Exploring the contribution of lymphatics towards diabetic kidney disease and their potential as a therapeutic target

A 3-year PhD Studentship funded by Diabetes UK is available within the Kidney Development and Disease Group (http://www.ucl.ac.uk/ich/research/developmental-biology-cancer/developmental-biology-birth-defects/kidney-development-and-disease-group) in the Developmental Biology and Cancer Programme, Great Ormond Street UCL Institute of Child Health. The studentship will commence in October 2020 under the supervision of Dr David Long and Professor Luigi Gnudi (King’s College London).

The aim of the studentship is to examine how lymphatic vessels contribute to diabetic kidney disease and their potential as a therapeutic target. The student will (i) use three-dimensional imaging technologies to study the lymphatics of diabetic kidneys down to the detail of single cells; (ii) isolate cells from diabetic kidneys and perform single cell RNA sequencing to see how gene expression changes in lymphatics on a cell-by-cell basis, and how lymphatics might be interacting with other cells in the diseased kidney and (iii) target kidney lymphatics using gene therapy; delivering VEGF-C, a lymphatic growth factor, to the diabetic kidney. The project will utilise multiple techniques ranging from animal husbandry, three-dimensional imaging technologies, flow cytometry, single cell RNA-sequencing and gene therapy strategies.

For a full project description please see the GOS ICH website: https://www.ucl.ac.uk/child-health/phd-studentship-kidney-research

Applicants should have, or expect to receive an upper second-class Bachelor’s degree and a Master’s degree (or equivalent work experience) in a relevant discipline or an overseas qualification of an equivalent standard. The student will receive a starting stipend of £19,000 per annum (including London weighting) as well as the cost of tuition fees for UK/EU students (applicants from non-EU countries can apply but will have to personally fund the difference between the home/EU rate and the overseas rate).

To apply, please send a current CV including the contact details of two professional referees as well as a cover letter to ich.dbc.admin@ucl.ac.uk.

Enquiries regarding the post can be made to Dr David Long (d.long@ucl.ac.uk).

Deadline for receipt of applications: 19th June 2020, 5pm

Interview date: TBC

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The Alenius lab has a fully funded postdoc position opening at at Umeå university, Sweden. Our group combines Drosophila  and mouse genetics to investigate the fundamental mechanisms that control neuronal activity. We are shifting gears for this project and the focus is to identify hormones that regulate taste and olfaction in Drosophila.

We seek an enthusiastic, highly motivated candidate with a strong background in either Drosophila molecular biology or cell signalling. The position involves exploring candidate hormones from a screen using state of the art Drosophila genomic tools, behaviour analyses and biochemistry. Thus, additional skills in Drosophila neuroscience, imaging, and behavior analysis are considered a plus.

Candidates are encouraged to send applications (cover letter, CV, and contact information of 3 references) to the link below. Application deadline is June 23, 2020.  Reviewing of applications will start immediately until the position is filled. Openings are available immediately. If you have questions do not hesitate to write: mattias.alenius@umu.se

Use this link to apply: https://umu.varbi.com/en/?jobtoken=1cd2fd52e7a1e1dc6ae07e1cc2602f2d469ad26d5

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A Press Release from the University of Pennsylvania School of Medicine – see the Development paper by Lisa Vrooman, Marisa Bartolomei and colleagues here.

An experimental study from researchers in the Perelman School of Medicine at the University of Pennsylvania links a specific procedure – embryo culture – that is part of the assisted reproduction process (ART) to placental abnormalities, risk for preeclampsia, and abnormal fetal growth. The team, led by Marisa Bartolemei, PhD, a professor of Cell and Developmental Biology, published their findings today in Development.

Millions of births across the world have occurred with the aid of ART, and while its use continues to rise globally, this revolution in human reproduction does come with some problems, the underlying cause of these issues remain unclear.

“The question has always been, is increased risk a function of infertility or is it due to these procedures, because you’re doing all these manipulations outside the normal environment,” Bartolomei said.

Bartolomei and colleagues used a mouse model to study the effects of four individual ART procedures – hormone stimulation, in vitro fertilization (IVF), embryo culture and embryo transfer – on placental development and fetal growth. All four procedures led to reduced fetal weight at mid-gestation, and at late gestation groups utilizing embryo culture still had reduced fetal weight, larger placentas, and altered placental cell composition. The full IVF procedure led to an increased risk of preeclampsia, and the embryo culture procedure, a necessary component of IVF, was associated with defective methylation of placental DNA, which has the potential to result in abnormalities in the placenta and possible adverse effects on the fetus.

“With the ART process, there’s hormone stimulation to produce eggs, the actual IVF, the embryo culture, and the embryo transfer procedure – there’s a lot going on,” said Lisa Vrooman, PhD, a postdoctoral fellow of Cell and Developmental Biology and first author on the paper. “In the mouse model, we were able to pull apart those four different procedures and look at how they individually contribute to placental development. We also looked at different time points – one close to placental formation, a mid-point, and then at term – to try to understand how placental development may be altered at these different time points.”

ART procedures in mice cause placental abnormalities unrelated to underlying infertility. Researchers found that the embryo culture procedure – where the fertilization of the egg with the sperm takes place in a medium meant to replicate the essential nutrients found in the oviduct and is placed in an incubator meant to mimic the womb – had the strongest effects on abnormalities and adverse outcomes.

“ART is more art than science”

“ART is more art than science,” Bartolomei said. “We don’t really know exactly what’s going on in the human body. Reproductive endocrinologists are looking at whether or not the embryo in the embryo culture developed in what we think is the right amount of time, with the right number of cells for the stage it’s in, and so on. The embryo sits in culture for a week, as opposed to oviducts in the mother’s body and the embryo culture is an attempt to simulate that environment.”

The authors conclude that efforts should be focused on optimizing embryo culture to ensure healthy outcomes for mothers and offspring.

This study is part of a larger effort to investigate infertility and reproduction at Penn through the National Centers for Translational Research in Fertility and Reproduction. Bartolomei’s research team partners with Christos Coutifaris, MD, PhD, Professor of Obstetrics and Gynecology, Monica Mainigi, MD, Assistant Professor of Obstetrics and Gynecology, and Jeremy Wang, MD, PhD, Professor of Developmental Biology at the School of Veterinary Medicine.

“This collaboration between clinical and basic researchers is designed to look at causes of infertility and when you have infertility using assisted reproduction, what are features that can be optimized for healthier outcomes – that’s the goal of this work,” said Bartolomei.

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Co-authors include Eric A. Rhon-Calderon, Olivia Y. Chao, Duy K. Nguyen, Laren Narapareddy, Asha K. Dahiya, Mary E. Putt, and Richard M. Schultz. Funding for this study came from National Centers for Translational Research in Reproduction and Infertility (HD068157), The Lalor Foundation, Ruth L. Kirschstein National Service Award (HD089623), Roy & Diana Vagelos Scholars Program, and the National Institute of Nursing Research (T32NR007100).

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Today let’s delve into a curious case involving induced pluripotent stem cells (iPSCs) and leukemic stem cells (LSCs). Most blood cells derived from iPSCs are unable to engraft in immunodeficient mice. However, Wesely and colleagues observed an exceptionally high engraftment efficiency of cell lines derived from an individual affected by acute myeloid leukemia (AML). In particular, in vitro they observed typical round cells together with cobblestone-like, firmly adherent cells. The latter displayed markers of immaturity, a more quiescent cell cycle, but foremost they were responsible for the successful engraftment in immunodeficient mice. Collectively, these properties prompted the authors to identify the cells as induced Leukemic Stem Cells (iLSCs). They proved that the iLSCs can become the round cells, but not vice versa, suggesting a stem cell nature. In addition, the adherent phenotype allowed the easy separation of the two populations. In-depth transcriptomic analysis, both at single-cell and population level, was coupled with the study of chromatin accessibility. The iLSCs displayed a molecular resemblance to the leukemic stem cells isolated from AML patients, based on a 42-genes signature. Finally, the authors identified the transcription factor RUNX1 as critical for iLSC phenotype maintenance, as it is involved in the expression of 16 of the 42 genes in the LSC signature. In conclusion, this work describes for the first time the derivation of LSCs from iPSCs. This could be a fantastic tool for the study of the cancer stem cell theory, as those rare cells are not prospectively isolated, but only studied after transplantation. Since these iLSCs were derived from a single patient, it will be interesting to isolate them from other AML-iPSCs lines.

Wesely et al. “Acute Myeloid Leukemia iPSCs Reveal a Role for RUNX1 in the Maintenance of Human Leukemia Stem Cells”

Doi: https://doi.org/10.1016/j.celrep.2020.107688

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The Korzelius lab has a funded position for a 3-year PhD at the University of Kent in Canterbury, U.K. We use the Drosophila intestine as a model system for age-related decline of organ function. Similar to the mammalian small intestine and colon, the fly intestine is maintained by a population of adult Intestinal Stem Cells (ISCs). Our previous work has identified key transcriptional regulators that govern ISC maintenance and differentiation (Korzelius et al., 2014 EMBO Journal, Korzelius et al., 2019 Nature Communications). Please visit our website for more information: https://www.kent.ac.uk/biosciences/people/3191/www.kent.ac.uk/biosciences/people/3191/korzelius-jerome

This PhD project will investigate how ISC maintenance and differentiation change during aging, focusing on some of the key transcription factors important for ISC maintenance and differentiation. This project will allow you to build skills working with different types of whole genome datasets (RNA-Seq, DamID) as well as building skills in genetics, molecular biology and image analysis. We will e.g. perform crosses with inducible expression of RNAi’s, lifespan assays, microdissection and staining of gut tissue and FACS-isolation of midgut cell populations for whole genome RNA-sequencing.

You will work in the dynamic environment of the School of Biosciences at the University of Kent. The School of Biosciences has a rich expertise on Cancer and Ageing research, and we will have close connections to the ageing-related research in the labs of Dr. Jennifer Tullet and Dr. Marina Ezcurra. You will also be able to work with our collaborators in Germany at renowned institutes such as the Max Planck Institute for Biology of Ageing in Cologne and the FLI-Leibniz Institute on Aging in Jena as well as Genentech Inc. in San Francisco, U.S.A.

We are looking for a curiosity-driving student that works both independently and as part of a team and is interested in a multi-disciplinary research project. The ideal candidate should have knowledge of molecular biology techniques such as DNA/RNA-isolation, PCR and cloning as well as genetics. Additional experience in either Drosophila husbandry and genetics, bio-informatics or immuno-histochemistry and confocal microscopy would be an advantage. Excellent writing and communication skills in English are necessary.

Please send a cover letter and CV and contact details for 2 references. Further details about the application process and the position can be found at https://www.kent.ac.uk/scholarships/search/FN25TRISCA02

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In the latest episode of Genetics Unzipped we’re off on our virtual travels, finding out about the highs and lows of fieldwork. From chasing butterflies up mountains to artificially inseminating kakapos with the help of drones and putting angry birds in paper bags until they poo, we talk to the researchers studying genetics and evolution in action. 

Every year The Genetics Society runs the Heredity Fieldwork Grant scheme, awarding up to £1,500 to cover the travel and accommodation costs for researchers wanting to carry out a fieldwork project in genetics. Our stay-at-home roving reporter Georgia Mills caught up with four intrepid explorers who’ve been off on their travels in locations as exotic as New Zealand, Lanzarote and the Lake District to hear more about their research and what they learned out in the field.

Genetics Unzipped is the podcast from The Genetics Society. Full transcript, links and references available online at GeneticsUnzipped.com

Subscribe from Apple podcasts/iTunes, Spotify and all good podcast apps to make sure you get the latest episodes and catch up on our back catalogue.

If you enjoy the show, please do rate and review on Apple podcasts and help to spread the word on social media. And you can always send feedback and suggestions for future episodes and guests to podcast@geneticsunzipped.com Follow us on Twitter – @geneticsunzip

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This post highlights the approach and finding of a new research article published by Disease Models and Mechanisms (DMM). This feature is written by Olivia Howell as apart of a seminar at The University of Alabama (taught by DMM Editorial Board member, Prof. Guy Caldwell) on current topics related to use of animal and cellular model systems in studies of human disease.

Within the brain, anomalies in neuronal migration can precipitate aberrant phenotypes such as epilepsy, a disorder in which atypical neuronal circuitry induces recurrent seizures alongside additional neurological abnormalities^2,3. X-linked infantile spasms syndrome (ISSX) is one such debilitating epileptic subtype hallmarked by intellectual disability and intractable seizures that first present in infancy⁴. Previous work has established a causative link between ISSX and mutations in the Aristaless-related homeobox (ARX) – a gene that influences tangential and radial migration of some GABAergic interneurons vital for repressing excitatory neuronal signaling^5,6,7,8. Despite recent progress, the precise pathogenesis of ISSX as well as safe, specific and effective treatments remain elusive. Consequently, characterization of early progenitor interneurons is crucial to understanding and managing this disorder.

In this report, Siehr et al. hypothesized that recapitulating pancreatic ARX functionality within a developing neuronal framework would elucidate the role of this gene in ISSX and the means by which E2 and ACTH mediate their anti-epileptic effects⁷. They therefore utilized an Arx^(GCG)10+7 mouse model that recapitulates the ISSX phenotype to uncover temporally increased levels of apoptosis within the neocortex of Arx-mutant mice. Because this abnormal pattern of apoptosis could not be ascribed to ARX cell death, Siehr et al. deemed it non-cell autonomous in nature. While the affected cell population remains unascertained, Siehr and colleagues have definitively eliminated cortical non-ARX expressing interneurons and inflammatory processes from consideration by examining postnatal neuronal survival and neuroinflammation.

In regard to therapeutics, E2 was found to mitigate ARX⁺ cell density and ISSX seizure phenotype but proved unable to rescue increased apoptosis – rendering the utility of this drug unresolved. Moreover, the unanticipated failure of ACTH to rescue ARX ^(GCG)10+7 mutants from seizure phenotype may ultimately lay the groundwork to model intractable ACTH-resistant ISSX cases and thereby explore alternative ISSX treatments.

Notably, the authors herein report the first known observation of ARX-associated apoptosis in an ARX ^(GCG)10+7 rodent model for ISSX – a corroboration of findings in pancreatic tissue expressing aberrant ARX that highlights the relevance of cross-organ systems research.  While too soon to conclude that apoptosis contributes to ISSX pathogenesis, these results underscore the broad, varied and lingering effects of ARX upon neuronal structure and development. Accordingly, one can expect that subsequent pharmacodynamic studies of E2 and ACTH may ascertain their therapeutic relevance to ISSX while also elucidating the relationship between ARX-mediated apoptosis and subclinical molecular features of ISSX pathology.

References

1. Siehr, M., Massey, C. and Noebels, J. L. (2020). Arx expansion mutation perturbs cortical development by augmenting apoptosis without activating innate immunity in a mouse model of X-​Linked Infantile Spasms Syndrome. Dis Model Mech 13, 1-10.

2. Hwang, H. M., Ku, R. Y. and Hashimoto-Toril, K. (2019) Prenatal environment that affects neuronal migration. Cell Dev. Biol. 7, 138. 

3. Jackson, M. R., Lee, K., Mattiske, T., Jaehne, E. J., Ozturk, E., Baune, B. T., O’Brien, T. J., Jones, N. and Shoubridge, C. (2017). Extensive phenotyping of two ARX polyalanine expansion mutation mouse models that span clinic al spectrum of intellectual disability and epilepsy. Dis. 105, 245-256. 

4. Olivetti, P. R. and Noebels, J. L. (2012). Interneuron, interrupted: molecular pathogenesis of ARX mutation and X-linked infantile spasms. Opin. Neurobiol. 22, 859-865. 

5. Olivetti, P. R., Maheshwari, A. and Noebels, J. L. (2014). Neonatal estradiol stimulation prevents epilepsy in Arx model of X-linked infantile spasms syndrome. Transl. Med. 6, 1-10. 

6. Poirier, K., Van Esch, H., Friocourt, G., Saillour, Y., Bahi, N., Backer, S., Souil, E., Castelnau-Ptakhine, L., Beldjord, C., Francis, F. et al. (2003) Neuroanatomical distribution of ARX in brain and its localisation in GABAergic neurons. Brain Res. Mol. Brain Res. 122, 35-46. 

8. Wilcox, C. L., Terry, N. A. and May, C. L. (2013). Arx polyalanine expansion in mice leads to reduced pancreatic a -Cell specification and increased a-Cell death. PLoS ONE 8, e78741. 
9. Mattiske, T., Lee, K., Gecz, J., Friocourt, G. and Shoubridge, C. (2016). Embryonic forebrain transcriptome of mice with polyalanine expansion mutations in the ARX homeobox gene. Mol. Genet. 25, 5433-5443.

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This post highlights the approach and finding of a new research article published by Disease Models and Mechanisms (DMM). This feature is written by Joseph I. Kaluzny as apart of a seminar at The University of Alabama (taught by DMM Editorial Board member, Prof. Guy Caldwell) on current topics related to use of animal and cellular model systems in studies of human disease.

Fibrolamellar Carcinoma (FLC) is a hepatocellular carcinoma that disproportionately affects young patients and is characterized by a fusion transcript, DNAJB1-PRKACA, which acts as a unique molecular driver and is sufficient for diagnosis (Graham et al., 2015). While liver resection and transplantation remain common management approaches (Kassahun, 2016), the lack of available therapy has motivated molecular mechanistic studies of the fusion.

Previous work has shown that the fusion is sufficient to drive FLC tumorigenesis in murine models (Engelholm et al., 2017). In a recent Disease Models & Mechanisms article, de Oliveira and colleagues chose to study the fusion in zebrafish due to their transparent larvae that provide non-invasive live imaging of liver morphology and inflammatory responses (de Oliveira et al., 2020). The researchers used a hepatocyte-specific promoter to overexpress the fusion and establish an FLC zebrafish line. Liver visualization in adults was achieved via outcrossing with a transgenic line expressing agfp-I10a (Fig. 2A in de Oliveira et al., 2020). The livers of 8- and 12-month-old FLC and control fish were resected for standard histopathological evaluation, which confirmed liver enlargement and abnormal hepatocellular architecture in FLC livers (Fig. 2B-C in de Oliveira et al., 2020).

The investigators then sought to determine if overexpression of the fusion caused alterations indicative of malignancy in larval zebrafish. The researchers confirmed hepatomegaly 7 days post-fertilization, suggesting the potential for zebrafish larvae to be used as a model to study the progression of early FLC, an area of interest for a progressive condition that primarily affects young patients (Fig. 3 in de Oliveira et al., 2020). Overexpression of the fusion increased neutrophil and macrophage infiltration into the liver, TNFα-positive macrophages, and caspase-a activity, confirming an inflammatory response in FLC larvae (de Oliveira et al., 2020). Targeting this inflammation with TNFα and caspase-a inhibitors limited FLC progression.

Despite this potential for therapy, there are many outstanding issues with the zebrafish FLC model, such as the presence of two fusion forms due to the genome duplication in zebrafish, the lack of fibrosis markers characteristic of human FLC progression (Kastenhuber et al., 2017), and alternate pro-inflammatory pathways that are unexplored or understudied in the field (Rigutto et al., 2009), which warrant further study.

References

de Oliveira, S., Houseright, R. A., Korte, B. G. and Huttenlocher A. (2020). DnaJ-PKAc Fusion Induces Liver Inflammation in a Zebrafish Model of Fibrolamellar Carcinoma. Disease Models & Mechanisms, 26 Feb. 2020, doi:10.1242/dmm.042564.

Engelholm, L. H., Riaz, A., Serra, D., Dagnaes-Hansen, F., Johansen, J. V., Santoni-Rugiu, E., Hansen, S. H., Niola, F. and Frodin, M. (2017). CRISPR/Cas9 Engineering of Adult Mouse Liver Demonstrates That the Dnajb1-Prkaca Gene Fusion Is Sufficient to Induce Tumors Resembling Fibrolamellar Hepatocellular Carcinoma. Gastroenterology 153, 1662-1673 e10.

Graham, R. P., Jin, L., Knutson, D. L., Kloft-Nelson, S. M., Greipp, P. T., Waldburger, N., Roessler, S., Longerich, T., Roberts, L. R., Oliveira, A. M. et al. (2015). DNAJB1-PRKACA is specific for fibrolamellar carcinoma. Mod Pathol 28, 822-9.

Kassahun, W. T. (2016). Contemporary management of fibrolamellar hepatocellular carcinoma: diagnosis, treatment, outcome, prognostic factors, and recent developments. World J Surg Oncol 14, 151.

Kastenhuber, E. R., Lalazar, G., Houlihan, S. L., Tschaharganeh, D. F., Baslan, T., Chen, C. C., Requena, D., Tian, S., Bosbach, B., Wilkinson, J. E. et al. (2017). DNAJB1-PRKACA fusion kinase interacts with beta-catenin and the liver regenerative response to drive fibrolamellar hepatocellular carcinoma. Proc Natl Acad Sci U S A 114, 13076-13084.

Rigutto, S., Hoste, C., Grasberger, H., Milenkovic, M., Communi, D., Dumont, J. E., Corvilain, B., Miot, F. and De Deken, X. (2009). Activation of dual oxidases Duox1 and Duox2: differential regulation mediated by camp-dependent protein kinase and protein kinase C-dependent phosphorylation. J Biol Chem 284, 6725-34.

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EWM2020 meeting is going online June 22nd-23rd.

follow by a Poster Session June 29-30th with new abstract submission

Details  at shorturl.at/mvFY7 & Twitter Ewbank Pujol lab  #EWM2020;  Wormbase

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Author:

Suvimal Kumar Sindhu, Graduate Student @ Indian Institute of Technology Kanpur, Kanpur, Uttar Pradesh, 208016, India Email: suvimal.sindhu@gmail.com

Having joined my Ph.D. programme at India Institute of Technology Kanpur in India, I always witnessed my senior colleagues defending their Ph.D. thesis with panache and grace; for juniors like me such visuals were highly captivating and motivating. During my Ph.D. I trained to manipulate gene expression and analyze its effect on the developing avian brain. Using these skill-set I created additional hippocampus-like regions (a center of learning and memory) in the chick brain, to understand its development in the brain (Sindhu et al., 2019). I proposed a mechanism for correct positioning of hippocampus in the avian brain. After years of arduous and passionate research work, my defense day was scheduled in the evening of April 17^th and I was thrilled, for I was ready to experience the joy and accomplishment, a vicarious pleasure experienced through my senior colleagues, and sincerely hoping to match the high standards set by them. 

While I was getting prepared for my D-day, the COVID-19 pandemic started to spread in India. Staying in an autonomous and highly secure residential campus, everybody — I know — thought that our work won’t be affected. However, things escalated quickly and in an unprecedented manner, merely two weeks prior to my defense most of the organizations, including my institute, got shut down. COVID-19 took away everybody “reasons for struggle” in life. Now the only possible thing was to “stay at home” and “work from home”. With a broken heart, I came back to my home located in a remote village in the Indian state of Bihar. Amidst all this, I was becoming anxious and restless, my dream to become a Doctor of Philosophy getting delayed till uncertainty. After more than one month of nationwide lockdown, institutions started to conduct virtual academic seminars and meetings. And I got the opportunity to defend my thesis on the last day of the same month – April. I was disheartened as it would not be the same as a traditional thesis defense, which I had always dreamt of, but this was the only option available under these situations.

[Image on request designed by www.hoodnscience.com]

Suddenly I realized that there would be logistical hurdles, and preparation in the absence of supervisor and lab-mates would be challenging. But, I was determined to do this and decided to troubleshoot every aspect of it. Considering the location of my home two major hurdles were there -1) frequent power failure of home supply and 2) unstable cellular-network. Arranging an alternative power source and a Wi-Fi device was not a problem; I was not sure whether the network – which is mostly congested under current situation – would stably transmit data needed to sustain a group video conference with around 50 participants.  More importantly, how much data will it consume? – 2GB, 20GB or, 200GB, any number was just a blind guess. To test these conditions a priori, arranging such huge participants that too with a free version of any video conferencing app was just not feasible. I thought of doing a couple of trial presentations to check if my slides are in order and the quality of audio and video are fine. My first mock presentation with my supervisor was quite upsetting; the connection lasted only for 10 minutes as the network was highly unstable. In the second trial, I changed my location within the limited possibilities and that improved the data speed to ~65MBPS. This time my mock presentation lasted for 50 minutes and it consumed ~270MB of data. This was my first experience to deliver a formal presentation online, and hence sometimes I became oblivious of my virtual audience. I had minimized the video thumbnail of participants to avoid cluttering my screen, which was shared with others for the slide show. However, as a trade-off, I lost touch with my audience, and at times felt speaking to myself. This was also due to the fact that to see the entire shared screen running my slide show.

Finally, the D-day arrived, 10 minutes prior to the scheduled time, I signed-in to the Zoom platform and shared my screen; there were ~10 people waiting for my presentation, which eventually rose to 45 people. The connection became unstable; with stuck video and breaking voice, it was a total chaos. I thought my device would not be able to handle the load, and my presentation will have to be postponed. Meanwhile, it was suggested to temporarily turn off only video transmission for the audience except for the oral board members. This idea was quite helpful and I was able to go through my defense presentation as well as discussion, which took around 90 minutes of time. At the end of the session around 1.8GB of data was consumed. Without the slide transition device and laser pointer, it was inconvenient initially, but I adapted to the keyboard and mouse pointer for managing the presentation. To remain in touch with my audience, this time I did not minimize the video of my participants; rather, I kept a few video thumbnails at the corner of my screen. This helped me in remaining aware of their presence and generated a sense of their physical presence.

I had never thought I would defend my thesis this way, but when the whole world is learning a new way to live, I learned a new way to defend and become a doctor under lock down.

(Edited by Sahil Batra, Graduate Student @ Indian Institute of Technology Kanpur, India)

Sindhu S.K., Udaykumar N., Zaidi M.A.A., Soni A., Sen J. MicroRNA-19b restricts Wnt7b to the hem, which regulates aspects of hippocampus development in the avian forebrain. doi:10.1242/dev.175729, Development, 146, (20):1-7

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