The 4th international chick meeting will be held in Sendai, Northern Japan, from August 29th to September 2nd, 2011. The meeting aims to build on previous meetings consolidating the links between the different disciplines within the bird community, exploring new frontiers in avian research and developing key community resources. The program is still being finalized, but session topics are listed on the website, and we are really happy that the plenary lecturers have all accepted. Despite the packed schedule, there will be plenty of chances for informal interactions, and break-out meeting. You can download the poster here.

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Just a quick roundup of some interesting bits of news.

Embryo research in France
This one’s rather interesting to read together with the interview with Margaret Buckingham we posted last week. France has very strict regulations in place for research on embryos or ESCs. Now, Nature reports that researchers in France are urging their government to authorize ESC/embryo research.
(This will be an interesting story to follow. If you’re in France, are you affected by this regulation? If so, would you like to write about it on the Node? Get in touch if you’d like to keep your colleagues around the world in the loop.)

EMBO installation grants
In December, EMBO announced that they’ve awarded Installation Grants to six researchers, allowing them to set up research groups in the Czech Republic, Poland, Portugal and Turkey. Many of the recipients are working, or have worked, in areas related to developmental biology: Szymon Świeżewski and Tomasz Wilanowski set up labs in Poland to study ncRNA-based gene regulation and Grainyhead-like transcription factors respectively. Alena Krejčí is starting a group in the Czech Republic to study Notch signalling in cellular metabolism, after a postdoc with Sarah Bray in Cambridge, and Cory Dunn moved to Turkey to work on mitochondrial DNA damage after a postdoc with Iva Greenwald at Columbia.

Research Blogging
We found a nice blog post about a Development paper on the Sanford-Burnham blog, with interviews with the authors. It’s also listed on Research Blogging – a site that indexes blog posts about peer reviewed research.
If you search for “developmental biology” on Research Blogging, you’ll find a few familiar posts, as we use this on the Node as well. We love to hear your stories behind papers (in any journal), and if you don’t have your own (or institutional) blog, you’re more than welcome to use the Node to show off your work.

Heard any other news that the Node should cover? Please sign up and post it yourself, to prevent delays

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On January 12th, about three quarters of the Australian State of Queensland was flooded as local rivers and creeks overflowed from rainfall. Needless to say, it’s been an extremely wet summer. One victim was the University of Queensland, which still stands next to the Brisbane River, the cause of the city of Brisbane’s troubles. Flood waters receded on January 14th.

To clarify, I’m not in Brisbane’s University of Queensland, but many other students are.  A few thousand in fact.To keep everyone in the loop, UQ students have a blog on the University’s website. the latest post from January 13th comes just after the flood reached record highs on their St. Lucia campus (they have several other campuses in other areas). It’s aim was to be informative to students on and off campus. Details include which buildings were affected, university closure dates, who to call if you need counselling etc. Rest assured, no biological buildings were harmed in the flooding.

In a quote from the chancellor, water levels reached those of recording breaking 1974. In the university news website, Brisbane has only experienced massive flooding 2x in its history, once in 1893, the other in 1974. It can now add 2011 to the short list.

(Tad jealous, if only the ANU had a student run blog too. On the other hand, happy to be missing out on the excitement up at UQ.)

UQ also keeps a Flickr photostream, with images of the recent flooding and clean-up. Click here

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(This interview originally appeared in Development)

Margaret Buckingham is Professor in the Department of Developmental Biology at the Pasteur Institute in Paris and she is also the current President of the French Society of Developmental Biology (Société Française de Biologie du Développement, SFBD). We spoke with her about the role of the SFBD and about ongoing changes in the French research system.

What is your laboratory currently working on?

We work on skeletal myogenesis and cardiogenesis. The skeletal myogenesis research involves studying gene regulatory networks that govern cell fate choices and the entry into the myogenic programme in the embryo, as well as satellite cell behaviour during muscle regeneration in the adult. For cardiogenesis, work involves examining the second heart field and lineages that contribute to different parts of the heart. We’re also interested in cardiac morphogenesis, and how the chambers of the heart are shaped as development proceeds.

How long have you been President of the SFBD?

I’ve been President since 2006; the term is for 3 years, renewable once, so that after 6 years somebody else should take over.

How old is the society?

There was originally a much older society in France called the Société de Biologie, that was founded in the 19th century and still continues today. The actual French developmental biology society was set up in the 1980s.

What does the SFBD do for its members?

One of our main activities is the annual meeting, which is very important and which brings together all of the developmental biology community in France. We very often hold that annual meeting as a joint meeting with another developmental biology society. For example, next year our annual meeting will be in Nice with the British Society for Developmental Biology, this year it was in Paris with the Japanese society, last year it was in Toulouse with the Spanish society. So this is tradition.

We also have smaller meetings like one with the French Genetics Society on microRNAs in plant and animal development in December 2010.

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Last week (January 19), stem cell pioneer Ernest McCulloch died at the age of 84. Together with James Till, McCulloch discovered stem cells in the 1960s. For their work, the pair won the Gairdner Award in 1969 and the Lasker Award in 2005. McCulloch was professor emeritus of the University of Toronto and former Director at the Ontario Cancer Institute at the Princess Margaret Hospital in Toronto. See the news article on UofT’s website for more information.

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Here are the research highlights from the current issue of Development:

New moves in haematopoiesis: rumba and samba

Vertebrate haematopoiesis relies on a pool of haemetopoietic stem/progenitor cells (HSPCs) that can self-renew and differentiate into all haematopoietic lineages. But what are the molecular mechanisms that regulate this process? Here, Zilong Wen and co-workers (p. 619) identify two novel factors that regulate zebrafish HSPC maintenance. During zebrafish development, HSPCs originate from the ventral wall of the dorsal aorta (VDA), migrate to the caudal haematopoietic tissue (CHT) and finally colonise the kidney. The researchers isolated and characterised two haematopoiesis-deficient mutants, rumba^hkz1 and samba^hkz2. In these mutants, HSPC specification in the VDA and subsequent homing to the CHT are normal, but further HSPC development within the CHT is compromised. Using positional cloning, they show that Rumba is a novel nuclear C2H2 zinc-finger protein and that samba encodes a protein that is homologous to human augmin complex subunit 3 (Haus3). Both factors, they report, act independently and cell-autonomously to regulate cell cycle progression in HSPCs, and thus are essential regulators of zebrafish haematopoiesis.

Pancreatic Hh signalling: a play in two acts

In amniotes, inhibition of hedgehog (Hh) signalling in the early embryonic endoderm is a prerequisite for pancreatic specification. By contrast, loss of Hh signalling in zebrafish severely disrupts pancreas development, suggesting opposite roles for Hh signalling in fish versus mammalian pancreas organogenesis. Zahra Tehrani and Shuo Lin (p. 631) now reconcile these contrasting functions by showing that the Hh pathway plays distinct roles during various stages of zebrafish pancreas development. Using genetic and pharmacological approaches to temporally modulate Hh activity, they show that Hh activity during early gastrulation is essential for the subsequent migration and differentiation of pancreatic precursors. This positive role of Hh acts to restrict Bmp signalling and to promote β-cell differentiation. By the end of gastrulation, they report, Hh signalling adopts a negative role by antagonizing retinoic acid (RA)-mediated induction of endocrine pancreatic precursors. These findings highlight sequential roles for Hh signalling in pancreas development and uncover antagonistic relationships between the Hh, Bmp and RA pathways during pancreas organogenesis.

Sox9+ progenitors make β-cells in embryo but not in adult

All pancreatic cell types, including insulin-producing β-cells, arise from pancreatic progenitors during embryonic development, but whether the adult pancreas contains β-cell progenitors remains a controversial issue. Using fate-mapping studies in mice, Maike Sander and colleagues (p. 653) now demonstrate that cells positive for Sox9 give rise to β-cells during embryogenesis, but not in the normal or injured adult pancreas. They generated Sox9CreER^T2 mice in which Sox9-expressing cells can be accurately and temporally labelled. Lineage tracing shows that these cells can generate all pancreatic lineages during embryogenesis. By contrast, they report, endocrine and acinar cell neogenesis from Sox9-positive cells does not occur in the adult pancreas. Using partial duct ligation (PDL) to induce pancreatic injury, they also show that Sox9-positive cells do not generate β-cells following injury; PDL initiates pre-endocrine programs but not complete β-cell differentiation. Given the increasing use of PDL as a model to study β-cell regeneration, these studies provide important insights into the specification and regeneration of β-cells.

The first author of this paper has also written a post about these exciting discoveries.

engrailed links Hh and Bmp muscle development signals

Myotome morphogenesis requires the specification of distinct muscle cell types. In zebrafish, the specification of medial fast-twitch fibres (MFFs) and slow-twitch muscle pioneers (MPs), both of which express engrailed (eng) genes, is regulated by hedgehog (Hh) signalling but the mechanistic basis of this regulation is unclear. On p. 755, Philip Ingham and co-workers demonstrate that the eng2a promoter integrates repressive and activating signals from the Bmp and Hh pathways, respectively, to limit its expression to MFFs and MPs during zebrafish myotome development. The researchers identified a minimal element in the eng2a promoter that can drive reporter gene expression specifically in MFFs and MPs. This element binds both Gli2, a mediator of Hh signalling, and activated Smads, mediators of Bmp signalling. They demonstrate that Hh activity antagonises Smad activation in myotomal cells and, conversely, that aberrant Smad activation suppresses eng2a expression. Their studies identify novel crosstalk between the Hh and Bmp pathways that may be mediated by direct interactions between Gli and Smad proteins.

Non-embryonic Nodals orchestrate early development

Vertebrate development and patterning require Nodal signalling. However, the upstream inducers of Nodal expression and the relative contributions of Nodal ligands from embryonic, extraembryonic and maternal sources to embryogenesis are unclear. Now, Benjamin Feldman and co-workers show that non-embryonic sources of Nodal-related ligands, activated in part by the transcription factor Mxtx2, account for the spectrum of zebrafish early Nodal signalling events (p. 787). They report that Mxtx2 activates and is required for the expression of nodal-related 2 (ndr2) in the yolk syncytial layer, an extraembryonic tissue, thus identifying a novel upstream component of Nodal signalling. They further demonstrate that the co-disruption of extraembryonic ndr2, extraembryonic nodal-related 1 (ndr1) and maternal ndr1 recapitulates Nodal mutant phenotypes: embryos show a loss of endoderm and anterior mesoderm specification. Based on their findings, the authors propose that endoderm and anterior mesoderm specification during zebrafish development is executed by a failsafe mechanism involving the combined action of non-embryonic Nodal-related ligands, and that this mechanism may be relevant to higher vertebrates.

Plus…

Technical advances, together with increasing collaborations between experimentalists and theorists, have highlighted the importance of stochasticity in cell and developmental biology. As reviewed by Andy Oates, this was explored in detail at the Company of Biologists’ recent workshop in Windsor, UK. See the Meeting Review on p. 601

Also see the earlier post by Fernando Casares about this meeting

(1 votes)

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In a follow up to Eva’s first post in our alternative careers series about how a research background in developmental biology can lead to a career path that lies outside of research, I hope that my description here of how I made the move from a PhD in developmental genetics to a career in publishing will be of use to anyone else out there in the community who is considering making a similar move.

My journey in science began with an undergraduate degree, not in genetics, but in pharmacology at King’s College, London, where the most important thing I learned was that I was much more interested in genetics and development than I was in pharmacology, interests that led me to a PhD with Ian Jackson and Cathy Abbott at the MRC Human Genetics Unit in Edinburgh. From there, I became a post doc in Val Wilson’s lab.

At the time of my PhD, Ian was a regular contributor to the journal club section of Trends in Genetics, and when short on time, he would ask me to write these brief pieces on a paper of interest in his place. I came to enjoy this writing exercise and, as a result of it, was offered other writing opportunities, such as summarizing new mouse knockout phenotypes for a knock out database then under development at BioMedCentral. (In fact, one of the journals I had to check every month for new knock out papers was Development.)

As my fondness for writing grew, another opportunity arose towards the end of my PhD that helped me to choose between the different career paths I was starting to consider: research, science journalism, or a job in science publishing. This opportunity took the form of a Media Fellowship from the British Science Association. These fellowships place British scientists with a media organisation for a couple of months, where they learn to work within the constraints of the media to produce interesting stories about science. I was placed with the Guardian, a national daily newspaper in the UK, where I spent several weeks under the tutelage of Tim Radford,  who was its science editor at the time. Under the guidance of Tim’s red pen, I wrote science-related stories covering a wide range of topics, from archaeological discoveries (see picture), to cancer, and even about why Mozart had such a foul tongue (he had Tourette’s, so the story went). I also had many a story ‘spiked’ by the news desk editor, when it failed to pass the “so what?’ barrier that most science-related stories have to pass. This experience taught me several important things: how to write concisely and engagingly about science; about the constraints that journalists work under; and about the importance of scientists learning to communicate clearly and succinctly with the media about their work. But it also left me a little disheartened about the difficulties of getting good science stories covered, even by a reputable newspaper such as the Guardian, when they have to compete for space with stories about politics, crime and celebrity gossip, all of which have a more tangible ‘human interest’ angle for most news desk editors.

As a BSA media fellow, you write about whatever story is sent your way

As a result, I returned to the lab knowing that a career in science journalism was probably not for me while suspecting that my scientific interests were too broad to remain in research. But first I needed to give research a proper chance because to leave it felt like an irreversible decision not to be taken lightly. I have never regretted my time as a post doc; I learned much about embryology from Val, which has stood me in good stead to this day. My postdoc also broadened my scientific horizons and contacts, while giving me time to learn more about career options in publishing.

In time, I successfully applied for the job of assistant editor at Trends in Molecular Medicine (TMM), having heard good things about the Trends journals while writing for them as a student. I joined the office in Cambridge, which became a training ground for a generation of British editors, many of whom still work in publishing today. From feedback on my application, it became clear that I was offered this post because my CV showed that I was demonstrably interested in writing and in science communication; skills that complemented my role on TMM, where I assisted with developmentally editing reviews and was responsible for copyediting the content of the journal, while occasionally writing news stories for its front section and being dispatched to do live conference reporting for BioMedNet. It was a great first job in publishing, but not, as I subsequently discovered, what I really wanted to be, which was a commissioning editor. And so within a year of being recruited to TMM, I successfully applied for the role of Editor of Trends in Genetics, where I began to learn properly, for the first time, the job of a commissioning editor.

I have at heart been a commissioning editor ever since. In science publishing, a commissioning editor’s job is to determine the content of a journal, book or journal section and then to invite people – such as scientists, science writers and commentators, to write for their publication. The commissioning part of the job requires an editor to travel widely to conferences and to keep in close contact with their field, so that they can identify the topics that are the hottest and most interesting to commission articles on. The editorial part of the job comes in developmentally editing articles to improve their focus, structure, scientific content and accessibility and in making editorial decisions about whether a manuscript should be revised, accepted or rejected in response to the reviewers’ and your own editorial assessment of it.

My own experience as a commissioning reviews editor was further strengthened when I moved from Trends in Genetics to Nature Reviews Genetics,where I joined Mark Patterson and Tanita Casci to launch NRG as one of the first Nature Reviews journals. Launching NRG was a hugely exciting project that taught me not only a fantastic amount about genetics from working with Mark and Tanita and our many great authors, but also how to launch a journal from scratch. When Mark stood down as Editor in Chief of NRG, I successfully applied for this role and from this position moved to Development: my first experience at managing a primary research (and not-for-profit) journal.

My signed copy of the launch issue of NRG

As Executive Editor of Development, I wear many hats: I manage the in house journal team, and commission and handle reviews and other front section articles, together with Seema Grewal, the journal’s associate reviews editor. I also work closely with Development’s Editor in Chief, first Jim Smith and now Olivier Pourquie, and our team of dedicated scientific editors in handling papers and author queries, and in developing the journal editorially. I am also responsible for the journal’s online presence. And in response to a Development readers’ survey in 2009, I kick started another new and exciting launch project that, once we had Eva on board, came to fruition as this: the Node, which I had the honour of naming.

Being a managing and commissioning editor is a highly interesting and rewarding role. As an editor, you learn about new scientific findings every day and have to assimilate a lot of new information quickly, and you work within a wider community, building sometimes long-standing relationships with researchers, authors and reviewers. I’m particularly fortunate in having the developmental community to work with, a community I’ve found to be tremendously collegial. And, occasionally, I’m asked to do other fun things, such as speaking at meetings about publishing and interviewing speakers at the CSHL symposia.

Getting that first foothold in publishing is by far the hardest, most competitive step of all. I was successful in making this initial move by being able to demonstrate my enthusiasm for writing about and communicating science, and by having gained experience while still in research that significantly strengthened my application for my first editorial job. Other Editors, particularly primary manuscript editors who mainly handle research papers, may  have taken different paths from research to publishing, and it’s our hope that they will also share those different career paths and their experience with you here on the Node.

(8 votes)

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The Node’s staff has kindly given me the opportunity to write a background piece, placing into context the results of our studies described in the paper, “Sox9⁺ ductal cells are multipotent progenitors throughout development but do not produce new endocrine cells in the normal or injured adult pancreas” (released today in Development; http://dev.biologists.org/lookup/doi/10.1242/dev.056499).

For many years, debate has raged in the pancreas biology field as to the source of new insulin-producing beta cells in the adult pancreas, both in healthy and injured states. This is a topic of great interest as many groups around the world are engaged in the quest to repopulate functional beta cell mass in diabetic patients, either through transplantation of hESC/iPSC-derived beta cells, or by stimulating growth of residual beta cells in such patients. Manipulating endogenous pathways of beta cell regeneration, should they exist, might prove to be one avenue of curing diabetes. Thus, this is a hot-button topic.

In 2007, when I joined Dr. Maike Sander’s laboratory, the diabetes field was heatedly pursuing the question of whether or not new beta cells can arise from pancreatic ducts. The possibility that ducts might harbor facultative progenitor cells capable of producing beta cells upon stimulation energized many labs to do experiments to test this theory.  All of this attention was mainly due to studies that observed beta cells closely juxtaposed to pancreatic ducts after pancreatic injury (Gu et al., 1994). This was complemented by exciting data showing that Ngn3, an endocrine progenitor marker, is re-expressed in the ductal epithelium of beta cell regenerative models, such as partial duct ligation (PDL) (Xu et al., 2008). Yet another study, published by Rovira and colleagues, demonstrated that cells at the very end of the ductal tree (centroacinar/terminal duct cells) could be isolated from mice and behave like progenitors cells in the dish as well as differentiate correctly in an embryonic environment (Rovira et al., 2010). These findings all pointed to pancreatic ductal cells as a source of new pancreatic beta cells. That is until groups started to create and test CreER mouse lines with expression specifically in ductal cells (Furuyama et al., 2010; Kopinke et al., 2011; Kopinke and Murtaugh, 2010; Means et al., 2008; Solar et al., 2009) in the hopes of tracing duct-derived beta cells. I am a part of one of those groups.

Sox9creER labeled pancreatic ductal tree

In our group, we created a Sox9-driven CreER^T2 BAC transgenic mouse line and were thrilled to find that we could efficiently and exclusively label the pancreatic ductal tree in the adult Sox9CreER^T2;R26R^LacZ mouse (show picture). Given that the Sox9CreER^T2 transgene labeled such a large percentage of ductal cells (~70%), we felt confident that if any beta cells arose from the ductal compartment after PDL, we would be the group to detect it. Therefore, I teamed up with Claire Dubois, a graduate student in Dr. Sander’s laboratory, to perform PDL on tamoxifen-injected Sox9CreER^T2;R26R^YFP mice. As predicted by Xu et al. (2008), we observed a large increase in Ngn3 mRNA in the ligated pancreatic lobe and a low signal for Ngn3 expression was found in duct-like foci derived from Sox9⁺ ductal cells after PDL. Much to our surprise though, PDL did not induce the production of new beta cells from lineage-labeled ductal cells. This suggests that Ngn3 expression is initiated in Sox9⁺ cells after PDL, but the presence of Ngn3 is not sufficient to initiate endocrine differentiation. Therefore our findings and the majority other studies published thus far do not support the hypothesis that adult pancreatic ductal cells contribute to the endocrine compartment during normal aging or after PDL.

Because many studies, including our study published today, agreed that acinar cells are maintained by self-replication and are not produced by other cell types (Desai et al., 2007; Jensen et al., 2005), I had focused on the question of endocrine neogenesis in the pancreas. However, Furuyama and colleagues recently created a knock-in Sox9^IRES-CreERT2 mouse line and showed that Sox9⁺ cells can produce acinar, but not endocrine cells, in the adult mouse (Furuyama et al., 2010). How do we explain the discrepancy between their findings and ours? While we don’t fully understand the reason, small, but possibly significant, differences in the experimental design could provide an explanation. The tamoxifen doses used by Furuyama and colleagues were extremely high and resulted in labeling of acinar cells upon tamoxifen administration. Likewise, we observed patchy acinar cell labeling with our highest dosage of tamoxifen. It is possible that acinar cells express Sox9 at low levels, but recombination only occurs when the concentration of tamoxifen reaches a certain threshold. However, with the tamoxifen dosages used in our study the percentage of labeled acinar cells did not increase during the chase period. As it is unclear how long CreER remains active after very high dosages of tamoxifen, it is possible that rather than arising from Sox9⁺ ductal cells, in Furuyama’s study acinar cells are continuously labeled for an extended period of time after the tamoxifen pulse. Thus, additional studies showing results similar to those of Furuyama et al. will be necessary before it can be concluded that ductal cells contribute widely to the production of acinar cells.

Does this mean that ductal cells are not capable of producing other pancreatic cell types? The ability of ductal cells to form endocrine and acinar cells during development and the ex vivo analysis of terminal duct/centroacinar cells (Rovira et al., 2010) would suggest that ductal cells can be multipotent under the right circumstances. Therefore, future comparisons of the embryonic and adult ducts, as well as their microenvironments, may provide the key to turning a duct cell into an acinar or beta cell.
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(8 votes)

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Is this Monday not quite giving you the results you were hoping for? Cheer up with a few science music videos.

This one, “Bad Project”, is being emailed around rapidly among scientists worldwide, so there’s a good chance you’ve already seen it. If not, it’s worth a watch for the costumes (made of lab supplies!) and dance moves alone.

The next video is a bit older, but a lot more positive about research, and an ode to a famous evo devo model organism.

Both videos were products of departmental science variety shows or contests. “Bad Project” was a submission for a Molecular and Human Genetics Retreat 2011 at Baylor College of Medicine, and “Bringin’ Stickleback” was a submission for the 2009 “MCB Follies” at the Department of Molecular and Cell Biology at UC Berkeley).

Have any of you ever made a video (music or otherwise) with or in your labs? Would you like to? (Asking for a reason, so please do share your thoughts. I’m looking at you, students and postdocs. You there, with your eye on the lab timer, reading the Node while waiting for your experiments… Have you ever filmed something in your lab?)

(5 votes)

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A friend of mine went straight from his PhD in computational (pharmaco)chemistry to an investigator position, and I have heard an unconfirmed second-hand story of one other person recently making this transition in a life science related area. But by and large, most PI jobs require that you have done at least one postdoc, and the suggestion of people skipping this stage entirely seems like an urban myth. Historically, however, a PhD degree is itself enough for an academic position, and in several fields (most notably the humanities) this is still the case.

By requesting applicants to do one or more postdocs, the need for them is propagated further, but the NIH is now trying to break the mold by introducing a grant specifically meant to skip your postdoc. They describe it as follows:

“Although traditional post-doctoral training is likely most appropriate for the majority of new Ph.D.s and M.D.s, there is a pool of talented young scientists who have the intellect, scientific creativity, drive and maturity to flourish independently without the need for traditional post-doctoral training. Reducing the amount of time they spend in training would provide them the opportunity to start highly innovative research programs as early in their careers as possible. “

Of course, this still requires them to find an institute that will hire them without the ubiquitously desired “postdoctoral research experience”, but arriving at the door with an NIH grant under your belt should help.

The deadline for this new grant is this Friday. Are any of you applying? What do you think of this idea? Let us know via the poll below.

(poll closed and archived)

(2 votes)

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