After the devastating earthquake last year forced us to cancel the chick meeting, we are happy to announce that the next chick meeting will be held in Nagoya, Japan. The meeting will be held from 14th to 18th November 2012.

Please check the website for further details.

(6 votes)

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My inbox is full of abstract submission deadline reminders and meeting registration announcements, so I thought I’d share a few. Which conferences are you planning to go to this year?

Abstract submission deadlines:
* February 21 (tomorrow!) – Abstract submission deadline for the JSDB/JSCB meeting (May 28-31, Kobe)
* March 2 – Abstract submission deadline for the BSDB/BSCB/JSDB meeting (April 15-18, Warwick)
* March 26 – Abstract submission deadline for the SDB Meeting (July 19-23, Montreal)

Registration open:
* The International Conference on Zebrafish Development and Genetics (June 20-24, Madison, Wisconsin) just opened abstract submission. Get yours in by March 27. Meeting registration starts later this week.
* The Santa Cruz Developmental Biology Meeting (August 8-11, Santa Cruz) launched their website and Facebook page. Abstract submission and registration will open later this Spring.

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At the start of February, EuroStemCell used our Twitter page @eurostemcell in a new way: We posted a series of fascinating facts and ‘test your knowledge’ questions about stem cells, using the hashtag #stemcellfacts. The tweets covered a lot of ground, from embryonic stem cells and blastocysts to skin stem cells, gut stem cells, heart cells and regeneration.

Thanks to Kate Blair for developing the #stemcellfacts concept and researching the content for the 30 tweets. You can see all the tweets collated with responses from other tweeters in our Storify summary.

We’ve got off to a flying start in 2012 with lots of other activities too – new blogs, translation into Italian, new educational tools and articles about embryonic stem cells. Find out more in our February newsletter. And as ever, we’re keen to hear you feedback at www.eurostemcell.org/contact.

(4 votes)

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Cambridge University Research has recently launched a series of videos called “Under The Microscope”, that showcase some of the microscopic research carried out at the university. Two of the eight videos they’ve published so far have featured developmental biology:

PhD student Matt Benton talking about beetle development.

Research fellow Erica Watson describes mouse development.

The “Under the Microscope” videos are meant for a wider audience, and it’s interesting to read some of the comments the videos get on YouTube, from people who are sometimes only thinking about development for the first time. But I thought even the seasoned developmental biologist might enjoy having a look at them.

Find all the videos on their video and audio page.

(7 votes)

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Last June, Eva summarised the Node’s alternative careers stories, personal accounts of how scientists made their transitions from research into various alternative career paths. As a friend of Andrea Hutterer, who is now the Fellowships Manager at EMBO, I witnessed her exciting leap from the bench into science management back in 2010, and now asked her to tell her story. I’m sure her experiences will interest the Node’s readers and complement the alternative careers stories already available on the site. Enjoy the interview!

Briefly tell us about your scientific career.

I studied biochemistry in Vienna and then did both my diploma thesis and my PhD in Jürgen Knoblich‘s lab at IMP and IMBA in Vienna. The focus of my thesis was asymmetric cell division in the nervous system of Drosophila. After that I joined Masanori Mishima‘s group at the Gurdon Institute in Cambridge, UK, for a postdoc. In his lab, I studied the process of cytokinesis.

Why did you quit research?

I was simply not sufficiently fascinated by one particular biological problem. My CV was good in scientific terms, so I think I could have gone ahead and started to apply for PI positions. But without being passionate about a question I think it’s hard to be successful, and being quite ambitious I decided it’s not the right career path for me.

What got you interested in research funding and policy? Did you consider other career paths?

Once I had decided to look into alternative careers, I needed to find out which career paths were open to me. I looked into loads of things – management consulting, scientific editing, medical writing, conference organising and science communication. In the end it was clear that science management was the best choice for me, as I would still have direct contact to scientists and thereby get a broad overview of scientific progress and emerging fields. On top of that, one can make a difference in terms of policy, for example by dealing with researchers’ employment conditions or gender issues.

Did you take any additional courses to polish your CV?

At the Gurdon Institute I was lucky enough to be able to take advantage of the fantastic careers service Cambridge University offers. In the beginning, I almost randomly took courses such as microeconomics, web-authoring and programming languages. This helped in a way that I found out quickly that pure economics were not entirely my thing and Perl was not my language. Other courses were more useful, for example when I learned the basics of using HTML to build websites or how to best write a CV for non-scientific jobs.

With regard to “polishing” my CV, it wasn’t so much the courses I listed but more how I organised the CV. I tried to emphasise my soft skills and highlighted extracurricular activities such as supervising younger students and organising retreats and symposia.

How easy was it to get your first job in funding?

It wasn’t easy at all, not even to get interviews. My scientific CV was good, but I had virtually no other relevant experience. Many employers appreciate even the smallest amount of experience more than a fantastic scientific CV, so what you really need when coming out of a PhD or postdoc is to get a foot in the door.

The first interview I got was with Cancer Research UK, but they didn’t offer me the job. I then got offered a job as Science Manager with the Medical Research Council (MRC) in Swindon, UK. I was quite over-qualified for this job since it didn’t even require a PhD, plus it came with a significant pay cut, but I was glad to have been offered it and accepted. In hindsight, it was the perfect stepping stone.

As preparation for the interviews, the Cambridge Careers Service again proved extremely helpful, because they offered mock interviews with the career advisor. It helped immensely to practise – I found out what I might be asked in an interview and I learned to explore different possibilities for answering these questions. I simply got an idea of what to expect during the process.

What does your work consist of?

On an everyday basis, I do some general administration, the details of which depend on the various fellowship application deadlines: I read proposals, find referees, talk to fellows, talk to my team [Andrea has three administrative staff to manage] and attend in-house management meetings. Every now and then I travel to career events to give talks about the programme, or attend workshops somewhere in Europe, which cover different aspects that come with the programme, such as a recent workshop on tracking research careers.

I also write grant proposals to try to get more money for the programme, and organise and attend the EMBO Fellows’ meetings in Heidelberg and the US. So it’s a very diverse job and I’m never even remotely bored!

Is there anything you miss about working in research?

At the MRC, although my colleagues were great I sometimes missed the international environment, which I do have here at EMBO. Sometimes I also miss standing at the bench, running around in the lab, being physically active. But I’m aware that that would have stopped sooner or later even if I had stayed in research and had become a PI.

What advice do you have for PhD students and postdocs wanting to leave academic research?

Find out why exactly you want to leave and what you would rather do. Even if you’re unclear whether research might be the right thing for you or not, start thinking about alternatives and get involved in non-scientific activities early on. There’s actually quite a lot one can do with our education. You just need to be clear about your goals, have a good non-scientific CV ready and work towards the new career profile. It might take a while until you get the job you have in mind, and you possibly need to be prepared to take pay cuts and will maybe feel slightly under-challenged in your first non-research job, but at least for me it was all worth it.

(14 votes)

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The ability to learn and form memories are cognitive functions associated with the brains ability to produce and co-ordinate new neurons effectively. These cognitive abilities are well known to degenerate with age due to diminishing neurogenesis. This study published in Nature, shows that reduced regenerative ability of the brain is due not only to intrinsic cues from the central nervous system, but also extrinsic blood-borne cues communicating with the neurogenic niche via closely surrounding blood vessels. This investigation aimed to find molecular differences in the systemic environment of ageing mice using a heterochronic parabiosis study to identify a correlation between blood-borne factors and neurogenic decline.

To address this, young mice (3-4 months) were exposed to the systemic environment of old mice (18-20 months). This was achieved by the intravenous injection of plasma obtained from an old mouse into a young mouse. The change in systemic environment produced mice with deficient synapse plasticity and reduced cognitive functions such as learning and memory. Proteomic analysis comparing the plasma of young and old mice revealed a correlation between ageing and a group of chemokines. Of particular interest was the chemokine CCL11 which has not been linked previously with ageing. Administration of CCL11 by intraperitoneal injection caused a reduction in adult mouse neurogenesis and in turn these mice demonstrated impaired learning and memory. Further investigation showed this chemokine to increase in an age dependent manner in human plasma and cerebrospinal fluid indicating similarity in age related systemic content across species.

Could the molecular content of our systemic environment be responsible for the neurogenic signs of ageing? This study gives convincing evidence for a link between certain age related blood-borne factors with diminishing neurogensis and cognitive function associated with ageing. The converse to this study is of course, what pro-neurogenic factors may be present in the systemic milieu. These could have potential in future therapy for age related neurogenic disorders.

The full paper can be found by following this link

http://www.nature.com/nature/journal/v477/n7362/full/nature10357.html

(5 votes)

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Dear Developmental biology community,

I would like to bring to your attention a potentially valuable resource for your teaching and research endeavors.  I am a neurodevelopmental biologist at Smith College.  I started teaching a course in Developmental Biology back in 2005, and since then have been utilizing web conferencing technology to bring the research behind concepts alive in the classroom.  My students have been interacting with leading scientists in the field of developmental biology holding organized Q&A video conferences focused on current and seminal research articles.  I am posting this to the Node as since I started using this pedagogical approach I have been recording these discussions, and with full consent provided, I have established an online repository of these recordings via my lab website.  I have each conference (40 now and growing) organized by topic for ease of searching, and each individual session is further broken down by specific question to facilitate quick access to your greatest interest.

Because these sessions are based on key research papers they are extremely applicable for any teacher or student to use in their own courses as supplemental resources to what is probably the very same topics being covered.  For instance, I often assign my students select conferences to watch to supplement their readings or coverage of the material.  Moreover, in class I will poise certain questions about a topic to my student and after some discussion, click on say, Dr. Cliff Tabin’s response to the similar question.  It provides a new and real perspective to the information that students truly appreciate and fosters long-term retention of the material.

There are also many other positive outcomes to both conducting and watching these conferences.  Namely students gain a very different and revealing perspective of not only where a particular field of Dev Bio is moving, but more personal understandings of who the scientists are and how they got to where they are today.  Listening to these remarkable scientists articulate their thinking process to address the research question is extremely illuminating to the developing scientist in your classroom.

So I invite and encourage you to check out these discussions as I am disseminating them for your benefit and use.  I hope you find them helpful.  Feel free to let me know what you think and, if you like them, how you might use them in your teaching.

“Bio Web Conferences” http://sophia.smith.edu/~mbarresi/lab/biowebconferences.html

Best regards,

Michael J.F. Barresi

P.S. additional post on stem cell documentaries coming….

(10 votes)

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A fully differentiated cell took a fascinating journey to become its present self.  For every cell, a precursor cell existed that gave rise to it.  And for every precursor cell, a stem cell existed that gave rise to it.  Understanding precursor cells is an important part in understanding stem cell biology.  Today’s image is from a recent paper in Development that discusses how neuron precursor cell divisions affect development of the cerebral cortex.

The cerebral cortex is the outermost layer or brain tissue, and is commonly referred to as “gray matter.”  During development, the different regions and layers of the cerebral cortex are formed from precursor cells.  These intermediate precursor cells (IPCs) arise from radial glial cells (RGCs), which come from neural stem cells. The different layers of the cortex are formed from radial migration of the postmitotic neurons produced by RGCs and IPCs.  The length of time each RGC or IPC cell resides in the cell cycle regulates the distance its daughter neuron can migrate—cells that exit the cell cycle earlier are able to migrate further, while neurons that are born later cannot migrate as far.  Exploring this connection between the cell cycle and formation of cortex layers, Mairet-Coello and colleagues recently published results showing how two different cyclin-dependent kinase inhibitors (CKIs) regulate different stages of precursor proliferation and affects development of the different layers.  Specifically, p57^KIP2 regulates the cell cycle length of RGCs and IPCs, which in turn affects neurogenesis of layers 5 and 6.  p27^KIP1, however, regulates the proliferation of IPCs, in turn affecting neurogenesis exclusively in layers 2-5.  In the images above, p57^KIP2(red) is found in actively dividing precursor cells (PCNA, green) in two different proliferative zones in the developing mouse brain, labeled SV and SVZ.  The SV contains proliferating RGCs and IPCs, while the SVZ mostly contains proliferating IPCs.  Arrows point to p57^KIP2-postitive proliferating cells.

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

Mairet-Coello, G., Tury, A., Van Buskirk, E., Robinson, K., Genestine, M., & DiCicco-Bloom, E. (2012). p57KIP2 regulates radial glia and intermediate precursor cell cycle dynamics and lower layer neurogenesis in developing cerebral cortex Development, 139 (3), 475-487 DOI: 10.1242/dev.067314

(1 votes)

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What do you look like? The website This Is What A Scientist Looks Like wants to know. The site, run by science writer Allie Wilkinson, is collecting photos of scientists to show people what we look like. It’s an attempt to combat the very stereotypical view of scientists many people have. Just do a Google Image search for the word “scientist”, and you’ll find many messy-haired men in white lab coats. While some scientists may indeed look like the stereotype, most others don’t! This Is What A Scientist Looks Like shows that scientists come in all shapes and sizes, have hobbies and families, and look like everyone else:

(If you’d like to submit your own photo to the project, submission info is on the site.)

(3 votes)

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Here are the highlights from the current issue of Development:

ROCKed to the heart

Noonan syndrome – a common cause of congenital heart disease – is often associated with missense mutations in the protein phosphatase SHP-2. Interestingly, some types of leukaemia are associated with another subset of SHP-2 missense mutations. Here (p. 948), Frank Conlon and colleagues introduce SHP-2 that contains Noonan-associated mutations or juvenile myelomonocytic leukaemia (JMML)-associated mutations into Xenopus embryos to investigate how SHP-2 regulates heart development. Embryos that express SHP-2 containing Noonan-associated mutations have morphologically abnormal hearts, they report, whereas embryos that express SHP-2 containing JMML-associated mutations have normal hearts. The cardiac abnormalities caused by the Noonan-associated mutations are coupled with a delay or arrest in the cardiac cell cycle and with defective incorporation of cardiomyocyte precursors into the developing heart. Notably, these defects, which are caused by disruptions in the polarity of cardiac actin fibres and in F-actin deposition, can be rescued by inhibition of the Rho-associated, coiled-coil-containing protein kinase 1 (ROCK), which indicates that SHP-2 acts via ROCK to regulate the cardiac actin cytoskeleton during heart development.

Breaking symmetry during lateral root formation

Lateral root (LR) formation, which is essential for the construction of plant root systems, is initiated by coordinated asymmetric cell divisions (ACDs) of LR founder cells in existing roots. In Arabidopsis, LR formation is regulated by auxin signalling through the auxin response factors ARF7 and ARF19, which transcriptionally activate the plant-specific transcriptional regulator LBD16/ASL18 and other LBD/ASL genes. Hidehiro Fukaki and colleagues now provide new insights into the biological role of LBD/ASL genes in LR formation (see p. 883). They show that LBD16/ASL18 is expressed in Arabidopsis LR founder cells prior to ACD and that the spatiotemporal expression of LBD16/ASL18 during LR initiation is dependent on a specific auxin signalling module. Moreover, inhibition of LBD16/ASL18 and related LBD/ASL proteins in LR founder cells blocks nuclear migration, ACD and LR initiation. These results indicate that the localised activity of LBD16/ASL18 and related LBD/ASL proteins establishes the asymmetry of LR founder cells that is required for LR initiation, a key step in the construction of the plant root system.

Untangling the Hairy segmentation clock

During somitogenesis, an oscillating gene network generates a segmental pattern in the presomitic mesoderm. In zebrafish, this segmentation clock centres on cycles of transcription and self-repression of numerous hairy-enhancer of split related (her) genes, which encode proteins that dimerise, bind DNA and repress transcription. On p. 940, Scott Holley and co-workers systematically examine the physical interactions between Her proteins and test the ability of various Her protein dimers to bind to cis regulatory sequences. Dimerisation of Her proteins is specific, they report, with Hes6 serving as the hub of the network. Not all dimers bind to DNA, they note, but those that do so have distinct preferences for different cis regulatory sequences. Finally, Her7 disproportionately influences the availability of Hes6 for heterodimerisation with other Her proteins. The researchers propose, therefore, that Her7 has two functions within the zebrafish segmentation clock – direct repression of transcription through formation of a DNA-binding heterodimer with Hes6 and modulation of the network topology via sequestration of the network hub.

Diet and stem cells TORtuously linked

Nutritional status must be coupled to stem/progenitor cell proliferation and differentiation to ensure the proper growth and homeostasis of tissues, but how does diet regulate stem cell behaviour? On p. 859, E. Jane Albert Hubbard and colleagues show that rsks-1 [the homologue of mammalian p70 ribosomal S6 kinase (S6K), a target of the serine/threonine kinase TOR, which regulates cell growth and proliferation in response to nutritional cues] links cell fate, cell cycle and nutrient response in C. elegans germline stem/progenitor cells. They show that rsks-1 is required germline-autonomously to establish the proper number of germline progenitors, a role that requires a conserved TOR phosphorylation site in RSKS-1. Their analysis also reveals genetic interactions between rsks-1 and Notch, which suggest a prominent role for rsks-1 in cell fate control. Furthermore, dietary restriction causes germline defects similar to those observed in rsks-1 mutants and loss of rsks-1 renders the germline largely insensitive to dietary restriction. The researchers propose, therefore, that TOR-S6K signalling is a key nutrient-responsive regulator of germline progenitors.

Apical ECM and epithelial junction integrity

Polarised epithelial cells form many of the body’s surfaces, including the outer epidermis and the lining of several internal tubular organs. The apical surfaces of these epithelial sheets secrete a specialised extracellular matrix (ECM) that is generally viewed as a passive protective layer against pathogens, but does apical ECM have any other roles? According to Meera Sundaram and colleagues, the apical ECM in C. elegans might help to maintain epithelial junction integrity and, consequently, epithelial tissue integrity (see p. 979). The researchers report that the extracellular leucine-rich repeat only (eLRRon) proteins LET-4 and EGG-6 are expressed on the apical surfaces of epidermal cells and some tubular epithelia, including those of the worm’s excretory system. Mutants lacking one or more of these proteins, they report, have multiple defects in apical ECM organisation and, although epithelial junctions initially form correctly in these mutants, they subsequently rupture. Together, these results suggest that eLRRon-dependent apical ECM organisation might modulate epithelial junction dynamics and integrity.

Bimodal control of HoxD gene transcription

Correct innervation of peripheral muscles by spinal cord motoneurons is required to coordinate body movements in vertebrates. Hox proteins play an important functional role in achieving this innervation by specifying neuronal fates along the anteroposterior axis of the developing spinal cord. However, the mechanisms that generate Hox gene expression patterns are poorly understood. Here (p. 929), Denis Duboule and colleagues use tiling array-based transcriptome analyses and targeted deletions in vivo to investigate the control of HoxD gene transcription in the developing mouse spinal cord. They report that there are two distinct blocks of HoxD transcription that are regulated independently and that define two general expression territories. These territories, they show, are associated with the future nerve plexii at the brachial and lumbar levels. Given these and other results, the researchers propose that the establishment of spatial collinear HoxD domains in the developing mouse spinal cord involves the bimodal control of HoxD gene transcription by two independent ‘enhancer mini-hubs’.

Plus…

Human pre-implantation embryo development

Renee Reijo Pera and colleagues summarize what is currently known about human pre-implantation embryo development and highlight how further studies of human pre-implantation embryos can be used to improve ART and to fully harness the potential of hESCs for therapeutic goals. See the Primer article on p. 829

Retinoic acid signalling during development

Retinoic acid is a vitamin A-derived signaling molecule that acts as ligand for nuclear receptors, converting them from transcriptional repressors to activators. Here, Muriel Rhinn and Pascal Dolle review the main functions of retinoic acid during embryogenesis. See the Primer article on p. 843

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