In an attempt to tighten the country’s budget, the UK government wants to cut a large number of arms-length non-governmental organisations. These “quangos” (quasi-autonomous non-governmental organizations) include regulatory bodies, advisory organs, and other committees.

Until last week, there were only vague speculations as to which funds would be cut, but the news has become more certain now that the BBC has received a leaked document specifically listing 177 non-governmental organizations that are to be cut. Among those is the Human Fertilisation and Embryology Authority (HFEA), which regulates legal and ethical aspects of anything involving IVF, but also sets standards and licensing requirements for any research done on human embryonic stem cells or human embryonic developmental studies in the UK.

Without the HFEA, who would oversee this area of research? This is a question the BBC asked HFEA chairwoman Lisa Jardine, who explained that the current functions of the HFEA would probably be split in three portions, with the research using human embryonic tissue ending up in a new regulatory body. Since that new body is not yet set up, she assumes that the HFEA will remain in charge of regulations until an appropriate alternative has been set up. (If you’re in the UK you can watch her response in a video, otherwise you can read a summary and partial transcript in this article on BioNews which gives a lot of background information).

On the HFEA website is a list of research projects that they have approved in the past. As you can see, it contains many fundamental developmental biology and stem cell research projects. Delays in approving such research in the UK would affect progress within the field, so hopefully Jardine’s prediction will hold true and cutting HFEA funding will not result in a gap in licensing.

The impending demise of the HFEA is not the only worry British stem cell and human embryo researchers have at the moment. The news comes at a time when UK-based researchers in all areas of science are threatened with cuts in research funding that would allow funding only for top and/or commercially viable projects. With scientists taking to the streets to protect funding for basic research, and with important regulatory bodies such as the HFEA under threat, interesting times are ahead for researchers in the UK.

Meanwhile, on the other side of the Atlantic, things could not be more different for hESC researchers: Not only is the US increasing basic science funding rather than reducing it, but it has just been announced that the federally imposed ban on stem cell research (previously on the Node) has been lifted, bringing US stem cell projects back on track. Quite the opposite story. Are any other countries currently awaiting regulations that affect stem cell or developmental biology research?

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(This interview originally appeared in Development on September 28, 2010)

The International Society for Stem Cell Research (ISSCR) held their annual conference in San Francisco this June. At the time, the President of the society was Irving Weissman, who is currently on the board of directors of the ISSCR as past President. He is Professor of Pathology and Developmental Biology and also the Director of the Institute of Stem Cell Biology and Regenerative Medicine at Stanford University School of Medicine, where he works on the generation of myeloid and lymphoid lineages from haematopoietic stem cells. At the ISSCR meeting, we asked Professor Weissman about his role on the board of directors of the ISSCR, and also about the meeting and the field of stem cell research in general.

Thank you for taking the time for a quick interview. Are you enjoying the conference so far?

Of course, for those few moments I have without administrative duties.

What have been your highlights of the conference these first two days?

Well, there are different kinds of highlights. There is of course the highlight that just before the conference we launched our (the ISSCR’s) website on people in clinics who are practising for-profit, unproven therapies (www.closerlookatstemcells.org). This is our way of providing patients and their care-givers with the kind of advice they need in order to avoid being promised treatments that have neither the hope of treating or curing the disease nor of providing good medical practice.

How long have you been involved with the ISSCR; was it from the very start?

Yes, I was a member of the founding group, but I didn’t want the job of ISSCR President until it was more established.

How have you seen the ISSCR change over the past eight years?

I think we went from under a thousand people to nearly four thousand, both as members and as people who are participating in these meetings. We have also formed an alliance with the journal Cell Stem Cell.
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A fateful look at early mouse lineage specification

The first cell lineages specified in the mouse embryo are the trophectoderm (TE), which generates the embryonic portion of the placenta, and the inner cell mass (ICM). The ICM subsequently forms the pluripotent epiblast (EPI, which produces the embryo) and the primitive endoderm (PrE, which generates other extraembryonic structures). Two papers shed new light on these crucially important early embryonic specification events.

On p. 3383, Janet Rossant and colleagues investigate the role that the intercellular adhesion molecule E-cadherin plays in the divergence of the TE and ICM. By embryonic day 3.5, the TE has formed a polarised epithelial layer that encloses the apolar ICM. The researchers show that the normal epithelial morphology of the TE is disrupted in mouse embryos lacking both maternal and zygotic E-cadherin function but that individual cells in the blastocyst still initiate TE- and ICM-like fates. Interestingly, most of the cells express the TE marker Cdx2, which suggests that organised epithelium formation is not necessary for TE-specific gene expression. Furthermore, individual cells in these embryos still generate an apical membrane domainthat correlates with Cdx2 expression. Thus, the epithelial integrity mediated by E-cadherin is not required for Cdx2 expression but is essential for setting normal TE/ICM ratios in mouse embryos.

On p. 3361, Anna-Katerina Hadjantonakis and colleagues identify a role for platelet-derived growth factor (PDGF) signalling in PrE expansion in mouse embryos. The PDGF receptor-α (PDGFRα) is an early marker of the PrE lineage and of extra-embryonic endoderm (XEN) cells, which can be isolated from mouse blastocysts as derivatives of the PrE lineage. By combining live imaging and lineage analysis, the researchers show that Pdgfra expression coincides with that of GATA6, the earliest expressed transcription factor in the PrE lineage. GATA6 expression, they report, is required for Pdgfra transcriptional activation, and PDGF signalling is essential for the establishment and proliferation of XEN cells in culture. Moreover, implantation-delayed Pdgfra-null mutant blastocysts contain reduced PrE cell numbers and, surprisingly, increased EPI cell numbers, indicating that reciprocal signalling between PrE and EPI tissues might regulate compartment size within peri-implantation mammalian embryos.

For more on early mouse lineage segregation, see also the review by Fredrik Lanner and Janet Rossant on p. 3351.

OMA-1/2: repressors of translation and transcription

Primordial germ cell specification requires global transcriptional repression. In C. elegans, the zygote (P0) undergoes four successive asymmetric divisions to generate the germline precursors P1, P2, P3 and finally P4, the germline founder. OMA-1 and OMA-2 (OMA1/2), cytoplasmic proteins degraded after the first mitotic cycle, repress global transcription in P0 and P1 by sequestering TAF-4, an RNA polymerase II pre-initiation complex component, while the maternal protein PIE-1 represses transcript elongation in P2-P4. Now, Rueyling Lin and colleagues report that OMA proteins repress transcription in P2-P4 indirectly by maintaining PIE-1 expression (see p. 3373). OMA-1/2, they show, repress zif-1 mRNA translation in oocytes; zif-1 encodes the substrate-binding subunit of the E3 ligase that marks PIE-1 for degradation. MBK-2, a kinase that is activated after fertilisation, controls OMA1/2 function, report the researchers. Thus, they suggest, MBK-2 phosphorylation of OMA1/2 acts as a key developmental switch in the oocyte-to-embryo transition by converting OMA proteins from specific translational repressors in oocytes to global transcriptional repressors in embryos.

Shh: new TWISTs to limb patterning

Sonic hedgehog (SHH) controls anterior-posterior (A-P) patterning in the mammalian limb. Its expression is normally restricted to the posterior limb bud but when expressed ectopically, it can change digit number and/or identity. Several transcriptional factors regulate Shh expression in the limb bud but how do they function together? On p. 3417, Xin Sun and co-workers report that interactions between two negative regulators of Shh expression (the ETS transcription factors ETV4/5 and the bHLH transcription factor TWIST1) and a positive regulator of Shh expression (the bHLH transcription factor HAND2) control A-P limb patterning in mice. By examining mutant limb buds, the researchers show that Twist1 is required to inhibit Shh expression in the anterior limb bud, and that it acts with the Etv genes to antagonise Hand2. Moreover, biochemical data indicate that the ETV proteins inhibit Shh expression by regulating the dimerisation of TWIST1/HAND2. Together, these findings highlight the importance of a precise balance between positive and negative regulators of Shh expression during limb A-P patterning.

Muscling in on motoneuron specification

Mammalian skeletal muscles contain several types of muscle fibres, each characterised by its contraction speed and molecular properties. Individual motor axons innervate a few dozen muscle fibres, usually all of the same type. How this striking ‘motor unit homogeneity’ is established is incompletely understood but, on p. 3489, Joshua Sanes and colleagues reveal that, in mice, signals from the muscle fibres influence the molecular properties of motoneurons that innervate them. The lack of markers for motoneuron types has impeded the study of motor unit homogeneity. Here, however, the researchers show that the motoneurons that innervate slow muscle fibres selectively express the synaptic vesicle protein SV2A and carry it to their nerve terminals. Notably, overexpression of the transcriptional co-regulator PGC1α in muscle fibres, which converts them to a slow phenotype, increases the number of SV2Apositive motoneurons. The researchers propose, therefore, that retrograde signals from muscles integrate with previously described anterograde influences of the nerve on the muscle fibre to match the properties of these synaptic partners to each other.

LIN-42-ing up development and stress

Environmental stresses, such as nutrient fluctuations, can affect developmental progression in animals. C. elegans larvae, for example, normally develop into adults through four larval stages under the control of heterochronic (developmental timing) genes such as lin-42, a homologue of the circadian rhythm gene period. But, when times are hard, C. elegans forms long-lived dauer larvae, an alternative third larval stage. Now, Ann Rougvie and co-workers report that lin-42 functions in dauer entry (see p. 3501). Loss of lin-42, they report, makes animals hypersensitive to dauer formation under stressful conditions, whereas misexpression of lin-42 in pre-dauer stages inhibits dauer formation. Other experiments suggest that LIN-42 acts in opposition to the ligand-free form of the nuclear receptor DAF-12, which integrates external cues and developmental decisions. Together, these results suggest that LIN-42 and DAF-12 are intimate partners in the decision to become a dauer larva and raise the possibility that Period-like proteins play a conserved role in coordinating intrinsic timing mechanisms with environmental conditions.

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A recent paper in PNAS describes the development of MiniPromoters: human DNA promoters of less than 4 kb, designed to drive gene expression in specific areas of the brain. The initiative is called the Pleiades Promoter Project, and so far they have confirmed brain-region specific activity in knockin mice for 27 of their MiniPromoters. The final goal is to produce 160 fully characterized MiniPromoters to drive gene expression in defined brain regions.

The project is a spin-off of the Mouse Atlas Project (hence the name “Pleiades”: in Greek mythology, the Pleiades were the daughters of Atlas). To create the MiniPromoters, the researchers have computationally identified regulatory regions associated with brain-region or cell-type enriched gene expressions. Information about region-specific expression came from the Mouse Atlas Project as well as from the Allen Brain Atlas, which maps the human brain.

Several MiniPromoters driving LacZ in different areas of the mouse brain. (Part of Figure 5 from PNAS paper)

The MiniPromoters are designed to work in both mouse and human brains. While the Pleiades website emphasizes the ultimate goal of selective target delivery in gene therapy, the MiniPromoters can also be used to drive reporter expression in cell types of interest, for example to follow development of particular areas of the brain.
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Thomson Reuters has predicted who they think will walk away with the Nobel Prizes in medicine, chemistry, physics, and economics. Their predictions for the prize for Physiology or Medicine include six names in four areas:
– Douglas Coleman and Jeffrey Friedman, for the discovery of leptin
– Ernest McCulloch and James Till, for the discovery of stem cells
– Ralph Steinman, for the discovery of dendritic cells
– Shinya Yamanaka, for the development of induced pluripotent stem cells

What do you think? Are any of these scientists going to be on the podium in Stockholm in a few months, or someone else?

I asked on Twitter, where Dean Griffiths guesses the prize will go to Shinya Yamanaka and John Gurdon, but is rooting for Till and McCulloch. Marios Stavridis thinks it’s too soon yet for Yamanaka, but that Till and McCulloch are long overdue a win.

Here’s my own guess: I think I agree with Marios that it’s too early for a win for Shinya Yamanaka. He’ll get it eventually, but probably not yet this year. And like Dean I’m also rooting for Till and McCulloch (I did my PhD in Toronto, so they’re “the home team” for me) but I also think Coleman and Friedman have a good chance. I watched the video for their Lasker Award (see previous post on the Node) and the whole story just screams “Nobel Prize” to me.

We’ll know soon enough, because the winners will be announced on October 4.

(2 votes)

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Today, the Lasker Foundation announced the winners of their 65th annual Lasker Awards, celebrating biomedical research. The winners all contributed to scientific research with strong implications for medical advancements:

Albert Lasker Basic Medical Research Award
Awarded to: Douglas Coleman & Jeffrey Friedman for the discovery of leptin, the “obesity gene”

Lasker-DeBakey Clinical Medical Research Award
Awarded to Napoleone Ferrara for the discovery of the role of VEGF in angiogenesis and the development of an anti-VEGF therapy for wet macular degeneration

Lasker-Koshland Special Achievement Award in Medical Science
Awarded to David Weatherall for lifetime research in the genetics of blood diseases, in particular for his work on thalassemia

The status of the awards becomes clear when you realize that in the past 65 years, as many as seventy-nine Lasker winners have also received a Nobel Prize. Winners of the Lasker receive $250,000 per award, and a statue, which you can see in the video below.

In Napoleone Ferrara’s award announcement video, he and others describe the role of VEGF in angiogenesis and wet macular degeneration:

Videos for the other winners are also available on the Lasker Foundation website.

Coleman, Friedman, Ferrara and Weatherall will receive their awards on Friday, October 1, in New York City.

And a little quiz: Aside from all winning a Lasker award this year, what connects these three research topics? (The simplest answer is only five letters long, but you can be more complicated. No prize, just for fun.)

(1 votes)

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From 4PM UK time on Wednesday September 22nd, the Node’s server is going down for some maintenance. Work will continue for several hours, and will cover most of the working day in North and South America. Apologies for the inconvenience. I’ll schedule some things to appear on the Node’s Twitter account to read while the site is down.

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I’m going to collect dates from my travel journal and batch post the most interesting bits.  See this post for my introduction and an explanation for all of this. Enjoy!

May 12, 2007 Beijing, China

The flight was outrageously long, but uneventful once I boarded. I didn’t find out until I got to Logan airport that my flight was to La Guardia but connecting out of JFK, so I had to catch a cab across Brooklyn. Then it was a bit of a game of musical chairs to get my seat. I boarded late so that I didn’t have to take part in the herd of passengers. Since my first trip to China as a tourist, I’ve observed a collective rush to board flights in no particular boarding order, so I routinely wait until everyone else has settled and board nearly last. On this flight, I was supposed to be in Seat 42A, but there was a guy in that seat. He was supposed to be in 41A, but there was someone in his seat who was supposed to be in 40A. I decided “screw it” and ended up in 40A. That apparently very much confused my graduate student companion when he came looking for me midflight and I was not the person in 42A. I was dead to the world for most of the flight anyway, so I didn’t notice much of a thing. My brain is sort of mush right now from the jetlag, and we’ve started right to work in our colleague’s lab getting things ready. I got to see the Olympic stadiums this morning. They’re super cool. And the institute of zoology is really nice. It’s a new building with new lab space. I love new lab space. We’re going to finish getting things ready today and tomorrow and maybe have a bit of time to see the Great Wall and the Imperial Palace before we head off for Inner Mongolia. No Jerboas yet, but there is a great big Tibetan rabbit sitting in the corner of the desk watching me type. It’s Dr. Yang’s pet, and it’s a little snotty and keeps sneezing. Kind of funny to see a rabbit sneeze.

May 13, 2007 Beijing, China

All I’ve managed to do so far is eat and sleep, and I have been wonderful at that. Ms. Xia (a research associate in our collaborating lab) brought me to lab yesterday morning to get started on the preparations for the fieldwork. That didn’t take very long, so she took me to an outdoor recreation store (like REI) and then to a tourist souvenir market. I quickly decided that I needed lunch and sleep, so after trying to choke down a bacon, egg, and pickle (!) sandwich, she took me back to the hotel for a “nap”. Said “nap” turned into a 5 hour sleep. I woke up in time to catch dinner, read a bit of my book, and go back to sleep for a full night. I think I’ve shown that jetlag what’s for though. I will have to say that Shaoyuan, my graduate student, knows good food. With the exception of that questionable sandwich (for which he wasn’t present, and I should have known better since the menu was in English), all of our meals have been fantastic. I had a really beautiful pork and tofu dish last night, and brunch today was a bowl of spicy chow mein noodles with mushrooms and chicken. I may still lose a little weight on this trip, but it won’t be for lack of trying to keep myself full at all times. I’ve also learned from every country I’ve visited that it’s better to go to places with no English menus and point at other people’s plates if you have to. If you’re willing to risk eating calf intestine, you’re likely to get a fantastic meal.

May 14, 2007 Beijing, China

Yesterday I made enough paraformaldehyde to fix a horse. That excites me in a weird way. We’re pretty much ready to go now. Traps, lots of food (for us and rodents), DEPC water, PFA, tubes and tubes and tubes… After the prep work, I caught the train downtown and walked for about 2 hours to get to the Forbidden City to meet Shaoyuan. If it’s true that the best way to learn a city is to get lost in it, then I must know Beijing pretty well by now. I had no idea how EVERYTHING on the map is very very very tiny compared to real life. And to you Texans out there – you aint got nuthin on China. Nothing is bigger in Texas compared to this place.

I was doing fine on time until I got to Tiananmen Square. The Chinese flag in the square is lowered every day at sunset and is cause for a huge spectacle. They shut down all foot traffic past the flag as a crowd of several thousand forms. I had to take the underground passages to get around everyone. But not until after I snapped a fantastic shot of a guy posing in front of the police formation. That’s one thing I love about Asia. People here will pose for a picture in front of just about anything. As a result, I’ve started a bit of a collection of my own pictures of people having their pictures taken in front of random things :) So after a bit of a walk around, Shaoyuan took me to some famous restaurant where we had the most AMAZING duck I’ve ever eaten in my life. It was so juicy, and the skin was the most perfect brown crispy deliciousness.That’s it for now. I’m going to help get things ready to leave tomorrow and then we’re going back down to see the inside of the Forbidden City and visit Chairman Mao’s preserved remains. More later…

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Hello Node Community:
I would like to inform you about the Development Travelling Fellowships. Are you a Graduate student or Post-doc wishing to make a collaborative visit to another lab?

You can apply to Development to fund your travelling expenses. Development offers up to £2,500, you do of course have to be working in the field of developmental biology and intend to visit another lab.

All the information you need can be found at http://dev.biologists.org/site/misc/fellowships.xhtml along with an application form.

See a report from one of our previous recipients here

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I am a graduate student from Indian Institute for Science Education and Research (IISER), Pune, India. I wish to share some of my work and life experiences in Japan from a recent visit. Our lab works on development and evolution of insect wings. I am interested in understanding the development of lepidopteran wings using Bombyx mori ( silkmoth) as a model system. Initially at my place it was an ordeal working experiments mostly for the lack of technical expertise on silkmoth experiments and lack of availability of resources.

We decided to carry out some experiments in the University of Tokyo, Kashiwa campus to study the development and evolution of insect wings, specifically lepidopteran wing development, using the silkmoth as a model organism. Expertise on studies in silkworm development is abundant in Japan as there are many research groups working on this various aspects of silkworm development. To be housed in one of the best universities in asia was a privilege and the facilities and research truly matched the stature of one of the best institutes in the world.

I was in Prof. Haruhiko Fujiwara’s lab which works on Silkworms, Butterflies and different aspects of their genetics and development. The facilities in the lab were really state of the art, organization of the lab was immaculate and expertise vast which helped my work progress smoothly. One hurdle was definitely that of the language which I should admit was a more than what I anticipated, most people in the campus speak in Japanese, study and even discuss science in Japanese, but it seemed trivial with the kind nature of the people, every time they put an effort beyond their way to help you in every situation in lab or on outside. A little Japanese learned beforehand came in handy at times and also got a smile across people there who always appreciated generously for every one of my efforts to speak their language.

I started experiments here as soon as I came in but for a week or so they really did not work as I had to get adjusted to the setup and find the reagents and understand the instruments (some of which had complete Japanese menus!). With the help of the friendly lab members things moved rapidly and was able to understand the techniques they used and apply to solve issues which had troubled me in research so far. In a lab of around 20 people everyone chipped in whenever I had problems to trouble shoot with the best they could and made work progress fast and life easier. The discussions with my sensei (used to address professor in Japanese) were very helpful to understand the development of silkworm and to apply techniques like immuno histochemistry and RNA in situs. As these experiments were done in the lab on a regular basis and also the worms were studied extensively here, hence work moved smoothly and results were easy to come once I was settled in. I could work out all the standardization of Chromatin Immunoprecipitaion (ChIP) with the abundant silkworm resource which was excellently maintained. There wasn’t a single hindrance for an experiment no matter when I wanted to perform them because of the excellent maintenance of the larvae and the whole-hearted support of the lab.

During this trip I also had a golden opportunity to interact with other developmental biologists at the JSDB 2010 meeting at Kyoto. The discussions in the conference included various interesting aspects of developmental biology ranging from growth control, organogenesis to mathematical modeling. The meeting had over 300 poster presentations, where I also got an opportunity to present my work so far and discuss with the best researches in japan and also world-over. It was interesting to discuss with various interesting research projects from japan and other places, also helping understand our own research problems better and flashing some new and interesting insights.

The talks by Prof Eric Wieschaus and Prof Roel Nusse were enlightening and it was really a great opportunity to interact with these scientists, who were very encouraging and made the science more interesting , by inducing many new questions in the mind and also helping our research interests through superlative discussions.  apart from the conference Kyoto as a citywas serene and beautiful, having been to Tokyo this part of the world seemed a page from the ancient and rich traditional Japan and a wholly different landscape from what I had seen or imagined.

People in Japan were very kind, polite, peace loving and sweet who helped in every step of my stay. There a lot of international students around especially in my residence where they were very cooperative and were as kind as Japanese themselves. They organized various events from the art of wearing Japanese yukata (traditional Japanese dress) to that of attending the local city festival on weekends. They helped with every problem and also make stay fun filled and enjoyable in every way.  Cycling was the best transport in Japan for there were free lanes; it was always fun riding to university through a very beautiful park. For being a vegetarian the other constant problem was food, which I had to cook to survive in a land where nothing was vegetarian. The versatile kitchen facility eased out cooking for my survival and sometimes the vibrant community joined in usually watching football worldcup cheering for Japan or South Korea. It was the charm of the place and people around that made problems gradually melt away etching wonderful memories, easing life and making work enjoyable in a very pleasant ambience.

This visit helped move rapid strides in answering my research question and allowed me to learn newer methods to apply and progress in my research work. I am sure a lot of research problems will be solved and this work will raise new and interesting questions for me to pursue further ahead in research. I hope my experience will encourage more people to work across borders to learn the best from all the great learning centers and Japan in particular, which has people who work really hard and help each other to reach greater heights in their endeavors.

I would like to thank the Development and APDBN fellowships for their encouragement and generous support for my travel and stay in Japan. I would like to thank the Prof Fujiwara and University of Tokyo for the kind invite, support and warm welcome into their facility. My sincere thanks to the lab members of his lab and also other labs which helped and supported to the fullest, whose untiring help and encouragement helped me enjoy both work and stay in Japan. I would like to thank my supervisor Prof. Shashidhara and IISER pune for initiating this interaction and supporting all the way in my graduate study. I would like to thank node for allowing me to share my unforgettable memories of  Japan.

(2 votes)

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