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Postdoctoral position in Stem Cell Biology to study cell plasticity and chromatin architecture.

Posted by , on 17 February 2021

Closing Date: 18 April 2021

We offer one fully funded postdoctoral position up to five years in the Laboratory of Genome Integrity located at the National Institutes of Health (NIH, Bethesda, MD). NIH is the largest biomedical research agency in the world, fosters world-renowned researchers and provides access to state-of-the art innovative technologies and scientific resources.

 

Our laboratory uses human and mouse embryonic stem cells (ESCs) as well as mouse embryos to understand the molecular mechanisms underlying cell fate decisions. The applicant should have or about to have a PhD in Developmental Biology, Genetics or similar, and must have demonstrated expertise on molecular biology/mammalian cell culture (preferably in embryonic stem cells). Knowledge in mouse embryology, single-cell RNAseq, chromatin architecture and/or next generation sequencing technologies will be considered as an advantage.

 

The applicant will be involved in a very exciting project investigating the relation between cell plasticity/totipotency and chromatin architecture (see our last publication about this topic, https://doi.org/10.1101/2020.12.20.423692). We seek a highly motivated, creative individual, eager to learn and develop new technologies and complex cell systems based on live cell/embryo imaging, single-cell technologies and CRISPR-based editing interested in understanding how a single cell can develop into a complex multicellular organism in vitro and in vivo.

 

Please send a brief cover letter, CV and three reference letters via e-mail to:

 

sergio.ruizmacias@nih.gov

https://ccr.cancer.gov/Laboratory-of-Genome-Integrity/sergio-ruiz-macias

 

  • Vega-Sendino, et al (2021) The ETS Transcription Factor ERF controls the exit from the naïve pluripotent state. BioRxiv, doi: https://doi.org/10.1101/2021.02.01.429223.
  • Olbrich, T., et al (2020) CTCF is a barrier for totipotent-like reprogramming. BioRxiv, doi: https://doi.org/10.1101/2020.12.20.423692.
  • Markiewicz-Potoczny, M., et al (2020) TRF2-independent protection of telomeres in pluripotent stem cells. Nature, 589: 103-109.
  • Mayor-Ruiz C, et al. ERF deletion rescues RAS deficiency in mouse embryonic stem cells. Genes & Dev. 32: 568-576, 2018.
  • Ruiz S, et al. Limiting replication stress during somatic cell reprogramming reduces genomic instability in induced pluripotent stem cells. Nature Commun. 6: 8036, 2015.



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One thought on “Postdoctoral position in Stem Cell Biology to study cell plasticity and chromatin architecture.”

  1. Dear
    Dr. Sergio Ruiz Macias,

    I am highly impressed and really interested in your work on acquisition of totipotency mediated by remodelling of chromatin and genomic instability.
    I have years of experience in iPSC biology, reprogramming of PBMCs and glioblastoma biology in relation to canonical Wnt signaling. During my doctoral course I got an opportunity to get rigorous training in most of the basic needs of biological research like various biochemical techniques, flow cytometry, confocal microscopy, human tissue handling and processing for cell-line establishment, lentiviral production and transduction, molecular cloning (over-expression and knockdown), xenograft mice- modelling, cellular reprogramming to iPSCs using Sendai virus mediated gene transfer, differentiation of iPSCs to various lineages (hepatic and cardiac) and mass-spectrometry analysis. During my graduate training I could publish nine research articles, three as first author, three as co-author and three as contributing author in reputed international journals.

    I performed extensive research on a ubiquitin ligase protein FBXO16. In my work, I could also successfully establish that FBXO16 is deregulated in higher grades of brain tumors leading to poor prognosis of the disease. FBXO16 inhibits the active Wnt/β-catenin signaling in glioblastoma through a mechanism independent of GSK-3β or β-Trcp1. FBXO16 interacts with β-catenin and induces proteasomal degradation through E3 ubiquitin ligase. Analysis of patient-derived recurrent glioblastoma cell-line confirmed a drastic downregulation of FBXO16 as compared to astrocytes. In-vivo mice model demonstrated a regressed glioblastoma tumor volume when FBXO16 is constitutively expressed. Collectively, these experiments support in understanding the biology of FBXO16 in suppressing glioblastoma. In addition, I also observed that FBXO16 could assist double strand DNA break repair processes and worked on the mechanistic aspect of the biology.

    The research that I executed drew the attention of the research community in the form of publications in various biomedical journals. For the first time I showed FBXO16, which functions as a novel tumor suppressor protein in glioblastoma (published in Neoplasia). In addition, the importance of my research was also appreciated by the public and highlighted the findings in an Indian Newspaper (2019). I am also a good collaborator, which is reflected by the publications contributed to various other research institutes. My contributions surfaced to some of the reputed journals like Nanoscale and Bioconjugate Chemistry.

    I also have a multitasking research experience, along with my PhD work I also contributed significantly to the project of generation of iPSC cell lines for a banking facility associated with our lab. The main aim of the facility was to generate iPSCs of Indian population from CD4+ T cells, which is a less invasive procedure, has less ethical concern and is controllable in the sample size as CD4+ T cells proliferated in-vitro (published in Stem Cell Research). We were successful in generating six different iPSC cell lines (17 different independent clones) which includes both normal and non-alcoholic fatty liver disease patients. The generated iPSCs were also used for the hepatocyte and biliary differentiation (utilized both growth factor and small molecules based) and in-vitro drug toxicity evaluations on 2D and hepatic, biliary and hepatobiliary organoids. This project experience provided me with valuable insights regarding the process and standardisation of iPSC generation, differentiation, organoid formation and drug toxicity assays.

    At this moment, I am seeking to utilize my years of experience in iPSC biology and expertise in WNT signalling regulated molecular biology of glioblastoma pathogenesis. Given the opportunity, I am confident that I will be able to contribute successfully to the projects I am associated with.

    Thank you for your time and consideration.

    If you require further information please contact me at mohsinaanj@gmail.com.

    Thank you and I’m looking forward to hear from you.

    Regards,

    Mohsina Anjum Khan.

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