In a paper published today in Cell, Detlev Arendt, Raju Tomer and colleagues reveal evidence that the cerebral cortex evolved much earlier than previously believed. Using a new technique to detect and image simultaneously expressed genes in a compact brain area, they discovered that the gene expression patterns in the olfactory processing region (mushroom bodies) of the marine worm Platynereis dumerilii are strikingly similar to that of the vertebrate cerebral cortex – too similar to have evolved independently. The last common ancestor of Platynereis dumerilii and vertebrates lived around 600 million years ago, which means that the origin of our cerebral cortex can be traced back to the Precambrian era.

Previous studies that compared brain regions between different organisms would look at shape and location of the tissues, and found no cortex-like structure in any invertebrates – not even those more closely related to us than Platynereis is. To see the similarities between the worm brain and the vertebrate cortex, Raju Tomer developed a technique called cellular profiling by image registration (PrImR). This method enabled him to see each cell’s gene activity in the worm brain, and compare this information with gene expression profiles of the vertebrate cerebral cortex.

(Image credit: EMBL/R.Tomer)

The image above shows a virtual Platynereis brain, composed of average images of the brains of 36 individual larvae at 48 hours old, with colour-coded gene activity patterns shown for each area of the brain.

The study suggests that we may need to reevaluate what is known about the evolution of the cerebral cortex. It would be interesting to use PrImR on other organisms to find out more about similar structures in other species.

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(2 votes)

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Grade 7 £28,983 – £35,646

We are seeking two Post-Doctoral Research Assistants for Professor Liz Robertson’s Wellcome Trust funded Research Group studying mammalian developmental biology at the Sir William Dunn School of Pathology.

Our programme focuses on defining the molecular cues responsible for cell allocation and tissue morphogenesis in the developing mammalian embryo.  We have exploited transgenic and ES cell technologies to investigate the key signalling pathways and transcriptional networks that regulate expansion of diverse progenitor cell populations.  Candidates with experience in construct design, high resolution imaging, cell sorting, microarrays, ChIP and/or proteomic approaches would be especially welcome.  We are seeking well trained and ambitious scientists with good organisational and communication skills.

Arnold and Robertson (2009).  Making a commitment: cell allocation and axis patterning in the early mouse embryo.  Nature Rev. Mol. Cell Biol.  10, 91-103

Morgan et al. (2009) Blimp-1/Prdm1 alternative promoter usage during mouse development and plasma cell differentiation. Mol. Cell. Biol. 29, 5813-27

Costello et al. (2009) Smad4-dependent pathways control basement membrane deposition and endodermal cell migration at early stages of mouse development.  BMC Developmental Biology 9, 54-70

Arnold et al. (2008) The transcription factor Eomes/Tbr2 regulates neurogenesis in the embryonic subventricular zone. Genes Dev. 22:  2479-84.

Maretto et al. (2008) Ventral closure, headfold fusion and definitive endoderm migration defects in mouse embryos lacking the fibronectin leucine-rich transmembrane protein FLRT3 Dev. Biol. 318: 184-193.

Arnold et al. (2008) Pivotal roles for Eomesodermin during axis formation, epithelium-mesenchyme-transition and endoderm specification in the mouse. Development 135:501-511.

Robertson et al. (2007) Blimp1 regulates development of the posterior forelimb, caudal pharyngeal arches, heart and sensory vibrissae in mice. Development 134: 4335-45.

To apply please send your CV, a cover letter and contact details of 2-3 referees to administration@path.ox.ac.uk.  Please quote reference LR/10/008

Informal enquiries welcome – please email Prof Liz Robertson at Elizabeth.robertson@path.ox.ac.uk (www.path.ox.ac.uk/dirsci).

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“You’re probably wondering why I’m here”, were the first words of Edward Marcotte’s talk at the SDB meeting last month. After all, he was about to speak about systems biology in a session on organogenesis. What followed was not only a new way to identify genes involved in developmental processes, but also a perfect example of the kind of unexpected discoveries that can be made using publicly available data.

Edward Marcotte is a bioinformatician at the University of Texas at Austin. His lab introduced the concept of phenologs to discover non-obvious disease models and candidate genes, and at the SDB meeting, as well as in a recent paper, he described exactly how “non-obvious” some of those models are: If a yeast model for angiogenesis doesn’t sound unlikely enough, the group also proposed a plant model for Waardenburg syndrome!

The concept behind phenologs is that a set of genes related to a phenotype in one organism may correspond to an orthologous set of genes in another organism. Orthologues are homologous genes between different species, but this does not necessarily mean that the same gene is linked to the same phenotype in both organisms. Marcotte looked at groups of orthologues: If a group of genes is linked to a certain phenotype in one organism, and that same group results in another phenotype in a second organism, then those two phenotypes are phenologs.

The concept of phenologs. (Figure 1B in the PNAS paper.)

In one practical example from the paper, known gene-phenotype associations from yeast were compared with known gene-phenotype associations from mice, using information from publicly available yeast and mouse genome databases. This showed that many genes that are associated with abnormal angiogenesis in mice have orthologous genes in yeast. Of course yeast doesn’t have a circulation system, so these genes can’t possibly be associated with angiogenesis in yeast, and indeed they’re not: In yeast, these same genes are involved in sensitivity to the hypercholesterolemia drug lovastatin. This suggests that lovastatin sensitivity in yeast could be a model for angiogenesis in vertebrates. To prove this, follow-up experiments showed that the transcription factor SOX13, which was identified as lovastatin-sensitive in yeast, is required for vascular development in Xenopus.

Even more surprising than finding angiogenesis genes in yeast, is that a similar comparison of phenologs suggests a plant model for Waardenburg syndrome. This disorder is caused by impaired neural crest development, and is marked by pigmentation defects and craniofacial malformations. Phenologs showed that many genes associated with Arabidopsis failing to grow in response to gravity (gravitropism) were orthologous to human genes mutated in Waardenburg syndrome, which suggests that other gravitropism genes may serve as starting points to look for other factors involved in neural crest migration.

While I was listening to this talk, I wondered whether the people who did the original yeast lovastatin screens could ever have imagined their data being used to find a new factor involved in angiogenesis. And the groups that identified gravitropism-related genes in Arabidopsis must never have thought that this could even remotely have anything to do with Waardenburg syndrome in humans! It illustrates exactly why it’s important to make data from screens and large-scale studies available to others: You often only use a small amount of the data, and buried among the rest of it is information that could be useful to people you’d never expect would benefit from it! The data in public databases speeds up research and opens up new subjects of investigation, and that is exactly why it’s there.

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(6 votes)

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Many human embryonic stem cell (hESC) researchers are now scrambling for funding and concerned about the future of their research, following a recent ruling in the United States by Chief Judge Royce C. Lamberth.  To understand this ruling, both how it came about and its implications moving forward, it’s important to take a look at the history, biologically and politically, of hESCs in the U.S.

In 1998, a group led by Prof. James Thomson, at the University of Wisconsin, isolated embryonic stem cells (ESCs) from humans for the first time.  These pluripotent cells are specifically isolated from four- or five-day-old blastocysts (pre-implantation embryos containing approximately 150 cells).

To generate the hESCs, Thomson’s group used blastocysts from in vitro fertilization (IVF) clinics with full donor consent. Since then, additional hESC lines have been created, often using blastocysts from IVF clinics that would otherwise be discarded (due to being damaged). Since IVF has become such a popular practice (now responsible for 1 in 100 births in the U.S.), there are now over half a million frozen embryos in the U.S. alone; there does not appear to be a shortage.

In 2001, President George W. Bush adopted a rather restrictive hESC policy, limiting the number of hESC lines that researchers could use and still receive federal funding; work with only 21 of the originally created lines could be federally funded (and no newly generated lines would receive federal funding). (However, work with other hESC lines could still receive private funding.)

President Barak Obama’s administration changed Bush’s policies. Specifically, in March 2009, Obama made it possible for researchers to receive federal funding for research on at least 75 different hESC lines; lines could be funded as long as the embryos used had full consent of the donors and the embryos would have otherwise been discarded (after use in an IVF clinic). However, federal funding could still not be used to generate new hESC lines.

Obama’s new policy quickly brought about a lawsuit, led by Nightlight Christian Adoptions and two adult stem cell researchers, Dr. James L. Sherley (a former MIT researcher who notoriously went on a hunger strike after being denied tenure) and Dr. Theresa Deisher (president and founder of Sound Choice Pharmaceutical Institute). The plaintiffs claimed that the new policy violated the Dickey-Wicker Amendment (established in 1996), which states that federal money cannot be used for any “research in which a human embryo or embryos are destroyed, discarded or knowingly subjected to risk of injury or death.” The Obama administration’s policy had bypassed this Amendment because it did not allow for federal funding of the generation of hESCs, but only for their downstream use.

To determine how valid the objection against hESC research is based on its use of human embryos, it’s important to understand two key aspects of hESCs’ unique biology and derivation. First, unlike adult stem cells, hESCs can be grown and expanded indefinitely, creating potentially an infinite number of hESCs from a single human embryo. Consequently, most research facilities that use hESCs do not generate the cell lines themselves, but purchase them from a banking facility (such as WiCell) or a collaborator. Second, researchers have shown that it is possible to generate a hESC line without damaging the embryo (although, admittedly, this is not how the hESC lines are typically created) (see Klimanskaya et al., 2006). Not only is it possible to create hESC lines without destroying a human embryo, or create potentially infinite hESCs from a single human embryo, but most researchers who work with these lines never encounter the donated human embryos used. However, this has not stopped Dr. Sherley and Dr. Deisher from appealing their suit.

Last year, the suit was dismissed because the plaintiffs would not be materially affected by a possible change in the policy. However, the suit went to the Court of Appeals, which reversed the ruling because it claimed that Dr. Sherley and Dr. Deisher were harmed by Obama’s policy; as they only worked with adult stem cells, theoretically they would have to deal with increased federal funding competition. In these economically tight times, one wonders how many other researchers might resort to prosecuting away their competition for funding sources. Dr. Sherley and Dr. Deisher became the only plaintiffs remaining.

On August 23rd, 2010, Chief Judge Royce C. Lamberth (who was appointed in 1987 by President Ronald Reagan) ruled to block Obama’s new hESC policy, asserting that federal funding could not be used in hESC research because the research “necessarily depends upon the destruction of a human embryo.” Judge Lamberth continued to state that, “If one step or ‘piece of research’ of an E.S.C. research project results in the destruction of an embryo, the entire project is precluded from receiving federal funding.”

Judge Lamberth claimed that his ruling was simply a return to “status quo,” but many are unclear, and understandably quite concerned, about the implications of the ruling; does this mean there will be a return to Bush administration policies, or can no hESC research be federally funded at all? The ruling has shocked the National Institutes of Health (NIH) and researchers alike, disrupting research in hESC laboratories across the country. However, the NIH already declared that the ruling would not affect grants that have already been paid this year, but renewals and grants currently being reviewed will be postponed. It will take some time to clarify the impacts of the ruling, although the Obama administration quickly announced, on August 24th, that it would appeal Judge Lamberth’s decision. However, it is not easy or efficient to simply put hESC research on hold; these cells are delicate, and require time to get going once they have been stopped.

Luckily, many hESC laboratories have alternative, private funding that is not affected by this ruling. The most significant remaining funder of hESC research is probably the California Institute for Regenerative Medicine (CIRM), which in 2004 was given $3 billion (through Proposition 71) to spend on stem cell research by Californian voters. (Luckily, my laboratory in the University of California, Santa Barbara, is one of such stem cell facilities funded primarily by CIRM.)

For more coverage on Judge Lamberth’s ruling against Obama’s hESC policies, see The New York Times’ article on “U.S. Judge Rules Against Obama’s Stem Cell Policy,” The Los Angeles Times’ article on “Ruling a blow to stem cell research,” National Public Radio’s article on “Obama Appeals Stem Cell Ruling; Some Work to Stop,” or The Forum on Science, Ethics, and Policy’s article on “Court Ruling Prevents Funding of Embryonic Stem Cell Research.”

I would be interested to hear about hESC policies in other countries, especially in the European Union. From what I’ve heard, there seems to be great variation, even within the EU.

(4 votes)

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At the recent SDB meeting in Albuquerque, Eric Olson took the stage twice: on Friday morning he spoke in the organogenesis session about the role of microRNAs in muscle, and on Sunday evening he entertained the attendees of the conference’s closing ceremony with his band, the Transactivators. In between these two performances, I asked him a few questions about science, music, and doing research funded by a country singer.

What are you working on at the moment?

We’re working on the role of microRNAs in responses to a number of muscle diseases. We’re looking at how microRNAs regulate the sensitivity of the heart after stress, and how they regulate atrophy of muscle or diseases of the vascular system. We’re trying to develop new therapeutics that can manipulate microRNAs in the settings of those disorders.

You also play in a band, can you tell me a bit about that?

I have a band I started about five years ago, called the Transactivators. It’s made up of all scientists, and we just play Rock ‘n Roll. We’re a cover band, so we play all the seventies and eighties rock music that everybody likes to listen to. We have a good following in Dallas. We play in a bar there and people seem to like to see us outside of our normal, scientific, daily functions.

How did you meet the other band members? Through work?

Yes, I knew that some people I worked with knew how to play music, but we’d never played together. So we started getting together. One thing led to another and it just took off.

Are there any other music projects that you’ve been working on?

No, this is the only one. I play at home by myself, but in terms of organized projects, this is the only one. It’s kind of tough because I’m really busy and I travel all the time. So just to coordinate everyone’s schedules is a challenge.

You also hold the Annie and Willie Nelson Professorship in Stem Cell Research at the University of Texas Southwestern Medical Center. How did that come about?

The president of our institution knew that I was interested in music. When Willie Nelson’s kids were coming to UT Southwestern to get a checkup, he arranged for me to meet Willie Nelson’s wife and kids, and we talked about what I was working on. Annie Nelson – his wife – got really excited, so she got Willie to throw a benefit concert and raise money for our stem cell effort.

[As a result] the lead guitar player of my band and me have been on Willie’s tour bus, and been backstage at several of his concerts.

What does Willie Nelson think of research? Does he know anything about it, or is he mainly interested in the therapeutic side of it?

He’s interested in worthwhile causes, and that includes stem cell research.

—

The Node sadly had to miss the closing banquet of the SDB meeting, so I didn’t get to see Eric perform, but Steve Farber of the Carnegie Institution of Washington was there, and said: “Eric gave a great seminar that got me thinking about microRNAs and their regulation. Then he and his band got a sizable proportion of the banquet attendees dancing on the lawn by the aquarium.  I was surprised when I heard some Jimi Hendrix in the mix. Way too much fun!”

For an impression of what the band looks and sounds like, watch this YouTube video.

(4 votes)

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Non-muscle myosin II translates cilia polarity

In the brain, cilia on the multiciliated ependymal cells that line the brain ventricles circulate cerebrospinal fluid over the brain surface. To generate this directional fluid flow, the ependymal cell cilia and their basal bodies must be orientated in one direction. This ‘rotational’ polarity is regulated by the planar cell polarity (PCP) pathway. Recent reports have revealed that the basal bodies are also localised at the anterior of the ependymal cells but how is this ‘translational’ polarity established? Using a new method for time-lapse imaging of ventricular walls, Kazunobu Sawamoto and co-workers now show that, in mice, the anterior migration of basal bodies in the apical cell membrane during ependymal cell differentiation establishes translational polarity (see p. 3037). Inhibition of the PCP protein dishevelled 2, which disrupts rotational polarity, does not affect translational polarity, the researchers report. Instead, their pharmacological and genetic studies identify non-muscle myosin II as a key regulator of translational polarity. Thus, different mechanisms regulate the orientation and distribution of basal bodies in ependymal cells.

SNP links Dlx gene regulation to autism

Several neurodevelopmental disorders, including autism, have been linked to the aberrant development of γ-aminobutyric acid (GABA)-expressing interneurons in the mammalian forebrain. Dlx homeobox genes control the development of these interneurons and now, on p. 3089, Marc Ekker and colleagues report that a rare, autism-associated single-nucleotide polymorphism (SNP) in an ultraconserved regulatory element (I56i) in the DLX5/DLX6 bigene cluster affects Dlx5/Dlx6 regulation in the mouse forebrain. The researchers show that the SNP, which lies in a functional protein binding site, reduces I56i enhancer activity in the developing mouse forebrain and in adult GABAergic interneurons. Notably, Dlx proteins have a reduced affinity for the variant I56i protein binding site in vitro, they report, which reduces the transcriptional activation of the enhancer by Dlx. The researchers propose, therefore, that impaired I56i enhancer activity by the SNP could affect the auto- or cross-regulation of the DLX5/DLX6 bigene cluster, thereby disrupting cortical interneuron development and contributing to the developmental abnormalities that underlie autism.

Symmetric neural progenitor divisions Notch up

During development, the balance between neural stem cell self-renewal and differentiation is carefully controlled to ensure that the correct number of neurons is produced to build functional neural networks. In the Drosophila optic lobe, as in the mammalian cerebral cortex, neuroepithelial (NE) cells initially divide symmetrically to expand the stem cell pool, before switching to asymmetric division to generate neurons. Andrea Brand and colleagues now report that Notch regulates this important cell fate transition (see p. 2981). By comparing the transcriptomes of microdissected NE cells and neuroblasts, the researchers show that Notch signalling pathway members are preferentially expressed in NE cells. Notch mutant cells are extruded from the neuroepithelium and undergo premature neurogenesis, they report. Furthermore, a wave of proneural gene expression transiently represses Notch activity in NE cells to enable the transition from symmetrically dividing NE cell to asymmetrically dividing neuroblast. This progression resembles that seen in the vertebrate cerebral cortex, leading the researchers to propose that neurogenesis regulation could be conserved between these two systems.

Changing identities: neuronal transdifferentiation

Traditionally, cellular differentiation is thought to be an irreversible commitment to a given cell identity. So, for example, differentiated neurons cannot generate new cells or adopt new identities. Now, however, Melissa Wright and colleagues provide evidence for the transdifferentiation of dorsal root ganglia (DRG) sensory neurons in zebrafish larvae (see p. 3047). Using time-lapse microscopy, the researchers track DRG neurons in wild-type zebrafish and in zebrafish mutant for the nav1.6 voltage-gated sodium channel. Some DRG neurons migrate ventrally from their normal position and then adopt a phenotype characteristic of sympathetic neurons in both types of larvae, they report, but more DRG neurons transdifferentiate in the mutant larvae. Furthermore, although the loss of sodium channel expression promotes the migration of DRG neurons, once in a new environment, these neurons transdifferentiate regardless of sodium channel expression. Thus, the researchers conclude, differentiated sensory neurons retain the plasticity needed to transdifferentiate when challenged by a new environment, a finding that suggests new strategies for the treatment of nervous system diseases.

Heartfelt responses to opposing FGF/BMP signals

Congenital heart disease – the commonest type of human birth defect – is the result of abnormal early heart development. In this issue, two papers investigate how opposing fibroblast growth factor (FGF) and bone morphogenetic protein (BMP) signals control the differentiation of the secondary heart field (SHF) and anterior heart field (AHF) cardiac progenitors during early vertebrate heart development.
On p. 3001, by isolating and culturing chick SHF mesoderm, which forms the myocardium and smooth muscle of the heart’s arterial pole (the outflow region of the heart), Mary Hutson and colleagues show that this tissue contains stem cells that can differentiate into myocardium, smooth muscle and endothelial cells. By treating SHF (arterial pole) progenitor cultures with combinations of growth factors and inhibitors, the researchers show that BMP promotes myocardial differentiation but not proliferation of the arterial pole progenitors, whereas FGF promotes their proliferation and smooth muscle cell differentiation but inhibits myocardial differentiation. These and other results indicate that myocardial differentiation of the SHF progenitors requires BMP signalling and downregulation of the FGF/ERK pathway and suggest that the FGF pathway maintains the SHF stem cell pool early but promotes smooth muscle cell differentiation later.

On p. 2989,, Eldad Tzahor and colleagues provide further insights into how opposing BMP and FGF signals regulate cardiogenesis by studying the differentiation of chick AHF progenitors, which contribute to the right ventricle and to the arterial pole. By perturbing signalling pathways in vitro and in vivo, the researchers show that, as in SHF progenitors, BMP promotes myocardial differentiation of AHF progenitors by blocking FGF/ERK signalling and that FGF signalling prevents their premature myocardial differentiation. They also show that BMP4 induces the expression of several neural crest-related genes and that cranial neural crest cells are required for BMP-dependent myocardial differentiation of the AHF progenitors. Thus, Tzahor and colleagues suggest, BMP and FGF signalling pathways coordinate the balance between the proliferation and differentiation of cardiac progenitors in the AHF through regulatory loops that act in multiple tissues.

(1 votes)

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Postdoctoral Positions are available for highly qualified and motivated candidates to study the physical principles of morphogenesis in the Davidson Laboratory at the University of Pittsburgh in the Department of Bioengineering. The laboratory focuses on studying the molecular-, cellular, and tissue-scale processes that regulate mechanical properties and force-production during morphogenesis. Projects involve a combination of biophysics, cell biology, bioengineering, and embryology.

Candidates will have recently completed a PhD and have strong background in either biophysics, cell and developmental biology, or cell- and tissue- mechanics. Candidates with expertise with biochemistry, quantitative microscopy, microrheology, microfabrication or computer simulation are preferred. The research environment at the University of Pittsburgh includes a dynamic community of bioengineers, developmental biologists, cell- and tissue-level biomechanics, and theoretical biologists. Nearby resources include the John A. Swanson Micro and Nanotechnology Laboratory and the Pittsburgh Supercomputing Center. Contemporary Pittsburgh is a diverse vibrant city undergoing a renaissance led by world class Universities and the University of Pittsburgh Medical Center. The University of Pittsburgh is an Equal Opportunity Employer. Women and minorities are especially encouraged to apply.

Interested applicants should forward their statement of research interests, CV, and a list references to:

Lance Davidson
Department of Bioengineering
Biomedical Science Tower 3, Room 5059
3501 Fifth Avenue
University of Pittsburgh
Pittsburgh PA 15260
(email) lad43@pitt.edu
(web) http://www.engr.pitt.edu/ldavidson/

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Worth 1000 words?

http://blogs.nature.com/news/thegreatbeyond/2010/08/a_zebrafishs_first_minutes_of.html

[update 31/8: I added the first of the videos (below) – Eva]

(The original paper is in Science)

(2 votes)

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It seems that following on the tracks of Cell Press, which is reducing the maximum number of supplemental figures to one per manuscript figure, now J. Neuroscience is doing away with it altogether. Hooray?

I agree that it is not a very good thing at times that the amount of Suppl Figs has risen (or sunk) from useful to occasionally ridiculous (20+ figures!). Yes, it is useful to be able to add a few control experiments, or the validation of a mouse knockout, and a good place to put especially large datasets, but now it’s become an excuse to either bury data that isn’t super solid (in hopes that reviewers won’t pay too much attention), or from the other side, an open invitation for reviewers to ask for more (It’s like a reverse Oliver Twist: “Can I have more please?”; “MORE!?”).

And for the most part, it’s a rather annoying exercise to have to go download the suppl materials. Why can’t journals not put the supplementary pdf together with the main paper pdf? I do it all the time, it’s a simple feature in Acrobat, so is that so much to ask for from a publisher? Cell Press does it, Nature Cell Biology does it, but that’s about it.

So, Supplementary/Supplemental figures/data? Good, bad, ugly? Discuss. Perhaps we can help influence some journals that are paying attention.

(3 votes)

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Some Canadian postdocs are awaiting the next academic year with bated breath: will they earn less than they did during their PhD, or twice as much as their colleagues?

Canada’s 2010 research budget, announced this past spring, was full of surprises for the thousands of postdoctoral researchers in the country. To promote top-level talent, the government put aside $45 million for the next five years to award a select group of postdocs with $70,000 per year. These Banting post-doctoral fellowships are almost twice as much as the average Canadian postdoc salary of approximately $35,000-$40,000. Applications for the prestigious awards have opened on August 10, and are being accepted until November 3, 2010. But the lucky few who get the top awards will also receive another, slightly less pleasant, surprise: postdoctoral fellowships in Canada are no longer tax exempt. Even postdocs who previously paid no taxes on the funding they received, will be charged next year. Until now, postdoctoral stipends often fell under the same – tax-free – umbrella as student scholarships. Surprisingly, this now means that a fully-funded PhD student can end up with more money than they will receive as a postdoc paying taxes on a basic postdoc fellowship!

With such mixed funding news, reactions from young Canadian researchers have been all across the board. What do you think: is the $45 million well spent on the new competitive awards (boosting the international prestige of these researchers, and perhaps being a way out of the previously discussed issue of “too many postdocs”), or would you rather have seen a continuation of the tax exemption for postdoc stipends? The Banting fellowships are open to international applicants, too: would knowing that there was a very small chance of a competitive postdoc salary lure foreign researchers to Canada, or would it succeed in keeping Canadian graduates from seeking top funding elsewhere in the world?

(image by lsiegert on Flickr)

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