This interview, the 59th in our series, was recently published in Development

The control of timing in development is crucial, both within and between tissues. Heterochrony involves shifts in the rate of development of some tissues relative to others, and although the first heterochronic genes were identified in Caenorhabditis elegans in the early 1980s, their role in inter-tissue developmental coordination is still not completely understood. A new paper in Development tackles this problem with an analysis of the role of lin-28, a key heterochronic gene, in worm fertility. We caught up with Sungwook Choi, first author and recently graduated PhD student in Victor Ambros’ lab at the University of Massachusetts Medical School in Worcester, to find out more.

When did you first get in to science, and biology in particular?

I have been interested in biology ever since high school. I remember, at that time, being intrigued by the fact that each cellular compartment has distinct functions. I majored in life sciences during my undergraduate studies and focused on plant developmental biology during my Master’s degree.

Why did you decide to make the transition from plant to animal development?

Studying plant biology – in particular the biosynthesis of jasmonic acid in Arabidopsis – gave me the opportunity to be exposed to basic molecular techniques and genetic analysis. Later, when I started my graduate studies in University of Massachusetts (UMass) Medical School, I became interested in small RNA biology. I was fortunate enough to join the laboratory of Victor Ambros and learned that microRNAs, such as lin-4 and let-7, are key regulators of animal developmental timing. Since then, I have expanded my studies beyond microRNAs to include various genetic factors that regulate the timing of animal development.

How did you find the other transition – moving from South Korea to the USA?

It was quite a smooth transition. Although language barriers were inevitable at first, I met many nice people who helped me inside and outside of the laboratory. Also, I greatly enjoy and appreciate the international environment that UMass Medical School fosters through its inclusion of people with different nationalities from diverse cultures.

Before your paper, what was understood about lin-28‘s role in coordinating developmental events?

lin-28 was first identified as a developmental timing regulator in C. elegans by Victor Ambros and Bob Horvitz in the 1980s. The loss of lin-28 causes precocious hypodermal development in larvae and its function has mainly been studied in this context. In particular, many studies have elucidated the genetic relationship of lin-28with other developmental timing regulators such as lin-4, let-7, hbl-1 and lin-46. This genetic regulatory network is called the ‘heterochronic pathway’. In terms of inter-tissue regulation, a 2016 study from Gary Ruvkun’s lab showed that the heterochronic pathway genes act in the hypodermis to regulate mTORC2 signalling in the intestine.

Can you give us the key results of the paper in a paragraph?

We first looked at why lin-28 loss-of-function mutants exhibit reduced fertility. We found that somatic gonadal structures of the mutants are abnormal, which negatively affect the reproductive process, especially spermathecal exit and ovulation. Then, we asked how lin-28 regulates somatic gonadal structure. By genetic epistasis and tissue-specific rescue experiments, we found that the hypodermal, not somatic gonadal, function of lin-28 in controlling developmental timing is crucial for somatic gonadal development. Therefore, our data indicate that timely hypodermal development guaranteed by lin-28function is essential for somatic gonadal morphogenesis.

Timely hypodermal development guaranteed by lin-28 function is essential for somatic gonadal morphogenesis.

Your data suggest that lin-28 affects somatic gonadal morphogenesis cell non-autonomously: how might an RNA-binding protein act from a distance?

Our data implies that the downstream targets of LIN-28, such as let-7 and lin-46, are still in the hypodermis, not in the somatic gonadal tissues. Therefore, LIN-28 binding to its target RNAs probably happens in the hypodermis. What we have not yet identified is the exact mechanism by which hypodermal precocious development can talk to somatic gonadal morphogenesis. We speculate that there might be actual signalling molecule(s) from the hypodermis to somatic gonad, and/or perhaps physical contact between two tissues could be aberrant in lin-28loss-of-function mutants.

When doing the research, did you have any particular result or eureka moment that has stuck with you?

When I tried to identify the physiological causes of infertility of lin-28(lf) mutants, I didn’t know where to start. Around that time, I went to the Boston Area Worm Meeting and heard the presentation from Erin Cram’s lab about ovulation and spermathecal exit of C. elegans. I came to the realization that lin-28(lf) mutants showed defects in spermathecal exit and from then on, I analysed the mutants focusing on aspects of somatic gonadal development.

And what about the flipside: any moments of frustration or despair?

For me, the frustrating moments about research are not the times when I disprove my research hypothesis. What is most frustrating for me is when established protocols or techniques are not working as expected for my experiments for reasons that I do not understand very well. However, I kept trying to analyse the technical challenges and to enjoy the process of problem solving as a researcher.

Congratulations on getting your PhD last August – what’s next for you?

I haven’t completely decided yet. I am interested in several areas of research including those that are more clinically relevant. Regardless of the topic, I want to do research that is necessary for the progress of the field, even if it may not be particularly fancy.

Finally, let’s move outside the lab – what do you like to do in your spare time in Worcester?

I like Worcester very much. There are many local restaurants and pubs in Worcester, and some famous diners, which I often visit for breakfast. Other than that, I enjoy Worcester’s plentiful cultural resources, like the diverse exhibitions at the Worcester Art Museum and the concert series in the downtown area.

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We seek to appoint a Research Technician/Graduate Research Assistant to work on a research project elucidating a signalling pathway governed by the imprinted genes Dlk1 and Grb10. The pathway regulates fetal growth, lean to adipose body proportions and energy homeostasis, with relevance to growth disorders, obesity and diabetes.

The successful candidate will use biochemical, cell and molecular biology approaches to identify key additional pathway components.

A BSc in a relevant subject is essential along with experience of successfully applying at least one of the following techniques: mammalian cell culture, western blotting, histology, nucleic acid purification and PCR.

This is a fixed term contract for up to 3 years funded by the Medical Research Council.

For further details about the role please contact Prof. Andrew Ward (bssaw@bath.ac.uk), however, please ensure that all applications are submitted via the University website, also attaching a copy of your CV. Apply via the URL:

https://www.bath.ac.uk/jobs/Vacancy.aspx?ref=CC6582

The University of Bath and both the Department of Biology and Biochemistry and the Department for Health hold Athena SWAN bronze awards and are committed to equality of opportunity. We encourage applications from under-represented groups, including women.

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We seek to appoint an ambitious Research Associate to work on a research project elucidating a signalling pathway governed by the imprinted genes Dlk1 and Grb10.

The pathway regulates fetal growth, lean to adipose body proportions and energy homeostasis, with relevance to growth disorders, obesity and diabetes. The successful candidate will use mouse genetic, biochemical and cell biology approaches to identify key additional pathway components. They will join the group of Prof. Andrew Ward on the main campus at the University of Bath.

A PhD in a relevant subject is essential along with a strong background in cell biology and signalling biochemistry. Experience in mouse genetics and/or embryology, or in RNA-seq or proteomic data analysis, would be an advantage.

This is a fixed term contract for up to 3 years funded by the Medical Research Council.

For further details about the role please contact Prof. Andrew Ward (bssaw@bath.ac.uk), however, please ensure that all applications are submitted via the University website, attaching a copy of your CV. Apply via the URL:

https://www.bath.ac.uk/jobs/Vacancy.aspx?ref=CC6584

The University of Bath and both the Department of Biology and Biochemistry holds an Athena SWAN bronze award and is committed to equality of opportunity. We encourage applications from under-represented groups, including women.

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The Tata lab in the Department of Cell Biology, Duke University School of Medicine has an open position for postdoctoral researchers to study cellular plasticity mechanisms in lung injury repair and tumorigenesis. We seek to understand the genetic and epigenetic basis of organ regeneration and tumorigenesis. We study the properties of stem/progenitor cells in diverse epithelial tissues (with a primary focus on lung) and their relationships with neighboring tissues in pathophysiological conditions. We utilize in vivo mouse genetics, live imaging, 3D organoids, genome-wide Cas9/Crispr based functional genetic screening, and next generation sequencing technologies to study the behavior of tissues at single cell level. We offer an inspiring intellectual, collaborative and multidisciplinary research environment to support your career goals and provide access to state-of-the-art facilities. Candidates with background knowledge and hands-on experience in transcriptional regulation, 3D-organoids and bioinformatics skills are particularly welcome.

Requirements

– A PhD or MD/PhD (or equivalent) in biological sciences (cell & developmental biology or a related field).
– Strong research background in transcriptional regulation, cell biology, molecular biology, mouse models of cancer, and/or biochemistry. Prior experience in stem cells, Cas9/Crispr gene editing, 3D-organoid cultures, chromatin biology and bioinformatics is advantageous.
– Evidence of successful completion of a research project (publications)
– Ability to work independently; interpret, present and discuss experimental data
– Excellent communications skills

To apply, please submit a cover letter (less than a page) that includes a short summary of interests, a CV, and the contact information of 3 professional references to Dr. Purushothama Rao Tata (purushothamarao.tata@duke.edu)

Applications will be reviewed until positions are filled. The positions are available immediately.

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Research Group Julien Royet: “Host pathogen interactions in the Drosophila model”

IBDM (UMR CNRS 7288) • Parc Scientifique de Luminy • 13288 Marseille Cedex 9 • France

A PhD position is available at the Institute of Developmental Biology of Marseille (IBDM) for a motivated student to work on a research project investigating the genetic basis of host-bacteria interactions in the Drosophila model. This is a full-time position for 3 years. The candidate must be free to start in September/October 2019. The candidate will benefit from a doctoral grant from the National Research Agency (ANR).

Background

It is now very well established that gut-associated bacteria can impact the behavior and the physiology of their eukaryotic host. The PhD thesis project is aimed at using the powerful genetic tools available in the Drosophila model and the relative simplicity of its gut microbiota to study, at the molecular level, the molecular dialog between the microbiota and its host. In two recent publications, (Kurz et al, Elife, 2017: Charroux et al, Cell Host Microbe, 2018), the lab has shown that a metabolite produced by gut-associated bacteria, called peptidoglycan, can cross the gut epithelium and reach the insect blood where it interferes with various organs (fat body, ovaries, brain…) and modifies functions (behavior changes, organ wasting…). The PhD studentwill use the newest genome editing technologies (Crispr…), genetic tools and latest imaging microscopy technics to dissect the precise cellular and molecular mechanisms of the dialog that exist between gut-resident bacteria and some specific cells of the host. Recent results showing that mice deficient in peptidoglycan-sensing proteins exhibit social behavioral alterations suggest that the mechanisms that we study in Drosophila also exist in mammals. The research will be performed in the Institute of Developmental Biology of Marseille, an internationally recognized interdisciplinary research center and a very stimulating scientific environment (http://www.ibdm.univ-mrs.fr/).

Profile of the candidate 

We look for an enthusiastic and ambitious student with a strong interest in the genetics of host-bacteria interactions. The candidate is expected to have a background in molecular biology and should hold a Master Degree in Bioscience Engineering, Biotechnology or Biology. The candidate should have a level of proficiency in English which is sufficient to communicate effectively with colleagues.

Applications

Application documents should include a motivation letter, a curriculum vitae and a grade transcript. Additionally, the applicant is expected to arrange for two letters of recommendation to be sent to the address below. The application deadline is May 1^th, 2019. Applications should be sent electronically as one single file in pdf format to Julien.royet@univ-amu.fr, leo.kurz@univ-amu.fr and Olivier.zugasti@univ-amu.fr

Publications

Kurz et al, 2017. Peptidoglycan sensing by octopaminergic neurons modulates Drosophila oviposition. Elife. Mar 7;6. pii: e21937.

Charroux et al, 2018. Local and systemic immune responses to microbiota are respectively controlled by cytosolic and secreted peptidoglycan degrading enzymes in Drosophila.  Cell Host and Microbe. Feb 14;23(2):215-228

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Background

Mutualistic relationships between bacteria and complex organisms have repeatedly evolved and this has allowed host organisms to exploit new environments and foods. One of the most extreme and fascinating cases of symbiosis in the animal kingdom is observed in annelid worms of the genus Riftia and Osedax. These animals are able to live in particularly extreme environments, including deep sea hydrothermal vents and carcases thanks to bacteria from the environment that they acquire as juveniles. Ultimately, this induces a drastic developmental change where they degenerate their guts and rely entirely on the bacterial symbionts to produce the essential nutrients they require for survival in those hostile environments. Which cellular and genetic mechanisms control this bacterial symbiosis? How did these mechanisms evolve? How did its change contribute to animal evolution?

• In this project you would rigorously answer these questions sequencing and comparing the genome of these symbiotic worms with their closest asymbiotic counterparts.
• You would have access to a large genomic database, field collections and in-house live organisms to fuel your investigation.
• You would gain experience of molecular techniques (nucleic acid extraction, next generation sequencing), bioinformatics (e.g. genome assembly, RNA-seq analyses, gene family evolution), and statistics.
• You will be encouraged to develop your own ideas and hypotheses.

The studentship is fully funded and available to EU and UK citizens. It will cover tuition fees as well as provide an annual tax-free maintenance allowance for 3 years at Research Councils UK rates (£17,009 in 2019-20).

Skills preferred

In a multidisciplinary project like this, candidates are unlikely to have a background in all disciplines involved.  The most important qualification is motivation, enthusiasm and that the project appeals to you. However, previous computational experience would be a plus. We can envisage strong candidates coming through a variety of routes including:

• practical molecular biology
• evolutionary theory and phylogenomics
• computational biology

To apply, students should have a first class degree or have received a MSc in a relevant field (i.e. marine biology, evolutionary biology, bioinformatics) or are about to finish their MSc.

For informal requests, do not hesitate to contact me at chema.martin@qmul.ac.uk

***Deadline for application: 05.04.2019***

***Apply online via QMUL website*** 

Supervisor Information

Dr. Chema Martin

Email: chema.martin@qmul.ac.uk

Website: https://martinduranlab.com/

Dr. Lee Henry

Email: l.henry@qmul.ac.uk

Website: https://www.qmul.ac.uk/sbcs/staff/leehenry.html

Dr Yannick Wurm

Email: y.wurm@qmul.ac.uk

Website: http://wurmlab.github.io

Related References

• Cavanaugh, C. M., Gardiner, S. L., Jones, M. L., Jannasch, H. W. & Waterbury, J. B. (1981) Prokaryotic Cells in the Hydrothermal Vent Tube Worm Riftia pachyptilaJones: Possible Chemoautotrophic Symbionts. Science 213, 340-342.
• Rouse, G. W., Goffredi, S. K. & Vrijenhoek, R. C. (2004) Osedax: bone-eating marine worms with dwarf males. Science 305, 668-671.
• Thornhill, D. J., Fielman, K. T., Santos, S. R. & Halanych, K. M. (2008) Siboglinid-bacteria endosymbiosis: A model system for studying symbiotic mechanisms. Commun Integr Biol 1, 163-166.
• Hilario, A. et al.(2011) New perspectives on the ecology and evolution of siboglinid tubeworms. PLoS One 6, e16309

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A postdoctoral position is available to study cell signaling mechanism using eye development as a model.  Among the current projects, we are studying how extracellular signals induce cytoskeletal dynamics to control cell shape and adhesion. We are also interested in the crosstalk between FGF and other signaling pathways. The aim is to combine mechanistic studies in vitro with mouse genetics in vivo. Potential candidate should be highly motivated with a Ph.D. degree in biomedical science and a strong background in biochemistry and cell biology.  Experience in mouse genetics is desirable but not necessary.  The successful postdoc candidate will receive training in genetic, molecular and biochemical approaches in vision research, interacting with basic scientists and physicians in a multidisciplinary environment. For details of the research projects, please visit:  https://www.pathology.columbia.edu/profile/xin-zhang-phd

Relevant Publications

1. Li H, Mao Y, Bouaziz M, Yu H, Qu X, Wang F, Feng GS, Shawber C, Zhang X. Lens differentiation is controlled by the balance between PDGF and FGF signaling. 2019. PLoS Biol. 17(2):e3000133.
2. Collins TN, Mao Y, Li H, Bouaziz M, Hong A, Feng GS, Wang F, Quilliam LA, Chen L, Park T, Curran T, Zhang X. Crk proteins transduce FGF signaling to promote lens fiber cell elongation. eLife. 7:e32586.
3. Garg A, Hannan A, Wang Q, Collins T, Teng S, Bansal M, Zhong J, Xu K, Zhang X. FGF-induced Pea3 transcription factors program the genetic landscape for cell fate determination. PLoS Genetics. 14(9):e1007660.

Please send CV with names and contact information of three references to: Xin Zhang, Ph.D., Departments of Ophthalmology, Pathology & Cell Biology, Columbia University, New York, NY 10032.  Email: xz2369@columbia.edu

The Columbia University Medical Center is located in New York City, which offers world-class museums, performing arts and numerous culture opportunities.  With top ranked Ph.D. programs, medical school and affiliated hospitals, it presents a collaborative and stimulating academic environment for research excellence.

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Research Group Julien Royet: “Host pathogen interactions in the Drosophila model”

IBDM (UMR CNRS 7288) • Parc Scientifique de Luminy • 13288 Marseille Cedex 9 • France

A PhD position is available at the Institute of Developmental Biology of Marseille (IBDM) for a motivated student to work on a research project investigating the genetic basis of host-bacteria interactions in the Drosophila model. This is a full-time position for 3 years. The candidate must be free to start in September/October 2019.

Background

It is now very well established that gut-associated bacteria can impact the behavior and the physiology of their eukaryotic host. The PhD thesis project is aimed at using the powerful genetic tools available in the Drosophila model and the relative simplicity of its gut microbiota to study, at the molecular level, the molecular dialog between the microbiota and its host. In two recent publications, (Kurz et al, Elife, 2017: Charroux et al, Cell Host Microbe, 2018), the lab has shown that a metabolite produced by gut-associated bacteria, called peptidoglycan, can cross the gut epithelium and reach the insect blood where it interferes with various organs (fat body, ovaries, brain…) and modifies functions (behavior changes, organ wasting…). The PhD student will use the newest genome editing technologies (Crispr…), genetic tools and latest imaging microscopy technics to dissect the precise cellular and molecular mechanisms of the dialog that exist between gut-resident bacteria and some specific cells of the host. Recent results showing that mice deficient in peptidoglycan-sensing proteins exhibit social behavioral alterations suggest that the mechanisms that we study in Drosophila also exist in mammals. The research will be performed in the Institute of Developmental Biology of Marseille, an internationally recognised interdisciplinary research center and a very stimulating scientific environment (http://www.ibdm.univ-mrs.fr/).

Profile of the candidate 

We look for an enthusiastic and ambitious student with a strong interest in the genetics of host-bacteria interactions. The candidate is expected to have a background in molecular biology and should hold a Master Degree in Bioscience Engineering, Biotechnology or Biology. The candidate should have a level of proficiency in English which is sufficient to communicate effectively with colleagues.

Applications

Application documents should include a motivation letter, a curriculum vitae and a grade transcript. Additionally, the applicant is expected to arrange for two letters of recommendation to be sent to the address below. The application deadline is May 1^th, 2019. Applications should be sent electronically as one single file in pdf format to Julien.royet@univ-amu.fr, leopold.kurz@univ-amu.fr and Olivier.zugasti@univ-amu.fr

Publications

Kurz et al, 2017. Peptidoglycan sensing by octopaminergic neurons modulates Drosophila oviposition. Elife. Mar 7;6. pii: e21937.

Charroux et al, 2018. Local and systemic immune responses to microbiota are respectively controlled by cytosolic and secreted peptidoglycan degrading enzymes in Drosophila.  Cell Host and Microbe. Feb 14;23(2):215-228

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This obituary by Colin Johnson recently appeared in Development.

Jarema Malicki, a pioneer in developmental studies of the vertebrate retina, died on 4th January 2019, shortly after being diagnosed with cancer. Here, I reflect on Jarema’s life and work, with a particular focus on his research interests in zebrafish as a model organism for vertebrate retinogenesis and human ciliopathies.

Jarema was born in Warsaw, Poland, in March 1965. The family visited their small ‘orchard’ property outside of the city at the weekends, and his father often took him into the Tatry Mountains near Zakopane.

These early experiences inculcated a deep life-long affection for the natural world and walking in the mountains; in particular, he loved the Tatry Mountains and the Tramuntana Mountains of Mallorca. He enrolled at Warsaw University as an undergraduate but in 1987, at some personal risk and with great ingenuity, he escaped the political repression and authoritarianism of the Communist regime. He initially headed east, not west: on leaving Poland, he took a train across Siberia, ostensibly as a holiday trip to Japan. He then entered the USA via California, travelling on to Maine by bus with little money or fluency in English, to stay with friends of his parents. He was forever grateful to Bates College, Maine, for accepting him onto their undergraduate study programme, and for their generosity with scholarships and part-time work as he built a new life in the USA. Jarema did not see his parents again until 1991 and did not return to Poland until 1994. He became a US citizen in 2010.

In 1989, after one year at Bates College, he enrolled on the molecular biology PhD programme at Yale University, working in Bill McGinnis’ lab. Bill had made his name by defining the spatial and temporal expression of homeotic genes during Drosophila development. It was an exciting time to enter the Drosophila field: new molecular biology techniques were providing insights into the role of maternal gene expression, and positional cloning of mutants was beginning to define the often unexpected functions of key players. But the extent to which these insights into fly development applied to other vertebrates, the development of which appeared so radically different, was at the time unclear. Studies were just beginning to show that homeotic genes and the homeobox were highly homologous in metazoans, and Jarema’s PhD work took this a stage further by showing that cis-regulatory elements in the mammalian HOX4B gene (now renamed HOXD4) and the homologous fly gene Deformed (Dfd) were functionally equivalent during head development (Malicki et al., 1992). Jarema was very proud that this research was published in Nature just as he was graduating from Yale in 1992.

Around the same time, Wolfgang Driever was pioneering the use of the zebrafish as a genetically tractable vertebrate model organism that was suitable for large-scale mutagenesis screening in his lab at Harvard Medical School (Boston, MA, USA). The Driever lab started the so-called Boston zebrafish mutagenesis screen in 1992, and Jarema joined the lab in 1993. Jarema was very excited to work on this new model organism for embryogenesis and organogenesis, and was enthusiastic to enter a promising new field at such an early point. He spoke warmly about the camaraderie in the Driever lab, the life-long friends he made during this period, and his enjoyment of sailing in Boston Harbor and Cape Cod as well as hiking in the hills of north eastern USA. The research culminated in the publication of the famous zebrafish issue of Development in December 1996 (Driever et al., 1996), in which Jarema co-authored 11 papers and was first author on two that described mutations affecting the retina and ear (Malicki et al., 1996a,b). The positional cloning of these mutants, which Jarema often gave whimsical names using Polish words, was a rich resource for molecular characterization of function in subsequent years, and provided the basis for many projects in Jarema’s labs in Boston and later in Sheffield, UK.

As a faculty member of Harvard Medical School from 1996 and Tufts University (Boston, MA, USA) from 2009, Jarema focused his research on the genetic basis of vertebrate eye and ear development, how it related to the underlying cell biology of polarity and intracellular transport, and how these cellular processes related to morphogenesis and embryonic patterning. Early successes were the characterization of retinal patterning loci derived from the mutagenesis screen. These included oko meduzy (now known as crb2a; translated as ‘jellyfish eye’), which encodes a crumbs gene homologue (Omori and Malicki, 2006), and glass onion (cdh2), which encodes N-cadherin (Malicki et al., 2003). But his seminal contribution during this period was work on nagie oko (mpp5a; translated as ‘naked eye’; Wei and Malicki, 2002), which encodes a large scaffolding protein in the membrane-associated guanylate kinase (MAGUK) family; subsequent work by Ronald Roepman and colleagues identified it as an interaction partner of the Crumbs complex (Kantardzhieva et al., 2005). This work contributed to the realization that MAGUK proteins regulate plasticity and adhesion at tight junctions by stabilizing multi-protein complexes, as exemplified by the Crumbs complex during retinal development. In a satisfying parallel narrative, mutations in several members of the Crumbs complex were found to be a major cause of human inherited retinal dystrophies. In Jarema’s mind, these insights vindicated the medical potential of zebrafish and the power of forward genetic screens in the model.

Another series of mutants from the screen had photoreceptor loss and kidney cysts, phenotypes that are associated with defective cilia formation. In a prescient paper, Jarema’s group demonstrated that oval (ift88) encoded IFT88, a component of the ciliary intraflagellar transport (IFT) system that is essential for cilia maintenance and sensory neuron survival (Tsujikawa and Malicki, 2004). This work presaged a worldwide effort over the next decade to identify human disease genes for human inherited retinal dystrophies and ciliopathies, and a growing recognition that the cilia is a fundamental mediator and regulator of developmental signalling and cellular homeostasis. Jarema’s lab demonstrated that elipsa (traf3ip1) encoded a second IFT protein, TRAF3IP1/IFT54 (Omori et al., 2008), which led to another satisfying link with medical genetics: mutations in TRAF3IP1/IFT54 are now known to cause Senior-Løken syndrome (Bizet et al., 2015), a ciliopathy that is characterized by nephronophthisis and retinal degeneration. Subsequent work on IFT by Jarema’s group revealed molecular mechanisms for the selective transport of specific ciliary cargoes such as opsin within the photoreceptor (Zhao and Malicki, 2011). These insights were the rationale for the recent development of an elegant zebrafish model of conditional in vivo opsin transport, and this remains an area of active interest by Jarema’s trainees and colleagues.

I first met Jarema in person soon after he had moved to the Bateson Centre at the University of Sheffield in 2012. With an established reputation in zebrafish genetics and an interest in inherited retinal dystrophies, he was an excellent recruit to the zebrafish community that was established in Sheffield by Philip Ingham. We hit it off instantly and over numerous visits, talking about ciliary biology and the challenges facing this new field, we eventually collated our conversations into a review article (Malicki and Johnson, 2017) and set up the ‘Northern’ Cilia Club (now part of the UK Cilia Network). Jarema was an enthusiastic and incisive writing partner: his approach was characterized by lucid and insightful scholarship, attention to detail and generous advice. Chatting to his students and trainees, I soon realized that he was equally rigorous, self-disciplined and dedicated in his professional commitments to them. He was tireless in supporting not only his Sheffield students but also those from the Erasmus Programme, as well as younger scientists from Poland. At the same time, he was keen to share his passions from outside of the lab: good food, good wine, good coffee and the great outdoors. These interests often aligned during lab weekends at his hideaway in the Tatry Mountains, or in meals at one of his favourite restaurants. Above all, he was motivated by his love of science: his enthusiasm inspired those around him to work a bit longer and to try a bit harder. Żegnaj ‘Gruba Rybo’.

Acknowledgements

I am grateful to Jarema’s many students, colleagues and collaborators who shared their memories and provided anecdotes of his life and science on which this obituary is based. I extend particular thanks to Frederick Walters, Lilianna Solnica-Krezel, Zhou Zhu, Xiaoming Fang, Pawel Lysyganicz, Pamela Yelick, Dominic Norris, Katarzyna Szymanska, Andrew Furley, Ronald Roepman and Marysia Placzek for their comments and feedback on the text, and to Zhou Zhu for the photograph.

References

Bizet, A. A., Becker-Heck, A., Ryan, R., Weber, K., Filhol, E., Krug, P., Halbritter, J., Delous, M., Lasbennes, M. C., Linghu, B. et al. (2015). Mutations in TRAF3IP1/IFT54 reveal a new role for IFT proteins in microtubule stabilization. Nat. Commun. 6, 8666.

Driever, W., Solnica-Krezel, L., Schier, A. F., Neuhauss, S. C., Malicki, J.,
Stemple, D. L., Stainier, D. Y., Zwartkruis, F., Abdelilah, S., Rangini, Z. et al. (1996). A genetic screen for mutations affecting embryogenesis in zebrafish. Development 123, 37-46.

Kantardzhieva, A., Gosens, I., Alexeeva, S., Punte, I. M., Versteeg, I., Krieger, E., Neefjes-Mol, C. A., den Hollander, A. I., Letteboer, S. J., Klooster, J. et al. (2005). MPP5 recruits MPP4 to the CRB1 complex in photoreceptors. Invest. Opthalmol. Vis. Sci. 46, 2192-2201.

Malicki, J. and Johnson, C. A. (2017). The cilium: cellular antenna and central
processing unit. Trends Cell Biol. 27, 126-140.

Malicki, J., Cianetti, L. C., Peschle, C. and McGinnis, W. (1992). A human HOX4B regulatory element provides head-specific expression in Drosophila embryos. Nature 358, 345-347.

Malicki, J., Neuhauss, S. C., Schier, A. F., Solnica-Krezel, L., Stemple, D. L.,
Stainier, D. Y., Abdelilah, S., Zwartkruis, F., Rangini, Z. and Driever, W. (1996a). Mutations affecting development of the zebrafish retina. Development 123, 263-273.

Malicki, J., Schier, A. F., Solnica-Krezel, L., Stemple, D. L., Neuhauss, S. C., Stainier, D. Y., Abdelilah, S., Rangini, Z., Zwartkruis, F. and Driever, W. (1996b). Mutations affecting development of the zebrafish ear. Development 123, 275-283.

Malicki, J., Jo, H. and Pujic, Z. (2003). Zebrafish N-cadherin, encoded by the glass onion locus, plays an essential role in retinal patterning. Dev. Biol. 95-108.

Omori, Y. and Malicki, J. (2006). oko meduzy and related crumbs genes are
determinants of apical cell features in the vertebrate embryo. Curr. Biol. 16,
945-957.

Omori, Y., Zhao, C., Saras, A., Mukhopadhyay, S., Kim, W., Furukawa, T., Sengupta, P., Veraksa, A. and Malicki, J. (2008). Elipsa is an early determinant of ciliogenesis that links the IFT particle to membrane-associated small GTPase
Rab8. Nat. Cell Biol. 10, 437-444.

Tsujikawa, M. and Malicki, J. (2004). Intraflagellar transport genes are essential for differentiation and survival of vertebrate sensory neurons. Neuron 42, 703-716.

Wei, X. and Malicki, J. (2002). nagie oko, encoding a MAGUK-family protein, is essential for cellular patterning of the retina. Nat. Genet. 31, 150-157.

Zhao, C. and Malicki, J. (2011). Nephrocystins and MKS proteins interact with IFT particle and facilitate transport of selected ciliary cargos. EMBO J. 30, 2532-2544.

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