome to apply. The applicant should have expertise in, at least, one of the following topics: quantitative image analysis, quantitative time-lapse microscopy and/or mathematical modelling. Some experience in programming is expected.
Application Deadline: November 18th 2020.
See the full advert and application instructions in the following link .
Meyer HM, Teles J, Formosa-Jordan P et al. (2017) Fluctuations of the transcription factor ATML1 generate the pattern of giant cells in the Arabidopsis sepal. Elife. 6, 1–41.
Formosa-Jordan P, Teles J and Jönsson H (2018) Single-cell approaches for understanding morphogenesis using Computational Morphodynamics, in Mathematical Modelling in Plant Biology, Morris R (eds) (Springer, Cham).
Torii KU (2012) Two-dimensional spatial patterning in developmental systems. Trends Cell Biol 22(8): 438–446.
The wings of vertebrates, like birds and bats, emerged relatively recently, and we understand that these wings evolved from forelimbs. Even for the mythological dragon there seems to be a consensus (at least in recent depictions) that their wings are also derived from their forelimbs. Insects, however, possess both wings AND limbs on their winged segments, suggesting that their wings are not evolved from modified limbs, which begs the question “where did insect wings come from?” Despite their status as the first animals to take to the skies, the answer to this question has remained poorly understood and under debate for over 200 years1,2. This debate has culminated in two leading hypotheses on the origin of insect wings, each linked to different origin tissues: a lateral outgrowth of the dorsal body wall (tergum) and ancestral proximal leg structures (pleuron in insects)2.
Historically, scientists have attempted to dissect the evolutionary origin of insect wings through identifying structures related to wings in non-winged segments of insects (wing serial homologs) and other wingless arthropods (wing homologs)3. The idea behind this approach is that the wing homologs in other segments have been modified to differing degrees, suggesting that wing homologs from wingless segments might provide us with a series of “snapshot” views into the evolution of wings and help us reconstruct how this complex structure came to be. Until relatively recently, attempts to identify wing-related structures in non-winged segments relied on these structures sharing morphological similarity with wings (i.e. looking like wings), which understandably limited the identification of wing homologs. Recently, with the application of molecular evolutionary and developmental biology (evo-devo) approaches, the diversity of the tissues identified as wing homologs has increased3. Some of these studies have even provided evidence that insect wings are not derived from either tergum or pleuron (ancestral proximal leg), but potentially from a combination of these two tissues (i.e. they have a dual origin)4–9.
In our recent paper, we applied this molecular evo-devo approach to the identification of wing-related structures in a crustacean10. The reasoning behind looking for “wings” in a crustacean is that crustaceans and insects share a common ancestor. Therefore, by identifying the potential wing homologs of a crustacean and comparing them to the wing serial homologs of insects, we can gain a better understanding of what tissues were present in the common ancestor of these groups that had the potential to become wings in insects. Parhyale hawaiensis, the crustacean we chose for our study (Fig 1), provided a great “model” crustacean for our investigation because their dorso-ventral body plan is very similar to that of insects, which makes comparisons between the two much simpler.
Fig 1. The crustacean Parhyale hawaiensis.
We started our search for wing homologs in Parhyale by identifying structures that are dependent on the gene vestigial (vg). vg is a critical wing gene in insects and has often been used for the molecular identification of wing homologs. We looked at expression and function of vg in Parhyale and noticed something striking. First, vg is expressed in both the tergal edge and the proximal leg segments. Second, when we knocked-out the function of vg via CRISPR/Cas9 genome editing, we saw that the development of BOTH of these tissues (tergum and proximal leg, related to insect pleuron11) was disrupted (Fig 2). We expanded our expression and function analyses to two more insect wing genes, nubbin (nub) and apterous (ap) and saw a similar outcome – these genes are expressed and/or function in both tergum and proximal leg segments (Fig 2). We were curious how big the overlap was between genes that function in wing development (wing gene network, WGN) and genes that function in tergum and proximal leg development of crustaceans, so we investigated the expression of a few additional wing genes in Parhyale. Many of these genes were also expressed in the tergum and proximal leg of Parhyale, and one of these genes, optomotor-blind (omb), showed impressive expression pattern overlap with the functional and expression domains of vg, nub, and ap (Fig 2).
Fig 2. The functional domains of vg, nub, and ap and expression domain of omb in Parhyale. Abbreviations are as follows: te, tergum; co, coxa; cp, coxal plate; gi, gill; ba, basis.
Through these investigations, we were able to show that a gene network similar to the WGN operates in both the tergal edge and proximal leg of Parhyale, suggesting that the evolution of this network precedes the emergence of insect wings. It also seems that both of these structures qualify as candidates for wing homologs of a crustacean. When we compare these structures to those that have been identified as wing serial homologs in the wingless segments of insects, we see a striking similarity; two separate tissues dependent on wing genes, one of tergal and one of pleural/proximal leg-related identity (Fig 3). The similarity between the wing-related structures in insects and crustaceans appears to point to a dual evolutionary origin of the insect wing and suggests that insect wings evolved through the merger of two previously distinct structures.
Fig 3. The evolutionary relationship among wing homologs. Blue and yellow represent tergal and pleural wing homologs respectively.
An aside about terminology: Historically, tissues related to wings on non-winged segments (either in insects or crustaceans) have been referred to as “wing homologs”. We are starting to see that this terminology is problematic especially when you consider the evolutionary order of the emergence of these structures. It seems that the “ancestral state” for wings is really two separate, previously existing structures in the form of tergum and pleuron (or ancestral proximal leg segments). Only in the winged segments of insects do these two previously separate structures seemingly merge to form the wing (Fig 3). Therefore, more accurate terminology for the wing-related structures on non-winged segments might instead be “tergal serial homologs” or “pleural serial homologs” as this is more representative of the ancestral state for these tissues. After all, it is becoming increasingly apparent with recent studies that these “tergal” and “pleural” serial homologs provide an “evolutionary hotspot” for the development of morphological novelties including, but not limited to, beetle thoracic horns, tree hopper helmets, beetle abdominal gin traps, and wings12.
References:
Grimaldi, D. & Engels, M. S. Insects take to the skies. in Evolution of the Insects 155–187 (Cambridge University Press, 2005).
Clark-Hachtel, C. M. & Tomoyasu, Y. Exploring the origin of insect wings from an evo-devo perspective. Curr. Opin. Insect Sci.13, 77–85 (2016).
Tomoyasu, Y., Ohde, T. & Clark-Hachtel, C. M. What serial homologs can tell us about the origin of insect wings. F1000Research6, 268 (2017).
Clark-Hachtel, C. M., Linz, D. M. & Tomoyasu, Y. Insights into insect wing origin provided by functional analysis of vestigial in the red flour beetle, Tribolium castaneum. Proc. Natl. Acad. Sci. U. S. A.110, 16951–16956 (2013).
Medved, V. et al. Origin and diversification of wings: Insights from a neopteran insect. Proc. Natl. Acad. Sci. U. S. A.112, 15946–15951 (2015).
Elias-Neto, M. & Belles, X. Tergal and pleural structures contribute to the formation of ectopic prothoracic wings in cockroaches. R. Soc. Open Sci.3, 160347 (2016).
Linz, D. M. & Tomoyasu, Y. Dual evolutionary origin of insect wings supported by an investigation of the abdominal wing serial homologs in Tribolium. Proc. Natl. Acad. Sci. U. S. A.115, E658–E667 (2018).
Tomoyasu, Y. Evo–devo: The double identity of Iisect wings. Curr. Biol.28, R75–R77 (2018).
Clark-Hachtel, C. M., Moe, M. R. & Tomoyasu, Y. Detailed analysis of the prothoracic tissues transforming into wings in the Cephalothorax mutants of the Tribolium beetle. Arthropod Struct. Dev.47, 352–361 (2018).
Clark-Hachtel, C. M. & Tomoyasu, Y. Two sets of candidate crustacean wing homologues and their implication for the origin of insect wings. Nat. Ecol. Evol. (2020). doi:10.1038/s41559-020-1257-8
Bruce, H. S. & Patel, N. H. Insect wings and body wall evolved from ancient leg segments. bioRxiv (2018). doi:10.1101/244541
Linz, D. M., Hu, Y. & Moczek, A. P. From descent with modification to the origins of novelty. Zoology143, 125836 (2020).
A four year postdoctoral position in the lab of Alex Gould is now available. Previous work in the laboratory, using Drosophila, has shown that the neural stem cell niche plays a critical role in sparing the developing CNS from stresses such as nutrient restriction and hypoxia (PMID: 26451484, PMID: 21816278). We are now looking for a highly motivated researcher to identify metabolic interactions between neural stem cells and their niche during stress protection. The successful applicant will have access to state-of-the-art techniques such as single-cell sequencing, gene editing and metabolomics. They will also have a unique opportunity to utilize cryogenic mass spectrometry imaging, a new method recently developed in the laboratory for visualizing metabolism in tissues at single cell resolution (PMID: 32603009). Applications are particularly encouraged from candidates with molecular biology and gene cloning skills. Prior experience with Drosophila is useful but not essential. Examples of other projects ongoing in the lab can be found at www.agouldlab.com and at www.crick.ac.uk/research/labs/alex-gould. The successful applicant will have good organisational and communication skills and a PhD in a relevant area (or be in the final stages of completion).
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