A ERC funded postdoctoral position is available in the laboratory of Julien Courchet at the NeuroMyoGene Institute within the University of Lyon, France.

Our group studies the molecular mechanisms underlying axon outgrowth and neural circuits formation in the mouse cerebral cortex. Our current research is supported by an ERC Starting Grant and funds from AFM-telethon to explore how a dynamic regulation of the energy metabolism is involved in axon morphogenesis and cortex development. We focus on a previously identified kinase pathway controlling terminal axon branching through the regulation of mitochondria trafficking and distributing in developing axons (Cell 2013). Building on this previous research, the proposed project will use a combination of whole cell metabolomics, real-time fluorescent videomicroscopy and live 2-photon imaging to characterize some of the molecular mechanisms involved in the local regulation of mitochondria function in developing axon in vivo.

The selected candidate will join a young research team within a dynamic and collaborative scientific environment at the newly created NeuroMyoGene Institute (INMG). The candidate will have access to state-of-the-art facilities for imaging and metabolic analyses, including high quality confocal and 2-photon microscopes, animal phenotyping centers and a seahorse analyzer. Our institute is located in a newly renovated laboratory space in the Rockefeller faculty of Medicine in close proximity to the Neuroscience and the Cancer Research Centers.

Applicants should have a PhD degree or equivalent with a strong background and practical experience in neurobiology, confocal microscopy and/or real-time imaging. Previous experience working with rodent models is required. Training in techniques relevant to cell signaling, metabolic regulation and optogenetics would be an asset. We are looking for a highly motivated candidate with a strong attitude towards independent work and good interpersonal and communication skills. Excellent written and spoken English skills are essential. Ability to speak French in not mandatory.

The initial appointment is one year and can be renewed for 2 additional years. Salary including benefits will depend on previous experience according to guidelines at the University of Lyon. Applications will be reviewed on a rolling basis until position is filled. Selected candidates will be invited for an interview early 2018. Project start date is expected during the first semester of 2018.

Interested candidates should contact Dr Julien Courchet (julien.courchet@inserm.fr) with their CV, a summary of their previous research (< 1 page), a brief statement of their research interests and career goals, as well as the contact information for at least 3 references.

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The MRC Weatherall Institute of Molecular Medicine (WIMM) has fully funded 4-year Prize PhD (DPhil) Studentships available to start in October 2018. These Studentships are open to outstanding students of any nationality who wish to train in experimental and/or computational biology.

The Institute is a world leading molecular and cell biology centre that focuses on research with application to human disease. It includes the recently opened MRC WIMM Centre for Computational Biology and houses over 500 research and support staff in 50 research groups working on a range of fields in Haematology, Gene Regulation & Epigenetics, Stem Cell Biology, Computational Biology, Cancer Biology, Human Genetics, Infection & Immunity. The Institute is committed to training the next generation of scientists in these fields through its Prize PhD Studentship Programme.

The fully funded studentships include a stipend of £18,000 per annum and cover University and College fees.

Further information on the studentships, how to apply, and the projects available can be found at:

http://www.imm.ox.ac.uk/wimm-prize-studentships-2018

Closing date for submission of applications:  Monday, 8 January 2018, 12 noon UK time.

Interviews will take place the week commencing 22 January 2018.

Pure Computational Biology Project Leaders

Hashem Koohy – Machine-learning in gene function, transcription regulation and immunology

Ed Morrissey – Quantitative biology of cell fate

Aleksandr Sahakyan – Regulatory chromosomal domains and genome architecture

Supat Thongjuea – Computational biology of single-cell transcription and gene regulation 

Molecular and Cell Biology Project Leaders

Ahmed Ahmed – Experimental therapeutics

Chris Babbs – Causes of congenital anaemia

Oliver Bannard – B cell biology

Andrew Blackford – DNA damage and disease

Walter Bodmer – Colorectal cancer, stem cells, differentiation & drug response

Marella De Bruijn – Developmental haematopoiesis

Zam Cader – Stem cell neurological disease models

Vincenzo Cerundolo – Tumour immunology, vaccine strategies

David Clynes – DNA damage, repair and cancer

Simon Davis – T-cell biology

Hal Drakesmith – Iron and infection

Christian Eggeling – Super-resolution microscopy in immunology

Ben Fairfax – Inflammation, genetics and cancer therapeutics

Marco Fritzsche – Biophysical immunology

Lars Fugger – Multiple sclerosis

Tudor Fulga – MicroRNAs in development and disease

Richard Gibbons – Chromatin, epigenetics & transcription

Anne Goriely – De novo mutations and human disease

Doug Higgs – Gene regulation and epigenetics

Ling-Pei Ho – Lung immunology

Georg Hollander – T cell development and thymus organogenesis

David Jackson – Lymphatic trafficking in inflammation and cancer

Peter McHugh – DNA repair

Adam Mead – Normal and leukaemic haematopoietic stem cell biology

Claus Nerlov – Tissue stem cell genetics

Graham Ogg – Translational skin research

Catherine Porcher – Transcription factors and blood development

Jan Rehwinkel – Innate detection of viruses

Irene Roberts – Trisomy 21, haematopoiesis and leukaemia

Tatjana Sauka-Spengler – Neural crest gene regulatory networks

Alison Simmons – Innate immunity & Crohn’s disease

Alain Townsend – Influenza and ebola, vaccination and treatment

Paresh Vyas – Leukaemic stem cells

Andrew Wilkie – Sperm and craniofacial mutations

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The Karam Teixeira laboratory (https://www.gen.cam.ac.uk/research-groups/karam-teixeira) at the University of Cambridge (Department of Genetics) is looking to recruit an outstanding Postdoctoral scientist to investigate the molecular mechanisms sheltering totipotency and controlling germline stem cell behavior in vivo. Using the Drosophila germline as a model for studying stem cells, we employ an integrated approach, combining high-throughput molecular analysis (next-generation sequencing) and computational investigation with developmental, microscopy, and genetic analyses (including CRISPR-Cas9 gene editing, tissue-specific RNAi knockdown, etc). We were previously able to assemble the complete genetic framework controlling germline stem cell self-renewal and differentiation in vivo, revealing conserved new aspects of stem cell biology (Teixeira et al, Nature Cell Biology, 2015; Sanchez et al, Cell Stem Cell, 2016). Moving forward, our goal is to build a refined molecular understanding of how protein synthesis control – a new frontier in gene regulation – governs stem cell fate transitions in vivo. Our lab is generously funded by the Wellcome Trust.

Candidates must have experience in a wide range of molecular biology techniques, and prior expertise in next generation sequencing would be an advantage. Experience working with fly genetics is a plus but not required. The successful candidate will be highly motivated, willing to join a young and dynamic research group, have good communication skills, and possess strong problem solving capacities.

How to apply:

To apply online, please follow the link: http://www.jobs.cam.ac.uk/job/15379/

Applications should include a cover letter, Curriculum Vitae, and the contact information of at least two references.

The position start date is flexible. Application deadline: November 17^th, 2017.

For an informal discussion about this position, please contact Dr. Felipe Karam Teixeira (fk319@cam.ac.uk).

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Andras Paldi, Daniel Stockholm, Alice Moussy

How do phenotypic differences between cells of the same clonal origin emerge? How exactly does the transition between the initial and final phenotypes occur? What happens in the cell during the transition? When there are two or more options, how is the choice made between them? How long does it take to acquire a new phenotype? What is the minimal difference required to consider two cells as phenotypically different? To define a cell type, should we consider only morphological, molecular differences or both simultaneously?

Despite the plethora of studies, these simple questions remain unanswered. Most of the studies focus on identifying the essential genes or environmental factors usually at the level of cell populations. The huge amount of molecular data accumulated over the past decades gave us the illusion of knowledge. Knowing the players is obviously essential, but this is only the starting point for the understanding. Unfortunately, our understanding of the process of differentiation remains desperately scarce, as the lack of clear responses to the above listed simple questions shows.

Recently, two important challenges came to modify the perception of differentiation. The first comes from the spectacular development of single-cell technologies. The second is that we have to come to realize how much phenotypic plasticity is a genuine characteristic of cells. The main lesson from the rapid development of single-cell detection techniques is the unambiguous demonstration of how different individual cells are and how poorly population-level averages represent them. The bulk of our knowledge on differentiation comes from studies of cell populations. Perhaps unconsciously, we took for granted that individual cells all follow with small variation the same sequence of events as what we could see at the level of cell populations. The unexpectedly high variation of individual cell phenotypes in populations that were believed to be homogenous (because of the morphological similarity of the cells, their clonal origin, their expression of some markers etc.) draw the attention to the phenotypic plasticity of the cells and to the fact that fate decisions are “taken” by individual cells.

Clearly, a coherent, systemic level explicative frame is needed that can account for the coherent population-level behaviour emerging from highly variable individual cell phenotypes and behaviour.

Our recently published work [1] was motivated by the wish to contribute to this effort. Although we used the extensively studied hematopoietic stem cell model, we were surprised how much these general questions fit to the model. The definition of the hematopoietic stem cell is widely debated, no precise description of the earliest events of differentiation and only very scarce information on the morphological changes during the same period were available. The study of hematopoietic stem cells is made difficult by the lack of exact criteria to identify them. Nonetheless, there is a consensus that CD34+ cell fraction in the umbilical cord blood contains high number of these cells. We decided therefore to privilege an integrated view and work on the whole population of CD34+ cells. Individual cells were randomly sorted from the population at different fixed time-points and their gene expression profile was analysed by single-cell RT-PCR. The structure of the population and its components were identified on the basis of the collected single-cell gene expression data. Parallelly, we set up a time-lapse system that allowed the continuous monitoring of the cells and their progeny during the first 96hrs after stimulation. Adding the continuous observations of the morphological changes and cell division timing of individual cells to the single time-point single-cell molecular analysis sampling of the same population provided a glimpse of the true dynamic nature of cellular fate decision.

The CD34+ cell fraction is traditionally considered as heterogeneous. Indeed, before cytokine stimulation every cell displayed a unique gene expression profile. However, no groups could be identified on the basis of their statistical similarity, this population is not a mixture of a limited number of “cell types”. When cytokines were added to the culture, every cell responded in a unique way. Again, every cell displayed a unique gene expression pattern that was different of the previous seen at t=0 hours. It was characterized by the simultaneous expression of different lineage-specific genes. This state is known as a multi-lineage primed pattern [2, 3]. A second round of change occurred during the second 24 hours. Two days after the stimulation of the cells two distinct transcription patterns emerged. One pattern was typical for myelo-erythroid progenitors, while the second was reminiscent of multipotent cells. Until now, the results overall confirmed the previous studies; the main novelty was the apparent rapidity of transition from the initial to a multilineage primed gene expression pattern and, just 24 hours later, to two distinct profiles. However, these snapshots did not allow us to deduce on the dynamics of the changes.

The real surprise came from the analysis of the time-lapse records. Individual CD34+ cells were placed in microwells and imaged for a week at 1 image/min. The resulting time-lapse records allowed us to record cell cycle lengths and morphological changes of each individual cell within individual clones. After stimulation, the cells usually displayed a polarized shape with a strong protrusion on one side called uropod. The first unexpected observation was to see that the unusual length of the first cell cycle. The cells made more than 50 hours on average to divide. This means, that the first major transcriptional change occurred during the first cell cycle and the second around the end of the first or the very beginning of the second cell cycle. After the first division, we could see two different morphologies; one was strongly polarized with a uropod, the second is spherical. The daughter cells usually inherited the morphology of their mothers. Polarized cells gave two polarized and round cells two round daughters. However, we were surprised to observe that a significant proportion of the cells did not conserve a stable morphology; they switched from one morphology to another and back many times during the cell cycle. The majority of their daughter cells also conserved the fluctuating phenotype

We called these cells “hesitant”. The overall picture suggest that stimulated CD34+ cells, after a brief passage through a multilineage primed state reach (without cell division!) one of the two alternative states characterized by a typical transcription pattern and cellular morphology. However, a significant proportion of cells fluctuate between the two morphologies. Does this morphological instability reflect transcriptome fluctuations? To answer this question, we have isolated individual cells with the three different – stable round, polarized or “hesitant” – behaviours and analysed their gene expression pattern. It appeared that the cells with stable morphology displayed one of the two expression patterns first observed at the 48 hors time point. The “hesitant” cells were characterized by an intermediate profile. The molecular analysis correlated to the time-lapse data suggests therefore that these cells are in an unstable state; their transcriptome undergoes fluctuations that are reflected in their fluctuating morphology also.

These are the key observations and the immediate conclusions of this work. However, these observations may contribute to the current tendency to reframe the issue of cell differentiation and stem cells in general. Cell differentiation can be approached using the concepts of stability and change – two complementary concepts widely used in biology. Stem cells may represent a highly unstable cell fraction contrary to the cells with stable differentiated phenotype. Unstable stem cells are actively exploring the space of available phenotypes before getting trapped by one of them. This is a kind of trial-and-error process. Under normal conditions, the unstable period is relatively short lasting; this is why the unstable cells we consider as stem cells are so rare in a normal tissue. However, a substantial change in the environment can destabilize many cells at the same time. This is what we see when CD34+ cells are stressed by the sudden addition of a cytokine cocktail. Due to the progressive adaptation to the new environment, the proportion of the “hesitant” stem cells decreases gradually as they attracted to the more adapted phenotypes. Importantly, this process seems to depend only indirectly on cell divisions. This interpretation is in remarkable agreement with earlier theoretical predictions and experimental work [4-8] and supported by recent experimental observations also [9-12].

Our paper was initially submitted to a well-known journal in stem cell biology. Beyond the disappointment of the rejections (every scientist is used to that), we were surprised by the poor quality of the reviews. The referees raised some technical concerns about the single-cell RT-PCR versus single-cell RNA sequencing, but not a single word about the time-lapse experiments that represented the major part of the paper, nor about the coupling the molecular and cellular scales, which is the true originality of the work. The reviews were very different when the manuscript was submitted to PloS Biology. The comments concerned all aspects of the work and the suggestions truly helped to improve the final version.

It would be naïve to think that a single paper can answer the fundamental questions raised at the beginning of this text. Clearly, we need a fresh view on cell differentiation that goes beyond the simple gathering and classification of molecular data and takes into account the true dynamics.

References

1. Moussy A, Cosette J, Parmentier R, da Silva C, Corre G, Richard A, et al. Integrated time-lapse and single-cell transcription studies highlight the variable and dynamic nature of human hematopoietic cell fate commitment. PLoS Biol. 2017;15(7):e2001867. doi: 10.1371/journal.pbio.2001867. PubMed PMID: 28749943; PubMed Central PMCID: PMC5531424.
2. Hu M, Krause D, Greaves M, Sharkis S, Dexter M, Heyworth C, et al. Multilineage gene expression precedes commitment in the hemopoietic system. Genes & development. 1997;11(6):774-85. PubMed PMID: 9087431.
3. Pina C, Fugazza C, Tipping AJ, Brown J, Soneji S, Teles J, et al. Inferring rules of lineage commitment in haematopoiesis. Nature cell biology. 2012;14(3):287-94. doi: 10.1038/ncb2442. PubMed PMID: 22344032.
4. Furusawa C, Kaneko K. A dynamical-systems view of stem cell biology. Science. 2012;338(6104):215-7. doi: 10.1126/science.1224311. PubMed PMID: 23066073.
5. Huang S. Non-genetic heterogeneity of cells in development: more than just noise. Development. 2009;136(23):3853-62. doi: 10.1242/dev.035139. PubMed PMID: 19906852; PubMed Central PMCID: PMC2778736.
6. Kupiec JJ. A chance-selection model for cell differentiation. Cell death and differentiation. 1996;3(4):385-90. PubMed PMID: 17180108.
7. Kupiec JJ. A Darwinian theory for the origin of cellular differentiation. Molecular & general genetics : MGG. 1997;255(2):201-8. PubMed PMID: 9236778.
8. Paldi A. Stochastic gene expression during cell differentiation: order from disorder? Cellular and molecular life sciences : CMLS. 2003;60(9):1775-8. doi: 10.1007/s00018-003-23147-z. PubMed PMID: 14523542.
9. Mojtahedi M, Skupin A, Zhou J, Castano IG, Leong-Quong RY, Chang H, et al. Cell Fate Decision as High-Dimensional Critical State Transition. PLoS Biol. 2016;14(12):e2000640. doi: 10.1371/journal.pbio.2000640. PubMed PMID: 28027308; PubMed Central PMCID: PMC5189937.
10. Notta F, Zandi S, Takayama N, Dobson S, Gan OI, Wilson G, et al. Distinct routes of lineage development reshape the human blood hierarchy across ontogeny. Science. 2016;351(6269):aab2116. doi: 10.1126/science.aab2116. PubMed PMID: 26541609; PubMed Central PMCID: PMC4816201.
11. Richard A, Boullu L, Herbach U, Bonnafoux A, Morin V, Vallin E, et al. Single-cell-based analysis highlights a surge in cell-to-cell molecular variability preceding irreversible commitment in a differentiation process. . Plos Biology. 2016;(14):e1002585. doi: doi.org/10.1371/journal.pbio.1002585.
12. Velten L, Haas SF, Raffel S, Blaszkiewicz S, Islam S, Hennig BP, et al. Human haematopoietic stem cell lineage commitment is a continuous process. Nature cell biology. 2017;19(4):271-81. doi: 10.1038/ncb3493. PubMed PMID: 28319093.

(1 votes)

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Doing a PhD is tough, the data from surveys supports that. However it is not insurmountable, and here we have a collection of some guidance from the Twitter community.  Let us know in the comments if you have any thoughts to add.

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The Department of Biology within the College of Natural and Health Sciences at The University of Tampa invites applications for a tenure track position in developmental biology at the rank of Assistant Professor starting in August 2018.

The University of Tampa is a medium-sized, comprehensive, residentially-based private institution of 8,913 undergraduate and graduate students. The University is ideally situated on a beautiful 110-acre campus next to the Hillsborough River, adjacent to Tampa’s dynamic central business district, which is a growing, vibrant, diverse metropolitan area. UT reflects this vibrancy; with 20 consecutive years of enrollment growth UT boasts 229 student organizations, a multicultural student body from 50 states and 140 countries, and “Top Tier” ranking in U.S. News and World Report.

Primary responsibilities will include an undergraduate teaching load of 12 contact hours per semester. The candidate is expected to teach introductory biology for majors, an upper division course in developmental biology, and other courses as needed.
Secondarily, the candidate is expected to engage in scholarly and research activity that involves undergraduates, advise students, and provide service to the department, college, university and broader community. Research activities must yield peer-reviewed publications.
PhD preferred (advanced ABD candidates considered), prior teaching and research experience with undergraduates is desirable.

Salary for this position is competitive and commensurate with experience.
Review of applications will begin January 2, 2018, and continue until the position is filled. Limited start-up packages and modest research space are available for tenure-track positions.

For application details please visit

https://utampa.wd1.myworkdayjobs.com/en-US/Faculty/job/Tampa/Assistant-Professor-of-Biology–Developmental-Biologist-_R0001530

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What is the role of wrt-2 and wrt-4 in left-right asymmetry in C.elegans?

Once upon a time a genetic screen identified a signalling pathway that caused Drosophila melanogaster embryos to develop a ‘lawn’ of denticles rather than forming them only at parasegment boundaries. Thus the so-called Hedgehog signaling pathway was born (Nusslein-Volhard & Wieschaus, 1980). This pathway has revealed itself to be one of the core signal transduction pathways in regulating animal development. Through gene duplication and diversification events, different types of hedgehog proteins have been found across vertebrates. The brilliantly named Sonic Hedgehog ligand is the best studied ligand present in mammals. Loss of expression of Sonic Hedgehog in mice causes defects in left right asymmetry (Levin et al., 1995).

The story was expanded into C.elegans by bioinformatics (Burglin, 1996). A search of the C.elegans genome for homologues of the carboxyl terminal ‘hog’ domain revealed a family of proteins which did not contain the amino terminal ‘Hedge’ domain but instead a novel domain dubbed ‘Wart’. Thus the warthog (wrt) genes were named. Further genome analysis revealed genes which contained the amino wart domain but lacked the carboxy hog domain. Together this made a family of ten warthog genes.

Previous research in my lab (the Woollard lab in the Biochemistry department at the University of Oxford) had linked the wrt-2 branch of the warthog family (figure 2) to defects in left right asymmetry, with wrt-2 and wrt-4 giving the highest penetrance phenotypes. However it was found that the GFP marker used in the previous strains to help quantify another phenotype (related to vulval development) caused defects of its own. This is where I come in. My project was to cross and create strains of worms without this GFP background and then requantify the left right asymmetry defects. I studied the single mutants wrt-2, wrt-4, wrt-8, as well as the double mutants wrt-4;wrt-2, wrt-8;wrt-2, wrt-8;wrt-4 and the triple mutant wrt-8;wrt-4;wrt-2. The double and triple mutant strains I created myself. The combined mutations allow investigation into redundancy between the genes, giving a glimpse into their evolutionary history. The wrt-7 gene has been shown to have no expression pattern and is likely a pseudogene, so due to my limited time in the lab I didn’t quantify the wrt-7 mutations.

On a side note: the C.elegans species is great. They’re heamaphrodites so you can just leave them on an agar plate to reproduce by themselves. Males do exist – enabling you to perform genetic crosses. They’re transparent, so no need to dissect anything. You can even freeze them and they’ll be alright in liquid nitrogen until someone needs them!

At first glance C.elegans may not seem very asymmetric. However one source of left right asymmetry is the relative positioning of the gonads and intestine either side of the vulva in the worm. This is best shown through pictures. In the wildtype worm (figure 3d) the picture in the lefthand plane shows that in the anterior part of the worm one can see intestinal cells and the intestinal lumen going down the centre. In the posterior part of the worm one can see the U shaped gonad that migrates away from the vulva (just visible in the bottom left hand corner of that picture) along the body, turns twice then travels back along the body (schematic figure 3c). The top picture of a whole worm (figure 3d) shows the opposite situation (the worm is laying on its other side) where the gonad can be seen at the anterior part of the body and the intestine at the posterior.

Thus the anterior/posterior distribution of gonad and intestine gives us a tool to study and quantify left right asymmetry in worms. After discussions with Emily (a recent biology graduate who had been working on the project before me) we decided to only quantify worms in which the posterior gonad was visible down the microscope. Thus, worms which I counted looked like those in the two lefthand plane pictures in figure 3d. This decision, although arbitrary in itself, allows our results when published to be more understandable and easier to replicate.

The pictures shown in figure 4 demonstrate some of the mutant phenotypes scored in this project. Basically I was looking for gonad tissue poking through anterior intestine tissue and intestine tissue poking through posterior gonad tissue. Worms with this phenotype were scored as mutant and were also further divided into anterior or posterior defects.

One of the most enjoyable parts of this project has been pipetting alongside Emily, who worked on this project before me and is continuing to develop it. In my 8 weeks I have seen first hand a small portion of the amount of research that has gone into studying the warthog genes. However chatting with Emily I have seen how my short project may in future count towards producing a scientific paper. At the moment Emily is taking the story of warthog genes in C.elegans back to its bioinformatics heart, producing a phylogenetic tree of all the warthog genes across the nematode family – trying to link evolution with phenotype. She is also expanding from the wrt-2 branch of the gene family into as many other members as she can get her hands on.

The highlight of my time in the project has been having so much independence in the lab, deciding day to day, week to week how I wanted to spend my time. This has been a fantastic insight into the life of a researcher and totally different to undergraduate labs. The lowlight would have to be the Saturday when I broke a pipette and in the process spilled a box of pipette tips all over my desk…

Thank you so much to everyone in the Woollard lab for being more friendly and welcoming than I could have hoped for.

Josie Elliott

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The paper, published in Nature Cell Biology, by the Semb Group at DanStem, shows that cell polarity (the cell’s ability to sense what is up and down) in progenitor cells not only contribute to the architecture and shape of organs, e.g. tubular systems, but also governs the fate progenitor cells.

Video: 3D volume rendering of two endocrine progenitor cells (green membrane and red nuclei). The cell on the left is immature and has a larger apical domain facing the lumen of the duct (labeled in red) while the other cell has downregulated the apical domain. Embryonic mouse pancreas grown and imaged live in vitro

Major scientific findings of the paper

The scientists answer a fundamental question as to how the limited number of genes in our genome can control the large complexity of our organism. The results illustrate how genes are re-utilized in a context-dependent manner to expand their ability to control, not only one, but a many complex cellular events during organ formation.

Epidermal growth factor (EGF) signaling is identified as an essential regulator of cell polarity throughout pancreas formation to regulate tube formation (early) as well as the birth of insulin-producing beta cells (late).

The paper answers a long-sought question: how progenitors in the developing pancreas are instructed to become insulin-producing beta cells.

This discovery can be utilized to increase the efficiency and robustness of differentiating human pluripotent stem cells into insulin-producing beta cells for future cell therapy in type 1 diabetes, and deliver new general concepts for how cues from the environment instruct organ-specific multipotent progenitors into their different fates.

Link to the paper

Löf Öhlin, Zarah, Pia Nyeng, Matthew Bechard, Katja Hess, Eric Bankaitis, Thomas U. Greiner, Jacqueline Ameri, Christopher V. Wright & Henrik Semb (2017). Context-specific regulation of apicobasal polarity by EGFR orchestrates epithelial morphogenesis and cellular fate. Nature Cell Biology, doi: 10.1038/ncb3628.

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The O’Brien Lab (http://www.stemdynamics.org) is part of the Department of Molecular and Cellular Physiology at Stanford University School of Medicine. Our goal is to uncover the ongoing dialog that adult stem cells have with the tissues they support, and understand how this dialog happens on the molecular and cellular levels. We use a simple invertebrate organ, the Drosophila midgut, to pioneer new imaging and computational approaches that address basic questions in stem cell biology.

The O’Brien Lab is seeking a highly motivated, detail-oriented Life Science Research Professional 1 (LSRP1) to join our dynamic laboratory environment. The LSRP1 will perform functions and activities involved in defined research projects, which principally involve live and fixed tissue microscopy of Drosophila organs, computerized image analysis (ImageJ/Imaris), basic MATLAB coding, and construction and maintenance of sophisticated Drosophila genetic stocks. The goals of the projects are to understand cellular interactions and signaling in stem cell based Drosophila organs.

*- At the time of the interview, applicants will be asked to provide evidence of their imaging skills in the form of publications, posters, report, or other documentation.

Interested applicants must visit https://stanfordcareers.stanford.edu/job-search and enter 76659 in the job number field.

For more information, contact Shruthi Balachandra: sbalacha@stanford.edu

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