If you’re into developmental biology, chances are you’ve spent some time in your life thinking about how cells change the shapes of tissues. What would cells need to do in order to prevent change of tissue shape, though? In the text below, I summarize my thoughts on why the question of not changing shape during growth might be of interest and discuss the findings from our PLoS Biology publication on the topic (Matejčić et al., 2018). I performed the experiments for this work in the lab of Caren Norden from the Max Planck Institute of Molecular Cell Biology and Genetics in Dresden and the theoretical work was done by Guillaume Salbreux from The Francis Crick Institute in London.
As tissues develop, they need to grow into their correct size and shape in order to function optimally. Biological studies in the past, as well as those today, investigated changes of tissue shapes during the process of morphogenesis, and how cells that build these tissues contribute to shape changes (for example, invagination or elongation). However, many tissues, such as the human ear or foot, establish their shape very early in development, and then need to continue to grow without changing their shape.
At first, such maintenance of the shape of tissues might seem like a very simple task; the cells building the tissue should only maintain an already established shape. But, as the size of a tissue changes, so might the conditions around it, making this task more complicated. A larger tissue may, among other changes, experience new physical constraints as its cells become more packed, stretched and/or compressed. As an example, imagine you have a cultured, 1000 µm x 1000 µm x 10 µm sheet of a simple, monolayered epithelial tissue. You want to scale this culture up 10 times while keeping its proportions constant (i.e., maintain its surface-to-thickness ratio). How would you go about this scaling task? You might wait for your epithelial sheet to proliferate and grow more, but it might only spread, making its apical surface bigger but keeping its thickness the same. You might then constrain its growth laterally, but cells might create a multilayered epithelium. In this case, cells might be extruded, stop dividing or the tissue might buckle. Therefore, keeping a tissue shape unchanged while it is increasing its size is not always as simple as adding more cells through proliferation. For similar reasons, it is also not trivial to predict which cellular parameters will affect tissue shape as its size changes. Despite the importance of such scaling of tissue shape during growth, this complex question had not previously been addressed.
The topic of tissue shape scaling during growth is best investigated in a tissue with a geometrically simple shape, that allows quantitative analysis, and where shape perturbations are easily detectable, as well as functionally significant. Such a tissue is the developing vertebrate retina, that establishes its shape early in development (during the first trimester in humans) and then maintains shape as it grows. It has a shape of a smooth hemispherical cup (Figure 1, left panel) and lies in the back of the vertebrate eye to transmit light impulses to the brain. As within the light path of a microscope, each component within the eye, including the retina, must be correctly shaped and aligned for light to propagate effectively. It is, therefore, not surprising that even small glitches in human retinal structure, in the form of wrinkles or thickenings, lead to distorted vision (macular pucker) and that its smooth shape is essential for optimal visual function. During embryonic development, the retina is a pseudostratified epithelium, a conserved and widely utilized tissue arrangement (Figure 1, right panel). As in all other pseudostratified epithelia, in the developing retina cells are long, spindle-shaped and all divide at the apical tissue surface.
All these features are present in the retinal neuroepithelium of the zebrafish – an experimental model with the advantages of easy manipulation, tractable tissue-wide live and fixed imaging as well as fast development. In the zebrafish, the retinal neuroepithelium undergoes a phase of shape scaling in just 24 hours (stages ~20-48 hours-post-fertilization (hpf), Figure 2), which allowed me to study this entire developmental process within a single imaging session. Together, these factors make the developing zebrafish retina an excellent system to study tissue shape maintenance during growth.
Our project on retinal growth began out of a curiosity; I dug into how cell parameters such as number, size, shape and differentiation contribute to the increase in retinal size. Through these 3D, tissue-wide quantitative analyses (Video 1), we learned that, initially, all retinal cells divide, and after the developmental stage of 36 hpf, they have a 35% chance of exiting the cell cycle. Cell loss is negligible for growth in this system, and cells during development get smaller and smaller and increasingly packed. Overall, we were able to show that retinal tissue grows exponentially, by proliferative increase in cell number.
Video 1
However, I mentioned earlier that to scale tissue shape during growth is not necessarily as simple as adding more cells through proliferation. For starters, we should know where in the tissue new cells are added; we know oriented divisions and non-uniform proliferation can affect tissue shape by causing non-isotropic growth. That’s why we first needed to confirm that cell divisions do not orient along a preferred axis. We also found that their spatial distribution is homogeneous in all developmental stages, meaning that new cells are added uniformly throughout the tissue. Together with the previous finding, we here showed that proliferation itself does not disturb isotropic retinal growth. But, as I will hopefully manage to convince you, there is still more to retinal scaling than “just” adding more cells. In the second part of this text, I describe our quantitative analysis of retinal shape, and the development of the shape of cells that build it.
One important metric to assess proportions of a geometrical object (e.g. your computer screen) is its aspect ratio. The aspect ratio – or height-to-width ratio – can serve as a measure of shape and shape scaling of the tissue, as in my epithelial-sheet-example from the beginning. Using the aspect ratio as a metric of shape, we could quantitatively show that the shape of the whole retinal tissue does not change during growth. In other words, retinal thickness and surface area increased in concert, allowing developmental shape scaling. The thick retinal neuroepithelial tissue is still an epithelial monolayer, with each cell attached at both the basal and the apical surface of the tissue. Due to this, this apico-basal thickening of the tissue we observed translates to an elongation of retinal cells; the already slender cells thin-out and elongate even further (Figure 3, Cell elongation panel). Was it possible that this change in the shape of cells was necessary to keep tissue shape unchanged by increasing its thickness as it grew?
Cell shape in many different developmental contexts is controlled by actin (rev. in Lecuit and Lenne, 2007; Paluch and Heisenberg, 2009; Salbreux et al., 2012). To understand what governs developmental cell elongation I measured, I looked at how actin is distributed in the retina. Indeed, the subcellular distribution of actin changed as the tissue grew. Precisely coinciding with cell elongation, actin was depleted from the lateral cell regions and remained prominent only at the apical- and basal-most cell processes (Figure 3, Actin redistribution panel). A simplified theoretical model by Guillaume Salbreux could explain such actin-based cell elongation by using the actin signal redistribution as a proxy for redistribution of the cellular cortical tension (Figure 3, Model panel). In combination with the measured rate of tissue volume increase, this model also recapitulated the overall constant aspect ratio of the retinal tissue during growth.
To test if cells indeed needed to elongate to allow scaling of tissue shape, I analyzed retinal development in the zebrafish mutant for histone deacetylase 1 (hdac1-/-), where eye shape was shown to be severely perturbed in the late stages of development (Stadler et al., 2005; Yamaguchi et al., 2005). From live light sheet imaging datasets, I found that cells in the hdac1-/- retina indeed failed to elongate (Figure 4, 40 hpf). In a very exciting finding, completely consistent with our working model, the lateral cell region in these mutants remained rich in actin signal even in late developmental stages. By simply keeping the cell tension ratio in our model unchanged we could theoretically recapitulate the divergence in shape between control and mutant tissue that we measured experimentally. This convinced us that redistribution of the lateral actin pool is necessary for cells to elongate and keep overall retinal shape intact. Upon growing further, the short-celled hdac1-/- retinal epithelia started disturbing their otherwise smooth tissue surface by folding apically (Figure 4, Video 2).
Video 2
A day later, retinal folds appeared throughout the hdac1-/- retinal tissue and created a structure resembling more a miniature folded brain than a retina (Figure 4, rightmost panel). This severe shape perturbation demonstrated again how important it is for the retinal cells to elongate to maintain tissue’s aspect ratio during growth.
In an interesting side observation, folded retinas of hdac1 mutants could still differentiate into a neuronal tissue, despite the tissue having a heavily disturbed shape that would subsequently interfere with light propagation. This fact decouples retinal differentiation from tissue shape and highlights the importance of precise timing of developmental events; proliferative growth, actin redistribution and differentiation all need to be temporally coordinated to give rise to a fully functioning retina.
We also found that the synchronous, tissue-wide redistribution of actin and cell elongation are non-cell-autonomous events that depend on the extracellular matrix (ECM). We think that the ECM composition (or structure) changes at ~36 hpf in an Hdac1-dependent manner, and that this change affects actin tissue-wide, coordinating its redistribution within all retinal cells. In the zebrafish retina, Hdac1 functions upstream of Wnt/ß-catenin and Notch signaling. In turn, Wnt/ß-catenin can affect expression of ECM-genes (rev. in Astudillo and Larraín, 2014). So, by inhibiting Wnt/ß-catenin at the right time during development, Hdac1 might indirectly cause a change in composition of the basement membrane, and the ECM – actin axis might then act on actin redistribution inside retinal cells. Considering the evolutionary conserved tissue architecture and the players governing shape maintenance in the retina, similar mechanisms might be at play in other growing pseudostratified epithelia, such as the human retina or brain.
…
Overall, we combined experiments and theory to investigate the maintenance of retinal tissue shape during growth. We identified actin redistribution from the lateral cell membranes as a simple developmental cue necessary to elongate cells and thus keep the overall aspect ratio of the retinal tissue unchanged. Our story highlights that uniform growth and constant shape during development are not default states but require maintenance at the cell level (Shraiman, 2005), and I hope it will motivate further studies of coordination growth and shape during development.
Altogether, we generated a rich, 3D tissue-wide dataset of retinal growth and shape, quantifying many cell-level parameters during development of the retinal neuroepithelium. It would be great to have such detailed studies of many other organs. I think such knowledge should then be used as a ground truth of wildtype development to get closer to rebuilding synthetic and simulated tissues, but also to “debug” development in systems such as organoids, to ultimately really understand in vivo development.
References
Astudillo, P. and Larraín, J. (2014). Wnt Signaling and Cell-Matrix Adhesion. Curr. Mol. Med.14, 209–220.
Fish, J. L., Dehay, C., Kennedy, H. and Huttner, W. B. (2008). Making bigger brains-the evolution of neural-progenitor-cell division. J Cell Sci121, 2783–2793.
Lecuit, T. and Lenne, P.-F. (2007). Cell surface mechanics and the control of cell shape, tissue patterns and morphogenesis. Nature Reviews Molecular Cell Biology8, 633–644.
Matejčić, M., Salbreux, G. and Norden, C. (2018). A non-cell-autonomous actin redistribution enables isotropic retinal growth. PLOS Biol16, e2006018.
Paluch, E. and Heisenberg, C.-P. (2009). Biology and Physics of Cell Shape Changes in Development. Current Biology19, R790–R799.
Salbreux, G., Charras, G. and Paluch, E. (2012). Actin cortex mechanics and cellular morphogenesis. – PubMed – NCBI. Trends in Cell Biology22, 536–545.
Shraiman, B. I. (2005). Mechanical feedback as a possible regulator of tissue growth. Proc. Natl. Acad. Sci. U.S.A.102, 3318–3323.
Stadler, J. A., Shkumatava, A., Norton, W. H. J., Rau, M. J., Geisler, R., Fischer, S. and Neumann, C. J. (2005). Histone deacetylase 1 is required for cell cycle exit and differentiation in the zebrafish retina. Dev. Dyn.233, 883–889.
Yamaguchi, M., Tonou-Fujimori, N., Komori, A., Maeda, R., Nojima, Y., Li, H., Okamoto, H. and Masai, I. (2005). Histone deacetylase 1 regulates retinal neurogenesis in zebrafish by suppressing Wnt and Notch signaling pathways. Development132, 3027–3043.
The winners of Nikon’s Small World in Motion 2018 Competition have just been announced, and overall first place has gone to a stunning developmental biology SPIM movie.
The Francis Crick Institute is recruitingEarly Career Researchers who wish to set up their first independent research programme at the Crick in any area related to biomedicine. We welcome applications from those who wish to work on a flexible and/or part-time basis.
Successful candidates will be offered a competitive salary with a 6-year contract, renewable once for a total of 12 years. The package includes:
Salaries and consumables for up to five researchers, including graduate students
Opportunity to expand through external grant funding
Ready access to Crick Core Facilities
Full lab setup in state-of-the-art laboratory space
Package applies to the duration of the contract
The Crick will provide mentoring and support to ensure its early career Group Leaders make the most of their time at the institute and develop a world-class research programme. Towards the end of the 12-year period we will support them to find leadership positions elsewhere, with potential for a transition start-up package for those remaining in the UK.
Applications from candidates with a PhD and postdoctoral experience should be submitted online at:
Location: University of Southampton, UK
Salary: £30,395 to £36,261 per annum Full Time – Fixed Term for 3 years
Closing Date: Monday 05 November 2018
Interview Date: See advert
Reference: 1061818BJ
A Research Fellow position is available in the laboratory of Mammary Stem Cell Biology & Breast Cancer headed by Dr. Salah Elias at the School of Biological Sciences (SoBS) – University of Southampton (UoS), to study the mechanisms of asymmetric cell division during mammary gland development and homeostasis. The position is available for 3 years tenable from February 2019, funded by the Medical Research Council (MRC). On appointment your post title will be Research Fellow.
The Project
Our lab focusses on studying the mechanisms that regulate mammary stem cell fate and dynamics in normal development and breast cancer. This exciting project is a collaboration between our group and Dr. Philip Greulich group based at the Department of Mathematical Sciences at UoS. It will employ combined cutting-edge in vivo single-cell lineage tracing, quantitative three-dimensional (3D) high-resolution imaging and single-cell RNA-sequencing as well as mathematical/computational modelling to (1) identify novel mechanisms that control mitotic spindle orientation in mammary stem cells; and (2) determine how these mechanisms influence cell fate outcomes in the differentiating mammary epithelium. The outcomes of this collaborative project are expected to provide important novel insight into the identity, dynamics and potential of mammary stem cells.
The Successful Candidate
We are looking for a creative, ambitious and skilled Postdoctoral Researcher Scientist willing to challenge an innovative project by adopting a pro-active attitude and an analytical approach, with a strong interest in interdisciplinary collaboration.
You will be responsible for the development of the project, which includes experimental design, data collection and interpretation. You will work in collaboration with Dr. Greulich group who will use mathematical modelling to compare the generated experimental data with predictions from stochastic models for cell fate dynamics, and test the project’s hypotheses via Bayesian inference. You are also expected to contribute to new ideas for research projects, develop ideas for writing grant proposals, prepare scientific reports, write up results for publication in international peer-reviewed journals, assist other members of our group or people working on collaborative projects to become familiar with new methodologies, act as a source of information and advice on scientific protocols.
You will hold a PhD* or equivalent professional qualifications and experience in epithelial stem cell and/or cancer biology (or related field). A strong evidence of proficiency in cell biology and quantitative advanced microscopy in vivo is necessary. You will have experience in animal models and have a personal licence to work with rodents or be prepared to obtain such a licence via attendance of in-house courses. Experience in molecular biology techniques including Next Generation Sequencing is desirable. Basic understanding of computational/mathematical modelling would be advantageous. You will be friendly and have excellent interpersonal skills with a desire to communicate with other researchers whilst maintaining the highest level of professionalism at all times.
The Environment
At SoBS, we use cutting-edge technologies for innovative research to define the basis of human health and disease, and develop interventions that benefit peoples’ lives. There is a strong interdisciplinary research focus bringing together researchers from Biological and Medical Sciences, Computer Sciences, Physics and Mathematical Sciences with experimental work housed in a £45 million building that encompasses cutting-edge research infrastructures. Our Imaging Microscopy Centre (IMC) provides access to several advanced optical microscopic modalities equipped to perform the 3D imaging of this proposal. Excellent Specific-Pathogen-Free (SPF) Animal and Histology Facilities are also available. SoBS offers a supportive and dynamic research environment, with comprehensive training and career development opportunities. You will have full access to all resources and undertake appropriate training in the use of the equipment of our state-of-the-art core facilities to accomplish your studies. SoBS has an outstanding Stem Cell and Developmental research theme, in which our group is perfectly embedded, with excellent potential for collaborations that extend to the closely located Cancer Sciences where breast cancer research is very active. You will thrive within a unique international, stimulating and challenging research environment, with an outstanding international research seminar series in addition to Stem Cells and Quantitative Biology-centred meetings co-organized by SoBS and Mathematical Sciences. The proximity of SoBS and Mathematical Sciences and the specialized expertise that each contributes provides a unique environment needed to achieve the maximum impact of this project.
For informal enquiries, please contact Dr Salah Elias S.K.Elias@soton.ac.uk and/or Dr. Philip Greulich P.S.Greulich@soton.ac.uk
It is anticipated that interviews will take place at the end of November 2018.
Equal Opportunities and Benefits
SoBS holds an Athena SWAN Silver Award, demonstrating commitment to equal opportunities and gender balance in the workplace.
The University of Southampton has a generous maternity policy and onsite childcare facilities; employees are able to participate in the childcare vouchers scheme. Other benefits include state-of-the-art on-campus sports, arts and culture
facilities, a full programme of events and a range of staff discounts.
Application Procedure
Closing Date: 5th November 2018. However, we encourage early applications as we will be reviewing applications on an on-going basis. Therefore the advert may close before the deadline if suitable candidates are identified. First review date: 29th October 2018
How to Apply: You should submit your completed application form online at www.jobs.soton.ac.uk. Please include (1) a cover letter outlining your scientific interests, describing how you meet the requirements of the position, and an outline of future goals; (2) a curriculum vitae, (3) contact information for at least two references.
References are requested along with your application, so please allow time for these to be received prior to the close date, to assist the department with shortlisting.
If you need any assistance, please call Samantha Stubbs (Recruitment Team) on +44 (0) 23 8059 4046. Please quote vacancy reference number 1061818BJ on all correspondence.
*Applications will be considered from candidates who are working towards or nearing completion of a relevant PhD qualification. The title of Research Fellow will be applied upon successful completion of the PhD. Prior to the qualification being awarded the title of Senior Research Assistant will be given.
Antibodies.com is proud to support researchers with travel grants up to £500.
The Award:
Each quarter, Antibodies.com offers a travel grant up to £500 to help cover the cost of attending a conference.
These travel grants are open to PhD candidates, lab managers, and post-docs from academic research institutions across Europe. The grant is intended to help cover the costs of registration, accommodation, and travel to a conference of choice.
For a chance to win, simply complete the application form at Antibodies.com; including a summary of your research or abstract for the conference.
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Soon after the rediscovery of Mendel’s laws of inheritance in plants, French scientist Lucien Cuénot published a paper in 1902, reporting his studies of the inheritance of pigmentation in the house mouse.
Cuénot’s results showed that Mendel’s laws of inheritance also applied to animals. This is a fundamental paper in the field of genetics.
The original paper was published in French & many people may not read French. Therefore, Google, myself, and Phil Soriano (Mount Sinai, New York) translated the original manuscript into English.
Shuo-Ting Yen & Chang-Ru Tsai (MD Anderson Cancer Center) did the Chinese translation. Seol Hee Im (Haverford) did the Korean translation. Vanessa Barone (Scripps Institution of Oceanography) did the Italian translation.
You can find these translations at the University of Texas Genetics & Epigenetics Graduate Program website under Historical Translations (https://bit.ly/2P0gJ4v). We hope this provides the opportunity for many people to read this classic paper in genetics.
Applications are invited for a Research Assistant position, funded by the Wellcome Trust, to join an international team in the Department of Genetics in central Cambridge. The project is led by Ben Steventon and is aimed towards understanding growth control of a population of embryonic stem cells called neuromesodermal progenitors. The project will involve experiments using both zebrafish embryos and aggregates of mouse embryonic stem cells, or gastruloids.We are looking for a highly motivated and well-organised person, with a first degree in biological or biomedical sciences and experience in molecular biology. The project will involve cutting-edge imaging techniques including the quantification of gene expression levels in situ and the development of tools for manipulating gene expression levels within single cells in vivo. Experience in mammalian cell culture is essential and additional expression in zebrafish genetics would be desirable.
Welcome to our monthly trawl for developmental biology (and related) preprints.
Another month, another net full of exciting science. Look out for WNT vampires, regenerating lampreys, polarising ctenophores, plus investigations into niche architecture, tissue mechanics and the dynamics of developmental signalling.
The preprints were hosted on bioRxiv, PeerJ, andarXiv. Let us know if we missed anything, and use these links to get to the section you want:
Planar cell polarity pathway and development of the human visual cortex
Jean Shin, Shaojie Ma, Edith Hofer, Yash Patel, Gennady Roshchupkin, Andre M Sousa, Xueqiu Jian, Rebecca Gottesmann, Thomas H Mosley, Myriam Fornage, Yasaman Saba, Lukas Pirpamer, Reinhold Schmidt, Helena Schmidt, Bernard Mazoyer, Amaia Carrion-Castillo, Joshua Bis, Shuo Li, Qiong Yang, Michelle Luciano, Sherif Karama, Lindsay Lewis, Mark Bastin, Matthew A Harris, Ian Deary, Joanna M Wardlaw, Markus Scholz, Markus Loeffler, Veronica Witte, Frauke Beyer, Arno Villringer, Hieab HHH Adams, M Arfan Ikrum, William S Kremen, Nathan A Gillespie, the ENIGMA Consortium, Nenad Sestan, Zdenka Pausova, Sudha Seshadri, Tomas Paus, the neuroCHARGE Working Group
Reconstructing the human first trimester fetal-maternal interface using single cell transcriptomics
Roser Vento-Tormo, Mirjana Efremova, Rachel A. Botting, Margherita Y. Turco, Miquel Vento-Tormo, Kerstin B. Meyer, Jongeun Park, Emily Stephenson, Krzysztof Polański, Rebecca P. Payne, Angela Goncalves, Angela Zou, Johan Henriksson, Laura Wood, Steve Lisgo, Andrew Filby, Gavin J. Wright, Michael J. Stubbington, Muzlifah Haniffa, Ashley Moffett, Sarah A. Teichmann
Myh10 deficiency leads to defective extracellular matrix remodeling and pulmonary disease
Hyun-Taek Kim, Wenguang Yin, Young-June Jin, Paolo Panza, Felix Gunawan, Beate Grohmann, Carmen Buettner, Anna M. Sokol, Jens Preussner, Stefan Guenther, Sawa Kostin, Clemens Ruppert, Aditya M. Bhagwat, Xuefei Ma, Johannes Graumann, Mario Looso, Andreas Guenther, Robert S. Adelstein, Stefan Offermanns, Didier Y.R. Stainier
The novel lncRNA lnc-NR2F1 is pro-neurogenic and mutated in human neurodevelopmental disorders
Cheen Euong Ang, Qing Ma, Orly Wapinski, ShengHua Fan, Ryan A Flynn, Bradley Coe, Masahiro Onoguchi, Victor H Olmos, Brian T Do, Lynn Dukes-Rimsky, Jin Xu, Qian Yi Lee, Koji Tanabe, LiangJiang Wang, Ulrich Elling, Josef Penninger, Kun Qu, Evan E Eichler, Anand Srivastava, Marius Wernig, Howard Chang
Avian chromosomes in Torgasheva, et al.’s preprint
Germline-Restricted Chromosome (GRC) is Widespread among Songbirds
Anna A Torgasheva, Lyubov P Malinovskaya, Kira S Zadesenets, Tatyana V Karamysheva, Elena A Kizilova, Inna E Pristyazhnyuk, Elena P Shnaider, Valeria A Volodkina, Alsu F Saifutdinova, Svetlana A Galkina, Denis M Larkin, Nikolay B Rubtsov, Pavel M Borodin
The Desmosome is a Mesoscale Lipid Raft-Like Membrane Domain
Joshua D Lewis, Amber L Caldara, Stephanie E Zimmer, Anna Seybold, Nicole L Strong, Sara N Stahley, Achilleas S Frangakis, Ilya Levental, James K Wahl III, Alexa L Mattheyses, Takashi Sasaki, Kazuhiko Nakabayashi, Kenichiro Hata, Yoichi Matsubara, Akemi Ishida-Yamamoto, Masayuki Amagai, Akiharu Kubo, Andrew P Kowalczyk
pheno-seq – linking morphological features to gene expression in 3D cell culture systems
Stephan M. Tirier, Jeongbin Park, Friedrich Preusser, Lisa Amrhein, Zuguang Gu, Simon Steiger, Jan-Philipp Mallm, Marcel Waschow, Bjoern Eismann, Marta Gut, Ivo G. Gut, Karsten Rippe, Matthias Schlesner, Fabian Theis, Christiane Fuchs, Claudia R. Ball, Hanno Glimm, Roland Eils, Christian Conrad
FAIRsharing, a cohesive community approach to the growth in standards, repositories and policies
Susanna-Assunta Sansone, Peter McQuilton, Philippe Rocca-Serra, Alejandra Gonzalez-Beltran, Massimiliano Izzo, Allyson Lister, Milo Thurston, Dominique Batista, Ramon Granell, Melanie Adekale, Delphine Dauga, Emma Ganley, Simon Hodson, Rebecca Lawrence, Varsha Khodiyar, Jessica Tenenbaum, J. Myles Axton, Michael Ball, Sebastien Besson, Theodora Bloom, Vivien Bonazzi, Rafael Jimenez, David Carr, Wei Mun Chan, Caty Chung, Geraldine Clement-Stoneham, Helena Cousijn, Saravanan Dayalan, Michel Dumontier, Esther Dzale Yeumo, Scott Edmunds, Nicholas Everitt, Dom Fripp, Carole Goble, Martin Golebiewski, Neil Hall, Robert Hanisch, Michael Hucka, Michael Huerta, Amye Kenall, Robert Kiley, Juergen Klenk, Dimitrios Koureas, Jennie Larkin, Thomas Lemberger, Nick Lynch, Lynn Schriml, Avi Ma’ayan, Catriona MacCallum, Barend Mons, Josh Moore, Wolfgang Muller, Hollydawn Murray, Tomoe Nobusada, Daniel Noesgaard, Jennifer Paxton-Boyd, Sandra Orchard, Gabriella Rustici, Stephan Schurer, Kathryn Sharples, Marina Soares e Silva, Natalie J Stanford, Inmaculada Subirats-Coll, Jason Swedlow, Weida Tong, Mark Wilkinson, John Wise, Pelin Yilmaz
Life Inside A Dinosaur Bone: A Thriving Microbiome
Evan Thomas Saitta, Renxing Liang, Chui Y Lau, Caleb M Brown, Nicholas R Longrich, Thomas G Kaye, Ben J Novak, Steven Salzberg, Paul Donohoe, Marc Dickinson, Jakob Vinther, Ian D Bull, Richard A Brooker, Peter Martin, Geoffrey D Abbott, Timothy DJ Knowles, Kirsty Penkman, Tullis C Onstott
Research Associate/Fellow position (3 years) to work on a BBSRC funded project investigating cell fate regulation during mammalian gastrulation in the laboratory of Dr. Ramiro Alberio (U. of Nottingham, UK), in collaboration with Prof. Jennifer Nichols (U. of Cambridge, UK) and Dr Matt Loose (U. of Nottingham).
Project description:
The project will investigate the molecular mechanisms of mammalian gastrulation. The project involves working with embryos and embryonic stem cells combined with next generation sequencing as a mean to understand cell fate decisions in early embryos. This post is suitable to candidates with experience in single cell RNA seq., embryology and micromanipulation. This post offers a unique opportunity to work in fast developing fields (stem cell biology, single cell genomics and gene editing) and to develop skills in state-of-the-art technologies.
Ideal applicant:
Highly motivated and self-driven, with a PhD (or near completion) in cell/developmental or related biological science with experience in some of the following areas: stem cell biology (preferably hESC), single cell RNA seq, gene editing, and bioinformatics. Experience in embryo dissection, generation of transgenic reporter cell lines, gene targeting and other genome editing techniques are also relevant for the project.
On the Sunday night of 2nd September of 2018, one month ago, most Brazilians were watching TV shows while a large part of our national story was burning out in the National Museum’s fire. In a few hours, a 200-year old institution and several biological, anthropological, and geological collections were consumed by the fire. Publications have been written in respectable journals and newspapers about the fact and its consequences for the whole of society (https://www.theguardian.com/world/2018/sep/03/fire-engulfs-brazil-national-museum-rio).
In this post, I would like to provide a brief personal view from a Brazilian Evolutionary Developmental Biology (Evo-Devo) researcher who also acts as the Director of one of UFRJ’s Institutes. Our Institute also hosts important scientific collections (http://www.macae.ufrj.br/nupem/index.php/colecao-de-peixes-npm), which could be or might be affected in the future if we do not improve our administrative practices.
First, as a Brazilian Evo-Devo researcher, the loss of holotype specimens from some of the most extensive invertebrate collections worldwide will not be recovered sooner or later. Some of the specimens collected by famous naturalists – such as one the Darwin´s greatest colleagues, the German Naturalist Fritz Muller – are of special interest for Evo-Devo researchers (https://onlinelibrary.wiley.com/doi/full/10.1002/jez.b.22687
), since it has been argued that many evolutionary secrets and different morphotypes might lie in the unexplored museums of the world. Unfortunately, in this situation we cannot come back and retrieve the samples and a part of Latin American Biodiversity is gone forever.
Although the reason for the fire is a case for the specialists, I would like to point out some issues which do not apply only for the National Museum of Brazil, but also for other public institutions. After the fire, some authorities and some of the public opinion of the country tried to put the responsibility onto our Rector, who has only been ahead UFRJ for three years and has been trying to obtain special funding to make the required changes in this historical building. This led to a strong response of our employees and students supporting our Rector and our democratic institution, our Federal University and the Museum, the first research institute in Brazil.
If you are a researcher from a developed country, you can´t imagine how much paperwork a Professor or a Director in a country like Brazil has to deal with to buy a simple equipment, or to develop a fire alarm system. The paperwork to hire a company or to develop such a project in Brazil impairs our scientific progress. This can be justified by the lack of qualified personal from the university, and our current low budget to hire a specialized company. In the past years, federal research money for Science has dropped over 60% and the Science and Technology Ministry has been largely neglected by the government.
To solve daily problems of infrastructure one must undergo a complex paperwork process which can take years and contain over a thousand pages and, at the end, the company might still not be hired due to lack of funding. Unfortunately, the corruption scandals in the past years led to a general impression that corruption is widespread all over the country. I can assure that most, if not all, professors and colleagues from my University are honest and, in many occasions, buy consumables for the university from their own salaries, to avoid undergoing this stressful and many times unsuccessful process of buying something using University money.
A second possibility, the donation of private money, rarely occurs. In general, wealthy people from Brazil do not donate to Universities or research institutes, as it is typical for US Universities. This situation is already changing with some great initiatives such as the Serrapilheira Institute (https://serrapilheira.org/en/), although the whole donation system is still in its infancy. Current Brazilian laws limit the use of the money that the University obtains from rents, museum tickets, donations, and any other source of funding. Money allocated in one year does not stay for the next year: it goes back to the Federal Government. Any money that enters in the University must undergo the same complex process that avoid any reasonable speed and progress that science needs. Thus, laws must change for science and technology improvement in Brazil.
Thus, although the museum tragedy cannot be solely attributed to lack of public funding and extensive inefficacy of paperwork and unreasonable laws to spend public resources by the University, these issues have contributed for the tragedy. Lastly, I believe that researchers from public universities have undermined the role and the importance of museums and collections for the Universities. I often see comments that museums are just repository of specimens, but particularly in the case of the National Museum a large part of Zoological, Anthropological, Paleontological research of our country was being carried out in this historical building. Importantly, immediately after the fire, the community of National´s Museum has risen together, and the collections are being restarted by the researchers and students.
The National Museum is ALIVE and I hope from now on, the Museum acquires the status it should never have lost, the home of our history and our knowledge, which fortunately lies in our public universities.
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