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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Here are the highlights from the current issue of Development:

Mechanical changes in cochlea development

Correct patterning of the mammalian inner ear sensory epithelium, which contains mechanosensory outer hair cells (OHCs) that detect and amplify sound vibrations and non-sensory supporting cells such as pillar cells (PCs), is essential for hearing. The cell surface mechanical properties of both OHCs and PCs are important for their function but how are these properties regulated during development? On p. 2187, Katherine Szarama and colleagues use atomic force microscopy to show that OHCs and PCs have different cell surface mechanical properties that develop over different time courses. By pharmacologically modulating cytoskeletal elements, they show that the increase in OHC stiffness observed during development depends primarily on actin whereas the development of the cell surface mechanical properties of PCs depends on microtubules. In addition, they report that fibroblast growth factor signalling regulates the developing cell surface mechanical properties of OHCs and PCs, in part by altering cytoskeletal dynamics. These new insights into inner ear development may eventually lead to better treatments for hearing loss.

Resetting after quiescence

During development, networks of regulatory genes control precisely timed sequences of developmental events. In C. elegans, heterochronic genes, which encode several transcription factors and microRNAs (miRNAs) that regulate the expression of these transcription factors, control stage-specific cell-fate decisions. Under adverse conditions, however, second larval stage (L2) worms enter a quiescent state called dauer. Intriguingly, when conditions improve, dauer larvae complete development normally. Here (p. 2177), Xantha Karp and Victor Ambros investigate how cell-fate progression is reset after dauer. Progression from L2 to L3 requires downregulation of the transcription factor Hunchback-like-1 (HBL-1), and, during continuous development, HBL-1 downregulation relies mainly on three let-7 family miRNAs. However, after dauer, the researchers report, lin-4 miRNA and an altered set of let-7 family miRNAs downregulate HBL-1. This shift in the programming of HBL-1 downregulation, they propose, involves the enhancement of lin-4 and let-7 miRNA activity by miRNA-induced silencing complex (miRISC) modulators. The employment of alternative genetic regulatory pathways can, therefore, ensure the robust progression of cell-fate specification after temporary developmental quiescence.

ExE progenitors make an eXit

In female mammalian embryos, inactivation of one of the two X chromosomes in each cell regulates X-linked gene expression. X chromosome inactivation (XCI) is dependent on the non-coding RNA Xist, which is expressed from and coats the inactivated X chromosome. Inheritance of a paternally derived Xist mutation causes embryonic lethality because the inactivation of the paternally inherited X chromosome that occurs in the extra-embryonic lineages of female mouse embryos during imprinted XCI fails. Now, Terry Magnuson and colleagues (p. 2130) describe the exact consequences of failed XCI within the extra-embryonic ectoderm (ExE). The ExE of X/X^Xist– embryos consists mainly of differentiated giant cells and their progenitors, they report, and less differentiated spongiotrophoblast precursors are not maintained. At E6.5, the ExE lacks CDX2, which is required to maintain the ExE’s multipotent state. Moreover, trophoblast stem cell lines derived from X/X^Xist– blastocysts completely reverse normal imprinted XCI patterns. These results suggest that dosage compensation is indispensable for the maintenance of trophoblast progenitors and that imprinted XCI is probably erased in ExE cells.

Gibberellin regulation of flowering

Several environmental cues, including day length, and endogenous developmental signals regulate the transition from leaf production to flower formation in plants. In Arabidopsis, the growth regulator gibberellin promotes this transition most strongly under short day (SD) conditions. Here (p. 2198), George Coupland and colleagues show how gibberellins also promote flowering in response to long days (LDs). The researchers deplete gibberellins in the vascular tissue or the shoot apical meristem by tissue-specific overexpression of GA2ox7, which catabolises gibberellins. Under LD conditions, gibberellins are needed in the vascular tissue to increase production of a systemic signal that is transported from the leaves to the meristem during floral induction. However, in the meristem, instead of activating the expression of the transcription factor SOC1 (which is needed to induce flowering under SD conditions), in response to LDs, gibberellins regulate the expression of SPL transcription factors, which are needed later during floral induction. Thus, the researchers conclude, gibberellins play spatially distinct roles in promoting flowering under long photoperiods.

Migrating primordial germ cells exploit endoderm remodelling

Cell migration through epithelial tissues occurs during development, infection, inflammation, wound healing and cancer metastasis. But how do cells overcome the impermeable junctions between epithelial cells? Leukocytes move out of blood vessels by loosening endothelial cell-cell junctions but do all cells actively remodel tissue barriers during migration? According to Jessica Seifert and Ruth Lehmann, who are studying Drosophila primordial germ cell (PGC) migration through the endodermal epithelium to the gonadal mesoderm, the answer to this question is no (see p. 2101). Although PGC migration requires activation of the G protein-coupled receptor Trapped in endoderm 1 (Tre1) within PGCs, the timing of PGC migration is dictated by the developmental stage of the endoderm. Now, using live imaging and genetic manipulation, the researchers show that PGCs take advantage of developmentally regulated epithelial remodelling, which causes discontinuities in the endoderm, to gain access to the gonadal mesoderm. Thus, Seifert and Lehmann conclude that, rather than actively remodelling tissue barriers, some migrating cells exploit existing tissue permeability.

Tcf21 seals cardiac fibroblast fate

The primary source of cardiac fibroblasts, which are essential for normal heart physiology, is a subpopulation of epicardial cells that has undergone epithelial-to-mesenchymal transition (EMT) and entered the myocardium. But does cardiac fibroblast specification occur early in the formation of the epicardium (which is a multipotent mesothelial layer of cells that spreads over the developing myocardium) or after the epicardial-derived cells have entered the myocardium? Here (p. 2139), Michelle Tallquist and colleagues resolve this puzzle by investigating the role of the transcription factor Tcf21 in cardiac fibroblast specification in mice. The researchers use lineage tracing to show that Tcf21-expressing epicardial cells are committed to the cardiac fibroblast lineage before the initiation of epicardial EMT. Moreover, Tcf21-null embryos fail to develop cardiac fibroblasts and Tcf21-null fibroblast progenitors do not undergo EMT. These results indicate that cardiac fibroblast specification occurs in the epicardium before EMT occurs and, importantly, these findings identify Tcf21 as an essential transcription factor for cardiac fibroblast cell-fate determination.

Plus…

X chromosome inactivation in the cycle of life

Bakarat and Gribnau review new insights into the molecular events occurring during the life cycle of X chromosome inactivation and, in the accompanying poster, provide an overview of the mechanisms regulating X inactivation and reactivation.

See the Development at a Glance poster article on p. 2085

Evolutionary crossroads in developmental biology: cyclostomes

Shimeld and Donoghue summarise the development of cyclostomes (lamprey and hagfish) and discuss how studies of cyclostomes have provided important insight into the evolution of fins, jaws, skeleton and neural crest.

See the Primer article on p. 2091

(note that this article is part of a series of Primer articles on organisms that represent an evolutionary crossroads in the study of evolutionary developmental biology – see the online Featured Topic to view other articles in this series)

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Postdoc position available at School of Natural Sciences and Regenerative Medicine Institute (REMEDI), National University of Ireland, Galway, to study the molecular mechanisms that control pluripotency and early lineage commitment in stem cells of the cnidarian Hydractinia. This animal is an established cnidarian genetic model organism, amenable to gene expression analysis and manipulation and classical genetics.

The successful candidate will have a PhD in developmental biology, cell biology, molecular biology or related area.

The position is available for 2 years in the first instance. Starting date will be September 2012 or shortly thereafter. Salary will be €38,286 per annum.

For further details please go to http://www.nuigalway.ie/about-us/jobs/ or to the lab webpage at http://www.nuigalway.ie/frank . To apply, email cover letter, CV and the names and contact info for 2-3 references to Dr. Uri Frank at uri.frank@nuigalway.ie .

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How much does it matter that the images we publish are neat and tidy? It’s a question I’ve been dealing with over the past couple of weeks, and I wanted to share some thoughts. Here at Development, as at many journals, we check all figures before publication to try and identify potentially inappropriate image manipulation. Whenever we do come across a figure that doesn’t comply with our guidelines on image processing, we contact the authors to ask for clarification, request that the author provides us with the original data – so we can check that nothing fraudulent is going on – and often also ask that the final figure be changed to properly represent the original data. I’m happy to say that problems are few and far between, and that those issues I have come across in the short time I’ve been here have been more a case of beautification than of fraud. But is it okay for authors to ‘clean up’ their images with Photoshop paintbrush tools or the like: not touching the data itself, but rather getting rid of specks of dust or extraneous bits of tissue that are there on the slide?

The images shown here don’t come from any paper, but have been kindly provided by a researcher to illustrate what I’m talking about.

This is a Drosophila wing disc, where clones of cells are marked with GFP, and the entire disc stained with phalloidin in red. Very often in preps like this, you get bits of irrelevant tissue associated with the disc on the slide. But this one looks very clean, right? Wrong. Here’s the original version – you can see that there’s a piece of trachea, stained red, off the left side of the wing disc.

So, thinking that this bit of extraneous tissue is problematic, the researchers have taken the simple solution of photoshopping it out: something that’s very clearly revealed by the standard checks we run on our figures: as shown here.

I’ve seen a seen a few of these cases recently, and in each, the 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. Journal guidelines are (or at least should be) pretty unambiguous, and the case above falls foul of this statement taken from our Guide to Authors: “Unacceptable manipulations include the addition, alteration or removal of a particular feature of an image, and splicing of multiple images to suggest they represent a single field in a micrograph or gel.” So while it may seem innocuous, it’s not permitted. Nor is it, at least to my mind, in any way necessary: are we really that easily distracted? Does that little bit of trachea really stop us from seeing the clones in the wing disc? It’s been pointed out to me that the image above could have simply been re-cropped to remove the offending tissue, and if it’s okay to do that, why isn’t it okay to selectively black out those parts of the panel? That’s a reasonable point, and selective cropping is an issue to which I’m not convinced there is a straightforward answer. But I’m guided by the basic principle that the presented data should accurately reflect what you saw down the microscope or on the blot or whatever, and that what may seem irrelevant to you (a higher molecular weight ‘background’ band on your Western) might actually be important to someone else (“Oooh look – this might be a post-translational modification of my protein”).

I well remember from my time in the lab the agony of discovering that the perfect picture was ‘ruined’ by a bit of fluff to the side of the embryo, or because the vibrotome knife had left streaks across the section. And then spending hours re-mounting or re-sectioning to avoid these imperfections. But we all know that science can be an inherently messy endeavour: cells don’t grow in neat rows, and Western blots often give us background bands. So why do we need to hide this when it comes to publication? Of course, it’s vital that the data are clearly presented and understood, but what’s most important is that they accurately represent the experiment, and there’s a danger of losing sight of this in the desire for a beautiful image.

Initiatives like publishing all the uncropped blots that have gone into making the figures in a paper (as pioneered by Nature Cell Biology) are aimed at addressing this issue: by all means show only the relevant bit of the blot in the main figure, but for those interested in the (literally) bigger picture, the whole thing – warts and all – is available. But it can be a pain to find and assemble these files, and we don’t want to make publishing harder than it already is – although there’s a school of thought that says if you can’t lay your hands on the original data, you need to be better at archiving it in the first place!

So what do the Node readers think? Have you been tempted to ‘prettify’ your data for publication, or have you actually done it? Are our guidelines clear enough on what you can and can’t do? Do you support initiatives to make the raw data available to the reader, or is it all too much of a hassle? We’d really love your input on what kind of requests or demands a journal should make in terms of data presentation, so please answer the poll below (it’s completely anonymous!) and give us your feedback in the comments section.

Katherine Brown is the Executive Editor of Development

(4 votes)

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