This is the final post from our developmental neurobiology seminar this semester. Two students wrote about our discussion of the importance of neuronal activity during synaptogenesis and their professor combined and edited the pieces. As usual, we focused  on development in the vertebrate retina. Hope you’ve enjoyed our contributions, we’ve enjoyed sharing our new-found understanding.

“Use it or lose it.” One of my mother’s favorite phrases, applicable to any number of situations. Fail to practice piano? Don’t use a toy for a while? Realize you’ve forgotten your high school Spanish? “Use it or lose it.”

The concept of “use it or lose it” can also be applied to synaptogenesis and neural circuit development (although I doubt my mother was thinking of this when she used the phrase). The idea of Hebbian connections – that synapse formation and elimination is dependent on activity – has been primarily supported by studies of the neuromuscular junction ^[1]. In general, input neurons converging on dendrites differ in synaptic activity, resulting in more active inputs outcompeting less active inputs for dendrite connection. Inputs with less active synaptic regions are ultimately eliminated ^[2],[3]. Essentially, the less active neurons don’t “use it” and so they “lose it”, with “it” being an electrochemical connection to a neighboring neuron.

Several years ago, investigations of developing connections in the vertebrate retina suggested that this idea of “use it or lose it” might not be the sole mechanism employed within the developing nervous system. Our class recently read and discussed a paper by Kerschensteiner et al. (2009) ^[4]. This detailed study suggested that, in contrast to the classical model, some neuronal connections are formed and maintained in the inner plexiform layer independently of synaptic activity.

Anatomy and Physiology Background: ON and OFF cells in the Inner Plexiform Layer

When light hits the mammalian eye, it changes the electrical properties of photoreceptors so that their downstream partners, bipolar cells, deliver a message to retinal ganglion cells (RGCs), which in turn relay information about visual cues to the brain (see Figure 1). The middlemen in this process, bipolar cells, can be depolarized when light hits photoreceptors (ON cells) or hyperpolarized when light hits photoreceptors (OFF cells). Bipolar cells communicate with RGCs by forming synapses with RGC dendrites in the inner plexiform layer (IPL). This layer is stratified primarily into two sections, an outer layer and an inner layer, where RGCs synapse with OFF and ON bipolar cells, respectively. There are three main types of RGCs – those that only synapse with ON or OFF bipolar cells (monostratified RGCs), as well as RGCs that synapse with both ON and OFF bipolar cells (bistratified RGCs).

Figure 1: Model of primary cell types and their connection patterns in the mouse retina. First, Photoreceptors (teal rods (R) and yellowish cones, (C)) synapse with horizontal cells (purple) and bipolar cells (RB and CB, green) in the outer plexiform layer (OPL). Next bipolar cells synapse with ganglion cells (G, blue) in the inner plexiform layer (IPL). Amacrine cells (red) also synapse with both ganglion cells and bipolar cells in the IPL. Notice the stratification within the IPL based on the ON/OFF status of the bipolar cells. (Reproduced for educational purposes from Development of cell types and synaptic connections in the retina (http://webvision.med.utah.edu/).

During retinal development, RGCs form stratified dendritic arbors with synaptic connections to either exclusively ON bipolar cells (ON RGCs), exclusively OFF bipolar cells (OFF RGCs), or ON and OFF bipolar cells (ON-OFF RGCs). In the latter, RGC dendrites form synapses with ON and OFF bipolar cells such that ON and OFF inputs reside on separate laminar arborizations (e.g., Figure 1). Typically, ON and OFF bipolar cells form similar numbers of synapses with RGC dendrites, regardless of whether the RGCs are monostratified (ON or OFF) or bistratified (ON-OFF).

Neuronal Activity Determines Synapse Density within ON and OFF Layers of the IPL

To test whether this classical “use it or lose it” model for developing neuronal connections held true in the retina, Kerschensteiner et al. created a new transgenic line of mice that were unable to release glutamate from their ON bipolar cells, which is crucial for signaling to RGCs. The authors made a transgenic mouse that coupled the transcription of TeNT, a bacterial protease that inhibits vesicle fusion (which is necessary for presynaptic signaling), with the promoter for mGluR6, a glutamate receptor expressed in ON bipolar cells but not in OFF bipolar cells. Thus, ON cells could not communicate with the RGCs, while OFF cells could. If the classical model explains the development of connections between bipolar cells and RGCs, one would expect retinas in the transgenic mice to have no or very few RGC – ON cell synapses, and many RGC – OFF cell synapses.

As expected, the resulting mice exhibited normal receptive field properties from OFF-RGC connections and reduced or absent responses from ON-RGC ones. The dendritic branching and stratification patterns as well as overall connectivity appeared identical in transgenic and wild-type mice. Normal RGC development in the presence of significantly reduced ON bipolar cell activity indicates that partner selection and dendritic stratification of post-synaptic RGCs occur regardless of bipolar cell activity. These data provide evidence that RGCs are programmed to synapse to either ON bipolar cells, OFF bipolar cells, or both, regardless of presynaptic glutamate release.

By quantifying the density of individual postsynaptic sites in RGCs adjacent to ON bipolar cells in transgenic mice, the authors found that loss of glutamate release correlated with fewer mature synapses adjacent to ON bipolar cells (~50% fewer synapses in transgenic compared to wild-type retinas, Figure 2B). In addition, as might be predicted from the “use it or lose it” model, the density of synapses in bistratified RGCs connecting with the silenced ON bipolar cells was decreased relative to the density of synapses in the arbors connecting with active OFF bipolar cells (Figure 2C).

Figure 2: Density of bipolar-RGC synapses changes in response to glutamate release. A) Post-synaptic densities (PSD95, red) form at specific sites along RGC dendrites (blue) when closely apposed to biploar cell termini (green). B) Heat maps of glutamatergic post-synaptic densities for OFF and ON arborizations in bistratified RGCs. C-D) Graphical comparison of data in B. Values from non-transgenic retinas in black, transgenic animals in red. D/A is dendritic density, P/A is post-synaptic puncta per arbor area, P/D is post-synaptic puncta per dendritic length. Images are select panels from Figure 2 in Neurotransmission selectively regulates synapse formation in parallel circuits in vivo, Nature August 2009 (Vol 460, pp. 1016-1020). Kerschensteiner, D., Morgan, J., Parker, E., Lewis, R. & Wong, R. Used with permission of Nature Publishing Group.

When Kirchensteiner and coauthors examined the underlying mechanism for this decreased density, the “use it or lose it” model didn’t seem to hold true. Using time-lapse imaging, the authors showed that the silenced ON bipolar cells eliminated synapses at a rate comparable to wild-type but initial synapse formation was dramatically reduced. These data indicate that glutamate release is necessary for synapse formation and that elimination of synapses may not be directly tied to the activity of presynaptic input.

When the authors examined synapses at the ultrastructural level, they found even more evidence that “use it or lose it” isn’t the best analogy for synaptogenesis in the IPL. They show that ribbon synapses, the synaptic vesicle anchoring structures implicated in rapid neuronal transmission, are more numerous in the silent ON bipolar cells than in the active OFF bipolar cells (or in active ON bipolar cells in wild-type retinas). These intriguing electron micrographs raise the possibility that post-synaptic signaling, perhaps in response to glutamate, limits ribbon synapse formation.

With this study, Kerchensteiner et al. helped elucidate the role of glutamate release in forming synapses between bipolar cells and RGCs. Interestingly, glutamate release regulates how many synapses are formed between bipolar cells and RGCs but not how many synapses are eliminated, contrary to the classical “use it or lose it” model of synaptic formation. In a follow-up study, published in 2011 ^[5], some of the same authors investigate this teamwork approach to syanpatogensis in the IPL, providing evidence that differential synaptic maturation of axo-dendritic appositions is shaped by presynaptic activity and occurs in a cell type-specific manner. Whether (and how) post-synaptic cells may influence this process still seems to be an open question.

Although the “use it or lose it” analogy doesn’t completely describe what happens during synapse formation in the IPL, it does provide a framework for thinking about what cells need to connect with each other. In the case of bipolar cells and RGCs, it seems that glutamate needs to be used for efficient and robust synaptogenesis or the cells lose out all together, rarely making functional connections.

——————

[1]Kasthuri, N., & Lichtman, J. (2003). The role of neuronal identity in synaptic competition Nature, 424 (6947), 426-430 DOI: 10.1038/nature01836

[2]Wong, R. O. L. & Lichtman, J. W. in Fundamental Neuroscience 2nd edn (eds Squire, L. R. et al.) Ch. 20, 533–554 (Academic Press, 2002).

[3]MILLER, K. (1996). Synaptic Economics: Competition and Cooperation in Synaptic Plasticity Neuron, 17 (3), 371-374 DOI: 10.1016/S0896-6273(00)80169-5

[4] Kerschensteiner, D., Morgan, J., Parker, E., Lewis, R., & Wong, R. (2009). Neurotransmission selectively regulates synapse formation in parallel circuits in vivo Nature, 460 (7258), 1016-1020 DOI: 10.1038/nature08236

[5] Morgan, J., Soto, F., Wong, R., & Kerschensteiner, D. (2011). Development of Cell Type-Specific Connectivity Patterns of Converging Excitatory Axons in the Retina Neuron, 71 (6), 1014-1021 DOI: 10.1016/j.neuron.2011.08.025

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Cosy Science is an informal pub gathering where scientists talk about their research over a pint of beer (or glass of wine!) with anyone who is interested in listening. It is mostly a monthly event, taking place at The Cittie of Yorke pub in London, and everyone is welcome!

As you may know, The Company of Biologists runs a series of workshops for scientists, and we collaborate with Cosy Science to bring some of the exciting research discussed at the workshops to the general public. Our latest workshop will focus on cell polarity, and one of the participants, Dr Suzanne Eaton (MPI-CBG, Dresden) will be joining Cosy Science next Wednesday (21st of May) to bring developmental biology to the pub! Suzanne will give a short talk about how cells communicate to build tissues, and its implications in regulating size, embryogenesis and cancer. After a short break to refill, the floor will be open for questions and friendly discussion. So if you’re in the area, bring along that friend who always wanted to know what developmental biology is all about, and enjoy an evening of pub science sponsored by The Company of Biologists!

Find out more information at the Cosy Science website

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Department of Molecular Biosciences, The Wenner-Gren Institute

Stockholm University is a leading European university offering a multicultural environment in one of the world’s most dynamic capital cities. With more than 60,000 students and 5,000 staff, the University facilitates individual and societal development by providing top quality education that is tightly linked to its internationally recognized research programs.

The Department of Molecular Biosciences, The Wenner-Gren Institute (MBW) unites 30 independent research groups pursuing fundamental questions in molecular cell biology, infection and immunobiology, and integrative biology. The department carries out experimental research primarily investigating the function of genes and cells in tissues and organisms.

Main responsibilities: We are looking for a highly motivated and focused individual to join Professor Christos Samakovlis’s research group. The successful applicant will utilize state-of-the-art approaches aimed at obtaining a fundamental molecular understanding of epithelial morphogenesis, regeneration and malignant growth in Drosophila. The laboratory utilizes genome-wide, tissue-specific RNAi screens, live-imaging and transcriptional profiling. The successful candidate is expected to participate in the comparative analysis of gene function in insect and vertebrate tissues.

Qualification requirements: The applicant must have received a doctoral degree from university in the field of molecular cell biology, developmental biology or genetics. Applicants must have demonstrated productivity in pursueing research in molecular cell biology or bioinformatics. Experience with the Drosophila model system is an advantage. Excellent English language skills, both written and spoken, are a requisite. Further information about the position can be obtained from Christos Samakovlis, christos.samakovlis@su.se

Application: 
The application deadline is June 13, 2014.

Applications should comprise the following:

1. CV, including full contact information and date of birth
2. Personal statement describing research interests (1-2 paragraphs), research
   experience (1–2 paragraphs) and career goals (1-2 paragraphs)
3. List of 2-3 references, please include name, e-mail address and telephone number Stockholm University is an equal opportunity employer

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A postdoctoral fellowship is available for at least three years at the SciLifeLab, Stockholm, Sweden. Science for Life Laboratory (SciLifeLab) is a national center for molecular biosciences with focus on health and environmental research http://www.scilifelab.se/. The center combines frontline technical expertise with advanced knowledge of translational medicine and molecular bioscience.
The position is associated with the laboratory of Professor Christos Samakovlis. Research at the laboratory addresses airway morphogenesis, epithelial regeneration and malignant growth in Drosophila. We utilize genome-wide, tissue-specific RNAi screens, live-imaging and transcriptional profiling. The successful candidate is expected to participate in a comparative analysis of gene function in fly and mouse tissues.

Qualification requirements: Research experience in mouse developmental biology is an important selection criterion and strong interest in genetics and molecular biology is advantageous. Applicants must have demonstrated productivity in pursueing research in developmental or molecular cell biology. Excellent English language skills, both written and spoken, are a requisite.
Additional information can be obtained from Christos Samakovlis, (christos.samakovlis@su.se), and http://www.su.se/mbw/

Application: 
The application deadline is June 13, 2014.

Applications should comprise the following:
1. CV, including full contact information and date of birth
2. Publication list and a personal statement describing research interests (1-2 paragraphs), research experience (1–2 paragraphs) and career goals (1-2 paragraphs)
3. List of 2-3 references, please include name, e-mail address and telephone number

Stockholm University is an equal opportunity employer

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The Journal of Experimental Biology is the leading journal in the field of comparative physiology and publishes papers on the form and function of living organisms, from the molecular and subcellular to the integrated whole animal. We are currently seeking applications for the role of full-time Scientific Copy Editor to provide maternity cover.

The role entails copyediting articles to a high standard, compiling and paginating articles within an issue, overseeing the journal production process and liaising with authors, academic editors and production staff to ensure that articles are published in a timely and professional manner.

Candidates for this position should have a degree (ideally a PhD) in a relevant scientific area, and previous copyediting experience is strongly preferred. Additional requirements include excellent literacy skills, high attention to detail, a diplomatic communication style, good interpersonal and IT skills, a flexible approach and the ability to work to tight deadlines.

This position represents an excellent opportunity within science publishing and offers a competitive salary and benefits. The position is a temporary role for a period of up to 12 months, likely starting in September 2014, and is based in our Cambridge (UK) offices. The post is full time (35 hrs) although part time might be considered.

The Company of Biologists is a not-for-profit organisation and publishes the three internationally renowned, established journals Journal of Cell Science, Development and The Journal of Experimental Biology, as well as the two newer Open Access journals Disease Models & Mechanisms and Biology Open. The organisation has an active programme of charitable giving for the further advancement of biological research, including travelling fellowships for junior scientists and contributions to academic societies and conferences.

Applicants must be eligible to work in the UK and should send a CV along with a covering letter that clearly states their current position and salary expectations, relevant experience and why they are enthusiastic about the post.

Please send applications by email to Miriam.Ganczakowski@biologists.com by 6 June 2014 using the reference JEBMat2014. Informal queries should be directed to Miriam Ganczakowski on 01223 426164.

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There are several things that could bring me to Switzerland. I guess that the Alps, cheese, and swiss chocolate would be 3 top-choices, I could talk about Swiss army knives and watches too, but I would never assume that the reason for my Switzerland visit would be… zebrafish. Of course not just as the ordinary wildtype zebrafish swimming in rivers of India. Not even the one nowadays available in the pet shops all over the world. I came to Switzerland for very specific (transgenic) zebrafish lines that could allow me to find out the answer for the questions I keep asking myself from the beginning of my PhD study.

Knowledge about the embryonic origin of paired teleost fins is a missing element that would help us to fully understand fin development and the fin to limb transition in evolution. It has been shown before that skeleton of mammalian limbs originates from lateral plate mesoderm; contrarily, it has been thought that rays in fish fins origin from trunk neural crest. Recent publications, including of my PhD supervisor Dr. Tomas Carney (AStar Singapore), have shown that it is not neural crest but paraxial mesoderm that gives rise to the osteoblasts (bone forming cells) in the zebrafish tail. This again rises the question about the origin of skeletal elements in paired fins. We had discussed ideas for possible answers but we were lacking tools to perform informative experiments.

 antibody staining performed on fin section of fish line for which I have traveled all way down to Switzerland

The laboratory of Prof. Christian Mosimann at the University of Zurich works on early cell fate determination of the lateral plate mesoderm, which gives rise to the circulatory system, the kidneys, and the limbs. The Mosimann lab has established unique transgenic zebrafish lines that allow visualization, tracking, and genetic lineage tracing of the developing lateral mesoderm. Prof. Mosimann and Dr. Carney had previously met at the International Zebrafish meeting in Barcelona in 2013, and over a glass of Rioja discussed the possibility to use the Tamoxifen-controlled Cre/lox technique developed by Christian to tackle the lateral plate contribution of the developing fins. So the plan was born to send me to Switzerland. With the financial support from the Company of Biologists who kindly awarded me with a travelling fellowship, I was able to collaboratively visit Zurich.

The University of Zurich and especially people from the Mosimann lab created a welcoming and productive environment to work. Despite the lab’s recent start in spring 2013, the place is buzzing with exciting science. The friendly, energetic atmosphere and unconditional support from all members of Mosimann lab made my stay highly enjoyable and productive. I had a chance to learn new techniques that members of Mosimann lab handled with real expertise. Anastasia Felker, a fellow PhD student in the Mosimann lab, is already an expert in cre:lox techniques while Christopher Hess, another PhD student, critically helped me with the molecular biology side of things. Even members of other laboratories have been ready to help me. I owe big thanks to Claudio Cantu from Basler group who has shared his work space with me and helped me to perform my crucial experiments on sectioned fins. I have gained new work colleges who then became my friends. Despite the serious hours spent in front of a cryostat and on the several fluorescent microscopes, I had ample opportunity to explore Zurich and the finer points of Swiss culture (including chocolate, cheese fondue, raclette, and snowboarding in the Alps). And yes, I now do own a Swiss army knife, and have acquired a similarly versatile new skill set to tackle my biological interests using zebrafish.

My farewell raclette wth the Mosimann Lab

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This article is a re-post of an article published at the F1000Research blog on the 8th of May, 2014. Eva Amsen is the outreach director of F1000Research.

Many of you will have been following the STAP stem cell saga: In January, researchers from Japan announced in Nature that they had produced induced pluripotent stem cells (iPS cells) by bathing somatic cells in acid. Other researchers were sceptical of these claims, and tried to reproduce the work. One of those scientists, Kenneth Lee of the Chinese University of Hong Kong, liveblogged his attempts on ResearchGate.

It soon became apparent that one of the underlying problems was that not a lot was known about the experiments in the original paper. Not all data was available, some data were potentially incorrect, and the protocol appeared to be insufficient to reproduce the work.

Lee pushed on, though, and using an updated protocol he systematically kept track of everything he did, and openly discussed it with others.

Today, F1000Research has published the full summary of Lee’s work, with all underlying data sets. Using white blood cells isolated from the spleen of neonatal mice – the same cells used in the original study – as well as lung fibroblasts, Lee was unable to replicate the original findings.

No iPS cell markers after acid treatment. Image from article.

Lee’s article has undergone a pre-refereeing check, and has now been sent to peer reviewers, whose comments you will be able to read underneath the article as and when they come in – with reviewer names. Once the article passes peer review (either in this version or after revisions), it will be indexed in PubMed and other external databases.

We use this completely transparent process for all articles we publish in F1000Research, and we believe that this particular case very clearly shows the benefit of a transparent system over the more traditional approach that has inevitably led to the ongoing problems following the original article in Nature: you will all be able to see what the invited reviewers think about Lee’s article, you can leave your own comments as well, and you can track any new incoming referee reports or comments on the paper by clicking “Track” on the article page.

You can also download the associated data sets to do your own analysis. We know that some other stem cell researchers have tried to replicate the acid bath experiments – now you can see how your data compare to those of the Lee lab. (And if you’d like to publish your own findings as a short Data Note, we’re currently waiving the article processing charge on those. Find out more here.)

Stem cell science has suffered from a closed publishing system perhaps more than many other disciplines, and it’s time to open up.

[You can find Lee’s article here, and download the associated press release (pdf) here.]

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by Jessica Chen and Jenna Galloway

Animals can contort their bodies into a diversity of movements: running, jumping, climbing, and swimming to name a few. All of these movements are possible because tendons transmit the force produced by the muscles to the bones. Most of us do not pay much attention to our tendons and ligaments until something happens to them. Sports and repetitive motion injuries are very common yet are complicated by slow and limited repair. Surprisingly, very little is known about how tendons and ligaments form and organize to make the appropriate connections within the musculoskeletal system, and then, maintain and repair themselves in the adult. Part of our limited knowledge concerning their developmental program had been due to the absence of early markers at stages that preceded the morphological detection of tendons. The identification of the transcription factor Scleraxis (scx)as a robust marker of tendon and ligament progenitors provided the means to gain an understanding of the molecular regulators of tendon cell induction and organization (Schweitzer et al., 2001). With these questions in mind, we developed the zebrafish as a model to study tendon biology in our recent paper in Development.

Why study zebrafish and do they have tendons? When we began these studies, we were often asked this question, and itforced us to consider if zebrafish would be an appropriate model to study tendon and ligament biology. Clearly, the forces fish experience in an aquatic habitat are much different than those felt by terrestrial land animals. As such, the tendons in these diverse species, which perform very different movements, could also be different. Previous molecular studies of zebrafish tendon tissues have focused on the myosepta, which connects the muscle segments along the body axis enabling undulatory swimming (Bassett et al., 2003; Charvet et al., 2013; Kudo et al., 2004). The myoseptal tissue functions as a tendon in transmitting force necessary for swimming, and we found that it expresses many tendon markers during developmental stages. At these stages, however, it primarily connects muscle to muscle, and in adult zebrafish, its structure is not similar to the linear tendons of mammals (Charvet et al., 2011; Summers and Koob, 2002). In contrast, we focused most of our studies on the cranial region when we began examining tendon markers in zebrafish embryos. We concentrated on this anatomical location for two principal reasons: here, cartilage and bone are primarily found developing in close proximity to muscle, and second, the pressure for prey capture and feeding would require a functioning musculoskeletal apparatus at very early stages. Indeed, it was in the cranial regions that we found the co-expression of many tendon markers, including scleraxisa, and also where, in adults, the tissue was similar on the ultrastructural level to that of the linear tendons of mammals.

In demonstrating that the zebrafish cranial tendon populations are homologous to their mammalian counterparts, we have expanded our ability to study this tissue in the context of musculoskeletal patterning. Although our work was the first to molecularly describe the head tendons and ligaments in zebrafish, the cranial musculoskeletal anatomy and functional morphology of ray-finned fishes has been studied for over a century (reviewed in (Ferry-Graham and Lauder, 2001)), and models of feeding mechanics in adult fish have detailed cranial tendon and ligament attachments in the context of their role during jaw movements (Liem, 1967; Westneat, 1990). During ontogeny, efficient feeding during developmental stages is linked to survival and thought to be evolutionarily advantageous (Houde and Schekter, 1980). We found it striking that the regions with robust co-expression of tendon markers coincided with pivotal points of force transmittance during larval feeding (Hernandez et al., 2002). Given the diversity of craniofacial morphology in teleosts, it would be interesting to understand how tendon and ligament progenitor induction and organization may play a role in shaping the cranial musculoskeletal anatomy. It is known that the neural crest-derived connective and skeletal tissues pattern the cranial muscle attachments in avian systems (Noden, 1986; Noden, 1988). Our work suggests that cartilage may have a role in tendon organization, and previous studies have found that a disruption to cartilage development results in distorted muscle shapes (Yan et al., 2002). Together, these results underscore the importance of tendon-cartilage interactions in musculoskeletal patterning, and future work in the zebrafish will begin to dissect the mechanisms underlying these processes.

Ultimately, we believe that the fish will provide new avenues for studying tendon and ligament biology in a powerful vertebrate genetic system. Findings from chemical screens in zebrafish have already demonstrated the potential for clinical translation in the treatment of a variety of human disease and developmental conditions (Bowman and Zon, 2010; Kaufman et al., 2009). Identifying the pathways that regulate tendon progenitor cell induction, growth, differentiation, and the formation of the attachment sites has relevance in the clinical setting where poor healing, scar tissue and high failure rates at the tendon-bone interface are quite common. The zebrafish system has the potential to not only expand our knowledge of the mechanisms underlying tendon formation and organization through the use of live-imaging and screen based approaches, but also the ability through the creation of injury and disease models and the development of drug discovery platforms to impact clinical therapies.

References

Bassett, D., Bryson-Richardson, R. J., Daggett, D. F., Gautier, P., Keenan, D. G., & Currie, P. D. (2003). Dystrophin is required for the formation of stable muscle attachments in the zebrafish embryo Development, 130 (23), 5851-5860 DOI: 10.1242/dev.00799

Bowman TV, & Zon LI (2010). Swimming into the future of drug discovery: in vivo chemical screens in zebrafish. ACS chemical biology, 5 (2), 159-61 PMID: 20166761

Charvet, B., Guiraud, A., Malbouyres, M., Zwolanek, D., Guillon, E., Bretaud, S., Monnot, C., Schulze, J., Bader, H., Allard, B., Koch, M., & Ruggiero, F. (2013). Knockdown of col22a1 gene in zebrafish induces a muscular dystrophy by disruption of the myotendinous junction Development, 140 (22), 4602-4613 DOI: 10.1242/dev.096024

Charvet, B., Malbouyres, M., Pagnon-Minot, A., Ruggiero, F., & Guellec, D. (2011). Development of the zebrafish myoseptum with emphasis on the myotendinous junction Cell and Tissue Research, 346 (3), 439-449 DOI: 10.1007/s00441-011-1266-7

Ferry-Graham, L., & Lauder, G. (2001). Aquatic prey capture in ray-finned fishes: A century of progress and new directions Journal of Morphology, 248 (2), 99-119 DOI: 10.1002/jmor.1023

Hernandez, L., Barresi, M. J., & Devoto, S. H. (2002). Functional Morphology and Developmental Biology of Zebrafish: Reciprocal Illumination from an Unlikely Couple Integrative and Comparative Biology, 42 (2), 222-231 DOI: 10.1093/icb/42.2.222

Houde, E., & Schekter, R. (1980). Feeding by marine fish larvae: developmental and functional responses Environmental Biology of Fishes, 5 (4), 315-334 DOI: 10.1007/BF00005186

Kaufman, C., White, R., & Zon, L. (2009). Chemical genetic screening in the zebrafish embryo Nature Protocols, 4 (10), 1422-1432 DOI: 10.1038/nprot.2009.144

Kudo, H., Amizuka, N., Araki, K., Inohaya, K., & Kudo, A. (2004). Zebrafish periostin is required for the adhesion of muscle fiber bundles to the myoseptum and for the differentiation of muscle fibers Developmental Biology, 267 (2), 473-487 DOI: 10.1016/j.ydbio.2003.12.007

Liem KF (1967). Functional morphology of the head of the anabantoid teleost fish Helostoma temmincki. Journal of morphology, 121 (2), 135-58 PMID: 6034528

Noden, D. (1986). Patterning of avian craniofacial muscles Developmental Biology, 116 (2), 347-356 DOI: 10.1016/0012-1606(86)90138-7

Noden DM (1988). Interactions and fates of avian craniofacial mesenchyme. Development (Cambridge, England), 103 Suppl, 121-40 PMID: 3074905

Schweitzer R, Chyung JH, Murtaugh LC, Brent AE, Rosen V, Olson EN, Lassar A, & Tabin CJ (2001). Analysis of the tendon cell fate using Scleraxis, a specific marker for tendons and ligaments. Development, 128 (19), 3855-66 PMID: 11585810

Summers, A., & Koob, T. (2002). The evolution of tendon — morphology and material properties Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology, 133 (4), 1159-1170 DOI: 10.1016/S1095-6433(02)00241-6

Westneat, M. (1990). Feeding mechanics of teleost fishes (Labridae; Perciformes): A test of four-bar linkage models Journal of Morphology, 205 (3), 269-295 DOI: 10.1002/jmor.1052050304

Yan YL, Miller CT, Nissen RM, Singer A, Liu D, Kirn A, Draper B, Willoughby J, Morcos PA, Amsterdam A, Chung BC, Westerfield M, Haffter P, Hopkins N, Kimmel C, & Postlethwait JH (2002). A zebrafish sox9 gene required for cartilage morphogenesis. Development, 129 (21), 5065-5079 PMID: 12397114

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Journal of Cell Science is looking for an enthusiastic intern who wishes to gain experience in science publishing.

Journal of Cell Science publishes primary research articles and a well-regarded front section of reviews and topical comment. Joining an established and successful team, including Academic Editor-in-Chief Michael Way, the internship offers an ideal opportunity to gain in-depth experience on one of the major journals in the field of cell biology. The intern will work alongside an experienced Executive Editor in our Cambridge offices.

The intern’s core responsibilities will include:

• Representation of the journal at scientific conferences and within the wider scientific community, with a view to promoting the journal and commissioning new front-section content
• Conducting interviews with early-career scientists
• Writing short summary pieces to highlight the key findings of some of the journal’s research articles
• Creative involvement in the journal’s development and marketing activities

The internship will last for 9 months at a salary of £15,000 pro rata. Applicants will have a PhD in cell biology or a related field and a broad knowledge of cell and molecular biology. Excellent time management, organisational and communication skills are essential, as are enthusiasm and self-motivation. Previous editorial experience is not required.

The Company of Biologists (www.biologists.com) is a not-for-profit organisation that publishes the three well-established, internationally renowned journals Journal of Cell Science, Development and The Journal of Experimental Biology, as well as the two newer Open Access journals Disease Models & Mechanisms and Biology Open. The organisation has an active programme of charitable giving for the further advancement of biological research, including travelling fellowships for junior scientists and contributions to academic societies and conferences.

To apply, please email your CV and a covering letter, quoting reference JCSINT2014, to Miriam.Ganczakowski@biologists.com. Candidates must be able to demonstrate their entitlement to work in the UK. Please direct informal enquiries to Miriam on 01223 426 164.

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As most of you will know, the Node is run by The Company of Biologists, a not-for-profit publisher of several journals, including Development. The Company of Biologists exists to benefit the scientific community, and as such all profits are given back to the community in different ways: by sponsoring meetings and societies, funding travelling fellowships and, most important for those reading this, allowing the Node to exist!

At the recent joint meeting of the British Society for Cell Biology and British Society for Developmental Biology, the company interviewed several researchers based in the UK that are associated with, and benefit from, the activities of the company. Watch the short video below for a quick snapshot of how The Company of Biologists helps the scientific community attending the Warwick meeting:

You can find more information about The Company of Biologists, and how you can apply to their grants and fellowships, by visiting their website.

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