I would have thought that all organisms heal a broken heart the same way humans do (bad movies and cheap wine), but I was wrong.  Some organisms, such as zebrafish and newts, are able to regenerate heart tissue where injury, such as myocardial infarction, occurs.  Understanding tissue regeneration is a necessary leap in generating successful stem cell therapies.  A recent paper in the Development describes the role of TGFβ signaling in zebrafish heart regeneration.

Mammals respond to myocardial infarctions by forming scar tissue at the site of the injury.  Zebrafish form scar tissue at the site of an infarction, but simultaneously begin a complex regenerative process to replace the scar tissue with healthy cardiac muscle.  This regeneration process involves the temporal and spatial coordination of both cardiac and non-cardiac cells, but the molecular players that regulate this process were unknown.  A recent paper by Chablais and Jaźwińska shows that TGFβ signaling is active during heart regeneration.  By timing and reversing inhibition of the pathway using a type I receptor inhibitor, Chablais and Jaźwińska found that TGFβ signaling is key for several steps throughout regeneration—scar deposition, tissue remodeling, and cardiomyocyte proliferation.

The images above show zebrafish heart sections after cryoinjury, which mimics myocardial infarction (left column: injured area in yellow, healthy tissue in blue).  In control sections (top row), cells both within and at the boundary of (arrowheads in zoomed image, seen in cardiomyocytes) the injured area show staining for phospho-Smad3 (green), a direct downstream TGFβ signal transducer.  New myocardium can be seen at the boundary of the injury (arrow in top left).  Treatment with the type I receptor inhibitor (bottom row) successfully suppressed pSmad3 staining and the invasion of cardiomyocytes, and eventually caused ventricular deformation.

For a more general description of this image, see my imaging blog within EuroStemCell, the European stem cell portal.

Chablais, F., & Jazwinska, A. (2012). The regenerative capacity of the zebrafish heart is dependent on TGF signaling Development, 139 (11), 1921-1930 DOI: 10.1242/dev.078543

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The Page laboratory at The Scripps Research Institute in Jupiter, Florida has a postdoctoral position available to investigate the role of genetic risk factors for autism in brain development, using mouse or Drosophila as a model system. This project will investigate brain growth, patterning and connectivity at a mechanistic level using genetic models as well advanced imaging techniques to characterize phenotypes in the developing brain. 

Requirements: In addition to a PhD in a related discipline, highly motivated candidates should have expertise in developmental biology, genetics and imaging. Interested candidates should send a cover letter, CV and contact details for three references to Damon Page, Ph.D., email: paged@scripps.edu.

TSRI embraces diversity & recognizes it as being a key to our success. EOE/M/F/V/D

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The Physics of Living Matter symposium is coming to London this year . This event, first popularised in Cambridge, is a forum for interdisciplinary research in cell and developmental biology.

For all the details and to register go to:

Physics of Living Matter 7

This year’s themes include:

Dynamic cell organisation

Emergent properties of cellular assemblies

Information processing at a molecular and cellular level.

Speakers

Chris Barnes (London, UK), Tariq Enver (London, UK), U. Gaul (Munich, Germany), C. Guet (Vienna, Austria), Martin Howard (Norwich, UK), Tony Hyman (Dresden, Germany), B. Lehner (Barcelona, Spain), P. Martin (Paris, France). J. Molloy (London, UK), B. Novak (Oxford, UK), T. Risler (Paris, France), R. Rodriguez Daga (Sevilla, Spain), E. Siggia (New York, USA), V. Sourjik (Heidelberg, Germany), JP Vincent (London, UK)

Featured Bragg lecturer

Professor Roger Brent, Seattle

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Here are the highlights from the current issue of Development:

Two-step loss of pluripotency

During early development, embryonic cells can form derivatives of all three embryonic layers. This pluripotency, which is regulated by a gene regulatory network that includes the transcription factors Oct4 and Nanog, is lost in mouse embryos between about E7.5 and E8.5. Here (p. 2288), Rodrigo Osorno, Anestis Tsakiridis and colleagues investigate the precise timing and mechanism of pluripotency loss in the mouse embryo. Pluripotency, they report, is extinguished at the onset of somitogenesis, and the loss of pluripotency coincides with reduced chromatin accessibility of the regulatory regions of Oct4 and Nanog, and decreased expression of these genes. Notably, pluripotency correlates with threshold levels of Oct4 and, consistent with this observation, the researchers identify a novel non-pluripotent state during which an increase in Oct4 expression can rapidly reverse chromatin closure and restore pluripotency. Finally, the researchers show that this temporary state is followed by permanent methylation-based epigenetic stabilization of the non-pluripotent state. Thus, two mechanistically separate events are responsible for the elimination of pluripotent cells during development.

Lateral inhibition at neurogenic wavefronts

During neurogenesis, lateral inhibition controls the final number of neurons. Neuronal precursors that express high levels of Delta prevent the neuronal differentiation of neighbouring cells by inducing Notch-dependent inhibitory signals in these neighbours. However, neurogenic wavefronts spread through non-neurogenic areas during development, so why isn’t lateral inhibition disrupted where these wavefronts contact non-neurogenic tissue? José María Frade, Saúl Ares and colleagues investigate this puzzle on p. 2321. The researchers show that Delta-like 1 (Dll1) is widely expressed by non-neurogenic precursors at the periphery of the developing chick retina. Using a mathematical model of lateral inhibition, they show that the absence of Dll1 ahead of the neurogenic wavefront reduces the robustness of lateral inhibition, enhances neurogenesis and alters the shape of the neurogenic wavefront, predictions that are consistent with previous observations in the retina of mice in which Dll1 was conditionally mutated. The researchers propose, therefore, that Notch-independent Delta expression ahead of the neurogenic wavefront optimizes neurogenesis by preventing perturbations in lateral inhibition and wavefront progression.

Hedgehog signals modular bone growth

The vertebrate skeleton provides structural support and protection for vital organs but how its component bones acquire their unique shapes is unknown. Here (p. 2371), Charles Kimmel and colleagues investigate the genetic regulation of morphogenesis in dermal bones, which are formed by direct differentiation of mesenchymal cells into osteoblasts, by analyzing the development of the zebrafish opercle. The researchers report that the Hedgehog (Hh) family ligand Indian hedgehog a (Ihha) is specifically expressed in a population of osteoblasts localized along the growing edge of this craniofacial bone. Loss of ihha function reduces pre-osteoblast proliferation and bone growth, whereas hyperactive Hh signalling in mutants for the Hh receptor ptch1 has opposite effects. Time-lapse and live-imaging experiments show that ihha-dependent bone growth is region specific and begins at the start of a second phase of morphogenesis, during which the opercle acquires a more-complex form. These results suggest that dermal bone development is modular, with different genes functioning at specific times and locations to pattern growth.

Lymphangiogenesis goes lyve1

The lymphatic system regulates tissue fluid homeostasis, aids immunity and helps absorb dietary fat. Because aberrant lymphatic growth is associated with cancer metastasis and chronic inflammation, a better understanding of lymphangiogenesis could identify therapeutic targets for these and other lymphatic abnormalities. The major trunk lymphatic vessel in the zebrafish embryo is a well-established model of lymphangiogenesis but the rest of the zebrafish’s lymphatic system is poorly described. On p. 2381, Phil Crosier and colleagues remedy this situation by generating transgenic lines in which the promoter of lyve1 (which encodes lymphatic vessel endothelial hyaluronan receptor 1) drives lymphatic vessel expression of fluorescent reporters. The researchers generate a map of zebrafish lymphatic development and characterize facial, intestinal and lateral lymphatic vessel networks for the first time. They also describe a novel mechanism that underlies the development of the lateral facial lymphatic. These results show that lymphatic vessel formation in zebrafish is more complex than previously thought, thereby increasing the versatility of zebrafish as a model of lymphangiogenesis.

Making dopamine neurons: less Nurr1 later is more

In vitro differentiation of stem cells has the potential to generate specific cell types for clinical use but, to date, this approach has mainly created cells with unsatisfactory phenotypes. Now, Sang-Hun Lee and colleagues generate mature dopamine (DA) neurons from rat neural progenitor cells (NPCs; see p. 2447). Midbrain DA neurons, which are the main source of dopamine in the mammalian nervous system, are lost in Parkinson’s disease. Previous attempts to induce NPC differentiation into DA neurons through the forced expression of Nurr1, a transcription factor that is expressed during midbrain development, induced DA-specific marker expression but failed to generate mature DA neurons. Here, by using an inducible retroviral vector system to express less exogenous Nurr1, and at a later time point than used previously, the researchers generate morphologically and phenotypically mature DA neurons from NPCs. Adjustment of the levels and timings of the expression of cell type-specific transcription factors to match physiological conditions, suggest the researchers, could facilitate the in vitro generation of other useful cell types.

Endoderm conduit for LR signals

Establishment of the left-right (LR) body axis is a crucial step in embryogenesis. In mouse embryos, a leftward flow of fluid in the node establishes an initial LR signal, which is transferred to the lateral plate mesoderm (LPM) where it triggers the gene expression program responsible for LR asymmetry. But how is the LR signal transferred to the LPM? On p. 2426, Yukio Saijoh and co-workers test the hypothesis that endoderm (which lies next to the node and covers the LPM) is involved in this process. The researchers report that expression of LR asymmetric genes in the left LPM is greatly reduced or absent in most mouse embryos null for the Sox17 transcription factor, which exhibit endoderm-specific defects. Interestingly, membrane localization of gap junction connexin proteins is impaired and intercellular transport between endoderm cells is disrupted in Sox17^–/– endoderm. Together, these results suggest that endoderm cells, possibly via gap junction communication, play an essential role in the transfer of LR signals during mouse LR axis establishment.

Plus…

Tudor domain proteins in development

Toshie Kai and colleagues discuss the emerging roles of Tudor domain proteins during development, most notably in the Piwi-interacting RNA pathway, but also in other aspects of RNA metabolism, the DNA damage response and chromatin modification. See the Primer article on p. 2255

The Prdm family: expanding roles in stem cells and development

Prdm factors either act as direct histone methyltransferases or recruit a suite of histone-modifying enzymes to target promoters. In their review, Hohenauer and Moore discuss the roles played by these proteins in stem cells and throughout development. See the Review article on p. 2267

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This (last…) month, several posts on the Node were about publishing issues.

Ivan Oransky wrote a guest post to tell the story of why he and Adam Marcus started the blog “Retraction Watch“, which tracks retractions across the literature.

“There are 44% more papers published every year than a decade ago, but at least 10 times the number of retractions per year.
Why the rise? (…) a few trends have manifest themselves. Some of the increase is due to more visibility for papers thanks to online publishing, and to the advent of plagiarism detection software. But journal editors Ferric Fang and Arturo Casadevall have made convincing arguments that the harsh competitive environment in which scientists work today has tempted more researchers to cut corners and commit fraud.”

Another publishing trend was picked up right here in the Development offices, where Executive Editor Katherine Brown noticed that several authors painstakingly removed “dirt” from images.

“[T]he aim of the authors was to ensure that the images were easily interpreted, and that readers weren’t diverted from the data by the extraneous bits of stuff. This may seem innocent, but it could be the first step on a dangerous slope, at the bottom of which lie the clearly fraudulent activities of deleting the bits of data that don’t fit our hypothesis, or making up data that do.”

Alfonso Martinez-Arias also considers the pressure of publication in his review of the book “Wetware” by Dennis Bray. He recommends the book, and ends by stating that “Wetware is a gust of wind that should encourage you to sail into the current of the unknown, without fear, with the imagination that is denied by the current interest in publications rather than Discovery.”

But before we end this publication-focused section of the monthly summary, I do want to point you to the three editorials written by the former and current Editors in Chief of Development, to mark the journal’s 25th birthday. It’s a great overview of the history of Development, and reflects the rapid progression of the field of developmental biology.

Competitions
There are a few competitions currently ongoing on the Node. First of all, there’s our essay competition. It’s open to anyone with research experience in developmental biology. The winner will be published in Development, and all nominees will receive a £50 Amazon gift certificate. See the announcement for full details. There is still time to start writing, so if you know someone who might be interested (a colleague or student) who may not have seen this yet, please spread the word!

Then there is another voting round for Woods Hole course images. Which of these colourful images would make a good journal cover?

You also voted for images from another course, the International Course on Developmental Biology from Quintay in Chile. Of the eight images, you selected this arrangement of zebrafish embryos as winner:

Also on the Node
–Smart signalling in the developing brain
-Updates from the BSDB meeting (part 1, part 2) and an interview with poster winner Stephen Fleenor.
-Several new job postings.

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The winner of the previous round of images from the 2011 Woods Hole embryology course appeared on the cover of Development a few weeks ago. But which of the following will receive the same honour? It’s up to you to decide: vote in the poll below the images for the one you would like to see on the cover of Development. (Click any of the images to see a bigger version.) Poll closes on June 19, noon GMT.

1. Widefield image of a pilidium larvae of the Nemertean ribbon worm, Cerebratulus lacteus, stained for F-actin (green; phalloidin), Acetylated tubulin (red) and DAPI (blue; nuclei). This image was taken by Joseph Campanale, Aracely Lutes, and Stephanie Majkut.

2. Confocal image of Crepidula fornicata (slipper limpet) embryo stained for FMRF (yellow), Acetylated tubulin (green) F-actin (purple; phalloidin) and DAPI (blue; nuclei). This image was taken by Juliette Petersen and Rachel K. Miller.

3. Confocal image of squid, Loligo pealei, embryo stained for for F-actin (green; phalloidin), Acetylated tubulin (red), anti-HRP (yellow), and DAPI (blue; nuclei). This image was taken by Juliana Roscito.

4. Confocal image of squid, Loligo pealei, embryo stained for for F-actin (red; phalloidin), Acetylated tubulin (green), and DAPI (blue; nuclei). This image was taken by Lynn Kee.

(10 votes)

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Earlier this month, you voted for your favourite image from the International Course on Developmental Biology.

The winner, exactly 100 votes ahead of number 2, was this zebrafish embryo image:

The image shows six Sox10-GFP transgenic embryos, in which GFP and DAPI fluorescence are merged. The picture was taken by Mariana Herrera Cruz (Instituto de Biotecnología, UNAM, Mexico); the following people also contributed to prepare the sample: Juan Pablo Fernández (INSIBIO (CONICET-UNT), Argentina), Miguel Angel Mendoza (Instituto de Neurobiología, UNAM, Mexico), Paulette Fernández (UNAM, Mexico) and German Sabio (Leloir Institute, Argentina); all of them were students at the International Course on Developmental Biology, UNAB, Quintay-Chile, January 2012.

The zebrafish will appear on the cover of Development in a few weeks, so keep an eye out for that!

And get ready for the next round of images from Woods Hole, which will be up later this week.

(6 votes)

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Wake your labmates and tell your friends – abstracts are due by Friday June 1 June 15!

The meeting
The Santa Cruz Developmental Biology meeting will be held Aug 8-11. Since 1992, the SCDB has been one of the premier meetings in Developmental Biology. The 20th anniversary meeting continues its emphasis on innovative developmental biology, focusing on morphogenesis, cell polarity, evo-devo, development and disease, patterning, neurogenesis, regeneration and stem cells. The meeting will be held on the beautiful, sunny UC Santa Cruz campus and is designed to foster interactions among scientists from labs around the world, from beginning students to leaders in the field. We have 27 invited speakers, and 19 more speakers will be selected from the abstracts submitted.

SCDB Young Investigator Award
If you are a grad student, postdoc, or junior faculty, you’re eligible to be considered for the SCDB Young Investigator Award. The awardee will be selected based on his or her meeting abstract and CV. The SCDB Young Investigator Awardee will speak in the opening session along with our Keynote Speakers Marty Chalfie, Lee Niswander, and Eric Betzig!

More information…
See the meeting web site at www.scdb2012.com

See you in Santa Cruz!

(4 votes)

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It was a summer afternoon in 2010 when Adam Marcus and I had the phone conversation that led to the birth of Retraction Watch.

We had each been covering medicine and science for more than a decade, and we had come to realize that we shared an unusual obsession: Scientific retractions. We had both experienced what happens when, as a reporter, you peel back the curtains on a mysterious retraction notice. Sometimes, there’s a story so big, major newspapers have to pick up on your coverage, as The New York Times and others did when Adam broke the story of Scott Reuben, the anesthesiology researcher who was forced to retract 22 papers – and go to jail – thanks to fraud.

We also both felt strongly that most journals did a pretty terrible job of publicizing their mistakes. Those realities, taken together with the fun I had been having with my blog Embargo Watch, which I’d founded about six months earlier, prompted me to suggest that we start a blog to monitor retractions as a window into the scientific process.

Adam was enthusiastic, so we launched on August 3, 2010. We figured we’d post a few times per week, whenever we saw an interesting retraction notice and could dig into it. There were fewer than 100 retractions per year, after all.

We – and others who thought this would be an interesting but limited project — were wrong. (more…)

(6 votes)

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Have you started writing your essay yet? The Node and Development’s essay competition, “Developments in development”, is looking for essays in which you express your views about the future of developmental biology.

In this competition, you’re writing for other scientists, but you’re not writing a scientific paper. It’s an opinion piece. You can use facts to strengthen your cause, but ultimately it will be your persuasive writing that gets you a place on the shortlist or in the front section of Development.

Resources for science writers
If you’ve recently written mostly scientific papers, it might be hard to adjust your writing style, so we’ve found some websites with advice and tips to help you out.

The first is a collection of science writing tips on the Guardian, “Secrets of Good Science Writing”, which they published in the weeks leading up to their own essay competition. Not all of their advice will apply, because they focus on writing for non-scientists, but some of the basic writing tips from professional writers are very useful. For example, in one of their entries, Ed Yong analyses Carl Zimmer’s writing, and points out how he achieves pacing by varying sentence length. It’s one of my favourite writing tricks.

The second link is a website called The Open Notebook. It’s a resource for and by science journalists. They share tips and tricks that you might find useful while you are writing your essay, and they list even more resources that are worthy of further exploration.

Know your audience
The sites linked above focus on popular science writing, but you will, of course, be writing for an audience of fellow scientists. How is that different? In some ways, it might be easier. One of the most difficult things of popular science writing is gauging what your audience knows. You can’t explain too little, or they won’t understand; you can’t explain too much, or they’ll get bored. For the Node and Development’s essay contest, you won’t have to deal with this: you know your audience! They are developmental biologists, and you can assume that they all know at least as much as a first year PhD student in the field.

Keep your audience in mind, and look at some of the other writing tips we’ve linked to. You still have several weeks to write, but the sooner you start on your first draft, the more time you have to work on the details.

Good luck!

(Full contest info. Deadline for submission is July 2nd.)

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