An Interview with Rong Li

Total Page:16

File Type:pdf, Size:1020Kb

An Interview with Rong Li SPOTLIGHT 1015 Development 137, 1015-1016 (2010) doi:10.1242/dev.050138 © 2010. Published by The Company of Biologists Ltd An interview with Rong Li Rong Li is an Investigator at the Stowers Institute for Medical Research, Kansas City, USA. Her lab is made up of a lively team who are all fascinated by cellular asymmetry, division and evolution. Rong joined Development as an editor in 2009. We interviewed Rong to find out about her work and career, her interest in developmental biology and her new role with the journal. and Fine Art. In the end, though, science helped me maintain a balanced perspective won, because I thought it would be easier to and has been an important source of advice pursue art as a hobby rather than the other and inspiration. way around. You run many different research You started your own lab at Harvard – projects at Stowers – which do you how did that happen? enjoy the most? I was recruited by Marc Kirschner, who had The best thing about being at the Stowers is just moved to Harvard Medical School to be that I can focus on my interests without the Chair of Cell Biology. Marc was one of distraction. When I moved my lab there in my professors at the University of 2005, I made a conscious decision to California, San Francisco, a scientist I really investigate questions that are truly admired. I left David Drubin’s lab at UC fascinating but are risky and open-ended, Berkeley before I had any publications as a either by adding new approaches to postdoc, because I just couldn’t pass on an scientific lines of enquiry I was already At what age did you realise you opportunity to work alongside Marc. pursuing or by developing new lines of wanted to be a scientist? research. This decision has shaped all of our When I was in high school. I was very Were there other important mentors current work. I particularly enjoy projects in interested in science and it was also in your life? which the outcome of each step is expected of me, partly because both my I left China for the US when I was very unpredictable, as they produce the most parents are geologists and partly because of young. Being far from home and my family, surprising and exciting findings. the attitudes prevalent in China in the early I couldn’t have gone very far without lots of 80s. High school students with good grades mentors at each step of my career path. They If you could find the answer to one in maths and physics were given a lot of include a senior chemistry professor who developmental biology question encouragement to take their study of science went out of his way to tutor and encourage tomorrow, what would that question and technology further. me when I had tremendous difficulties with be? the language as a freshman at Yale, the I would want to know how precise and How did you choose your college? people I worked with as an undergrad who reproducible developmental patterns arise I applied to a US college – Yale – as I was introduced me to the art of experimental as a result of dynamic, often promiscuous planning to study molecular biology. To be biology, one of my graduate mentors, Tim interactions of lots of molecules present in honest, I hardly knew what molecular Mitchison, who later became a close fluctuating amounts. I’m intrigued by the biology was at the time but I was certain that colleague in the same institution, and, of idea, as elaborated in Stuart Kauffman’s I would have to go abroad to get the best course, Marc Kirschner, who gave me book, The Origins of Order, that biological education possible in that field of science. unwavering support when I struggled systems operate on the edge of chaos. mightily as a starting Assistant Professor. Kauffman argues that such systems are best Did you ever want to be anything able to coordinate complex tasks and are else? poised to evolve under selective forces. It An artist! As a child I was very interested in I left China for the US when will be interesting to explore this idea in art and did a lot of drawing and painting. At specific cellular and developmental home this wasn’t considered a promising I was very young. I couldn’t systems. The complexity and dynamic basis for a future career but, after reaching have gone very far without nature of developmental systems will Yale, I signed up for a double major, taking require the application of non-traditional roughly equal numbers of courses in lots of mentors at each step approaches. Molecular Biophysics and Biochemistry of my career path. What have you discovered in your scientific work that has been a real If I had to name my one most important surprise? Interview by Kathryn Senior* scientific mentor, it would be my PhD thesis I love surprises, even if they prove me Freelance Science and Medical Writer advisor Andrew Murray. Andrew taught me wrong, and I’ve had a few good ones! One *Author for correspondence how to think and what to strive for in surprise that had a profound impact on how ([email protected]) science. Over the years, Andrew has always I think about biological systems came from DEVELOPMENT 1016 SPOTLIGHT Development 137 (7) studying a yeast cell. We supplied a non- processes. I also think that studying cell student days. When I return home from polarised yeast cell with high doses of biology in the context of development rather work, my favourite outside activity activated Cdc42 GTPase and were amazed than in generic cell culture models is much nowadays is playing with my children. to observe that it polarises robustly, albeit in more meaningful. It is so important to find random directions, without the influence of ways to move beyond specific gene-centric If you could give one piece of advice any existing spatial asymmetry. Before this views and to promote studies that attempt to to a young scientist starting out on experiment, we had thought that the origin explain morphogenetic phenomena from the their first degree today, what would it of cell polarity came from the inductive perspective of complex dynamic systems. be? power of external, pre-existing spatial cues, I’d like very much to contribute to this To realise that a large percentage of such as existing structural ‘landmarks’ or effort. experiments fail miserably on a daily basis, diffusible chemoattractant gradients. The especially if one strives to answer unmistakable ability of cells to break What do you enjoy about your role significant questions. The key to symmetry and polarise without these cues, with the journal? maintaining the energy and drive to move just by reaching a certain internal I get a lot out of being the first to read some forward continuously is to recognise that biochemical state, highlights the principle of of the best work in developmental cell each non-trivial negative result reveals ‘self-organisation’. I had heard of this but biology. Through the process of evaluating something useful. This can be a glitch in never really considered it in my own work; these manuscripts, I hope to learn a lot more thinking or a problem in the experimental now, I think about it all the time, even when about developmental biology, get to know approach. Being able to learn something, no considering problems outside cell polarity. and interact with researchers in this matter how small, from a negative result community, and help shape new takes you forward because it enables you to You run a large group – how do you perspectives for research on developmental be better at designing and interpreting the find the management and mentoring systems. next experiment. Quantum leaps in the side of science? discovery process are built upon many small I learned a lot from my own mistakes What do you feel is the main benefit steps that seem insignificant individually. running a lab at Harvard, which was much of the journal in this field of science? smaller than the one I have right now (about Development is a leading journal in the field What one thing would people be 20 people currently). When I was rebuilding of developmental biology. It serves the surprised to learn about you? my lab at Stowers I decided to change my developmental biology research community We have a small weekend farm outside approach to become a much more dedicated by dedicating itself to the best work in this Kansas City in a beautiful area of rolling mentor. This is one side of science that I field, and hopefully also by broadening the meadows, hickory woods and creeks. We really enjoy these days. vision and approach of the field with grow, with the help of a professional farmer, cutting-edge thinking and methodology in alternating crops of corns and soybeans, and Where would you like to be and what cell and systems biology. The fact that all of have a good-sized vegetable garden. Both would you like to be doing in 20 years the Editors are scientists themselves with my husband and I grew up in a big city but time? expertise in various areas separates the farmland all around Kansas City I’d like to be exploring the subject of Development from journals whose Editors prompted us to try a rural lifestyle. So far, theoretical biology because I personally feel are not research scientists. Free access to weekend and holiday living on a farm has that the post-genomic biology needs some certain papers and freely available color been a most unusual and rewarding overarching theories.
Recommended publications
  • PSOC@PENN SPRING-Webinars 2021 Revised
    Physical Sciences in Spring 2021 Webinar Series Oncology Center PSOC@Penn Mondays @ Noon (EST) For webinar link, please contact <[email protected]> 01.25.2021 “Predicting interactions between cell collectives and their environment” M. Lisa Manning, PhD Professor, Department of Physics, Syracuse University, NY https://thecollege.syr.edu/people/faculty/manning-m-lisa/ 02.01.2021 TBA 02.08.2021 “Abnormal Mechanics in Brain Tumors” Meenal Datta, PhD Research Fellow in Radiation Oncology, Massachusetts General Hospital https://connects.catalyst.harvard.edu/Profiles/display/Person/17 0359 02.15.2021 “Sensing matrix rigidity: transducing mechanical signals from integrins to the nucleus” Pere Roca-Cusachs Soulere, PhD Group Leader (IBEC) & Associate professor, Cellular and Molecular Mechanobiology, University of Barcelona https://www.ibecbarcelona.eu/member/156/Pere+Roca - Cusachs+Soulere/ 02.22.2021 “Host-microbiota interaction in lung cancer development and response to immune checkpoint therapy.” Chengcheng Jin, Ph.D Assistant Professor, Department of Cancer Biology, UPenn https://www.med.upenn.edu/apps/faculty/index.php/g2000 03.01.20 “Polarity signaling ensures epidermal homeostasis by coupling cellular mechanics and genomic integrity” Sandra Iden, PhD Professor, Head of Dept. Cell & Developmental Biology, Saarland University, Homburg/Saar, Germany https://www.uni-saarland.de/en/chair/iden.html 03.08.2021 “Entropy as a driver to tissue structural heterogeneity in health and disease” Zev Gartner, PhD Professor, Department of Pharmaceutical Chemistry, UCSF, California https://www.gartnerlab.ucsf.edu/people.php 03.15.2021 “T cell circuits that can sense antigen density with an ultrasensitive threshold” Rogello Hernandez-Lopez, PhD Postdoctoral Fellow, Wendell Lim Lab, UCSF https://limlab.ucsf.edu/people/rogelio.html 03.22.2021 “TBA” Robert T.
    [Show full text]
  • 2016 Symposium Program
    Center for Innovative Drug Discovery 2016 San Antonio Drug Discovery Symposium Target Discovery and Drug Development in Texas June 9th and 10th 2016 8:00 AM –5:00 PM UTSA Main Campus, University Center, Denman Ballroom UTCIDD.org Day 1 8:00 AM-8:30 AM: Continental Breakfast and Registration 8:30 AM-8:45 AM: Welcome from Symposium Co-Chairs Stanton F. McHardy, Ph.D., Co-Director, Center for Innovative Drug Discovery, Director, Max and Minnie Tomerlin Voelcker Medicinal Chemistry Core Facility, UTSA Matthew Hart, Ph.D., Director, Center for Innovative Drug Discovery High Throughput Screening Core Facility, UTHSCSA 8:45-9:00 AM: Introductory remarks Dean George Perry, Ph.D., Semmes Foundation Distinguished University Chair in Neurobiology, Dean of the College of Sciences and Professor of Biology, UTSA 9:00 AM-9:50 AM: Plenary Keynote Presentation, Chair: Stanton McHardy, Ph.D. 9:00 AM-9:50 AM: Craig Lindsley, Ph.D., William K. Warren, Jr. Chair in Medicine, Professor of Pharmacology and Chemistry, Director, Medicinal Chemistry, Vanderbilt University “ Neuroscience Drug Discovery in an Academic Environment ” 9:50 AM-10:10 AM: Coffee Break 10:10 AM-12:10 PM: Session One, Chair: Bruce Nicholson, Ph.D. Identifying and Characterizing Molecular Drug Targets 10:10 AM-10:40 AM: Michael White, Professor, Cell Biology, Associate Director, Simmons Comprehensive Cancer Center, Sherry Wigley Crow Endowed Chair in Cancer Research, Grant A. Dove Distinguished Chair for Research in Oncology UT Southwestern Medical Center “Targeting mechanistic subtypes of neoplastic disease” 10:40 AM-11:10 AM: Gaston Habets, Ph.D., Sr.
    [Show full text]
  • Scientists Identify New Paradigm in Genetics, Paving Way for Development of Better Drug Targets to Save Lives 4 December 2015
    Scientists identify new paradigm in genetics, paving way for development of better drug targets to save lives 4 December 2015 Agency for Science, Technology and Research estimated to be as low as 25 per cent, partially due (A*STAR)'s Institute of Medical Biology (IMB) and to the high number of drug candidates found to be Singapore Immunology Network (SIgN) have resistible only during trial stage. This represents the identified a new paradigm for the identification and loss of time and resources which could otherwise evaluation of genes for cell survival. By challenging have been used to develop more effective drugs long-held notions on gene essentiality and drug and therapies. development, the study holds great potential to predict future drug resistance, thereby saving lives Now, A*STAR scientists have redefined the and optimising the use of resources. The study underlying concept of gene essentiality by putting was published on 25 November 2015 in the online forth a new genetic paradigm. Previously, genes issue of Cell. were divided into non-essential ones that are dispensable for cell viability, and essential genes Traditionally, basic and applied genetics have that are required for cell survival. The new study relied on the core concept of gene essentiality, found that essential genes can be further split into which states that certain genes are essential for a two kinds - one being the kind that cells need for cell's survival. When the cells in question are survival, known as 'non-evolvable' essential genes, cancer cells or pathogenic microbes, drugs can be and the other being those that cells can find ways developed to block these essential genes, so as to to survive without, by an evolutionary process of eradicate these harmful cells.
    [Show full text]
  • Scientists Offer Insight Into Adaptive Ability of Cells 26 November 2008
    Scientists offer insight into adaptive ability of cells 26 November 2008 The Stowers Institute's Rong Li Lab has published regulation or chemotherapeutic drug treatment work findings that shed light on the ability of cells to to limit their growth." adapt to disruptions to their basic division machineries – findings that may help explain how The work establishes an exciting new path for the cancer cells elude the body's natural defense Rong Li Lab. mechanisms or chemotherapy treatment. The work was published in the November 26 issue of Cell. "These findings validated our view that evolvability is a trackable and important subject for study," said Working with yeast cells, the team disabled a Rong Li, Ph.D., Investigator and senior author on motor protein, type II myosin — which normally the paper. "We are now working to determine powers cell division — and observed the cellular whether there are many distinct mechanisms of response. As predicted, blocking division initially evolvability correlating with varying types and resulted in severe growth and cytokinesis defects. degrees of cellular disruptions. Additionally, we But after several selection passages, some cells would like to explore the possibility of predicting the were able to solve the problems. Unexpectedly, likely evolutionary paths and outcomes based on these cells ended up with more than the normal the architecture of molecular networks present in number of chromosomes. The abnormal the cell; and in extending our research into chromosome numbers led to changes in the mammalian cell systems to directly study the role of patterns of gene expression, which correlated with aneuploidy in the evolution of cancer." the cells' ability to evolve new ways to complete division and resume growth.
    [Show full text]
  • Presented by the Maryland Biophysics Program
    Movement of cells is key to life, from the collective motion of cells during development, to the migration of immune cells as they fend off invaders and deformations of neurons as they wire up the brain. Talks will feature both experiments and modeling of cell dynamics from multiple angles. 8:30 am Refreshments and on-site registration (no fee) 9:00 am Introductory Remarks 9:15 am Modeling cellular volume and pressure Sean Sun (Johns Hopkins University) regulation: Implications for cell shape and motility 10:00 am Mechanisms of actin-based force generation in Rong Li (Stowers Institute) cell polarity and cell division 10:45 am Break 11:00 am Actin-driven dynamics of the neuronal Thomas Blanpied (UMD Medical School) postsynaptic density 11:45 am Cytoskeletal dynamics during lymphocyte Arpita Upadhyaya (University of Maryland) activation 12:05 pm How cells crawl: a role for actin arcs in the Dylan Burnette (NIH) leading edge advance of migrating cells 12:25 pm Lunch and poster session* 2:00 pm Spontaneous waves and symmetry breaking of Anders Carlsson (Washington University) f-actin in cells 2:45 pm Excitable actin dynamics at the leading edge of Dmitrios Vavylonis (Lehigh University) crawling cells 3:30 pm Break 3:45 pm Cell shape dynamics: From waves to migration Wolfgang Losert (University of Maryland) Molecular force productions, cell-shape 4:05 pm changes, and tissue patterning during Glenn Edwards (Duke University) Drosophila development Reception 5:00 pm Presented by the Maryland Biophysics Program Supported by IPST, & the Biology, Chemistry, and Physics Departments Organizers: Wolfgang Losert, Arpita Upadhyaya For more information: Caricia Fisher ([email protected]) *Poster submission is encouraged.
    [Show full text]
  • Mechanisms of Branched Actin Network Formation Through
    MECHANISMS OF BRANCHED ACTIN NETWORK FORMATION THROUGH COORDINATE ACTIVATION OF ARP2/3 COMPLEX by LUKE ANDREW HELGESON A DISSERTATION Presented to the Department of Biology and the Graduate School of the University of Oregon in partial fulfillment of the requirements for the degree of Doctor of Philosophy December 2014 DISSERTATION APPROVAL PAGE Student: Luke Andrew Helgeson Title: Mechanisms of Branched Actin Network Formation through Coordinate Activation of Arp2/3 Complex This dissertation has been accepted and approved in partial fulfillment of the requirements for the Doctor of Philosophy degree in the Department of Biology by: Bruce Bowerman Chairperson Bradley Nolen Advisor Alice Barkan Core Member J. Andrew Berglund Core Member Kenneth Prehoda Institutional Representative and J. Andrew Berglund Dean of the Graduate School Original approval signatures are on file with the University of Oregon Graduate School. Degree awarded December 2014 ii © 2014 Luke Andrew Helgeson iii DISSERTATION ABSTRACT Luke Andrew Helgeson Doctor of Philosophy Department of Biology December 2014 Title: Mechanisms of Branched Actin Network Formation through Coordinate Activation of Arp2/3 Complex Fundamental cellular processes such as motility and endocytosis rely on the actin cytoskeleton to translate biochemical protein interactions into mechanical forces. Cells utilize an extensive collection of actin binding proteins to comprehensively regulate actin networks during these dynamic cell operations. Branched actin networks, which are geometrically and functionally disparate from linear networks, are required for numerous cellular actions. Actin-related protein 2/3 complex (Arp2/3 complex) nucleates branched actin filaments upon activation by regulatory proteins known as nucleation promoting factors (NPFs). Often, several biochemically distinct NPFs are required for the same cellular structure, leading us to hypothesize that multiple NPFs can coordinately activate Arp2/3 complex to regulate the nucleation, architecture and assembly of branched networks.
    [Show full text]
  • Overstuffed Cancer Cells May Have an Achilles' Heel 22 July 2019
    Overstuffed cancer cells may have an Achilles' heel 22 July 2019 the June 6 issue of Nature. The new experiments focused on a chromosome number abnormality known as aneuploidy. Normal human cells, for example, have a balanced number of chromosomes: 46 in all, or 23 pairs of different chromosomes. A cell with chromosomes that have extra or fewer copies is called aneuploid. Li says, "aneuploidy is the #1 hallmark of cancer," and is found in more than 90% of solid tumor cancer types. Aneuploid yeast cells on the left have difficulty drawing When cells gain chromosomes, Li says, they also in fluorescent molecules. Whereas, the normal yeast get an extra set of genes that produce more than cells on the right are able to rapidly draw them in. Credit: the normal amount of protein that a cell makes. Rong Li and Hung-Ji Tsai This excess can give cells growth abilities they normally wouldn't have, sometimes allowing them to overgrow and develop into a tumor. In a study using yeast cells and data from cancer Because aneuploid cells have unbalanced protein cell lines, Johns Hopkins University scientists production, they have too many free-floating report they have found a potential weak spot proteins that are not organized into a complex. This among cancer cells that have extra sets of increases the concentration inside of the cell chromosomes, the structures that carry genetic compared to outside. To compensate for the material. The vulnerability, they say, is rooted in a increased concentration, the cells draw in water, a common feature among cancer cells—their high phenomenon that leads to hypo-osmotic stress.
    [Show full text]
  • Scientists Probe Mechanism of Asymmetry in Meiotic Cell Division 7 October 2008
    Scientists probe mechanism of asymmetry in meiotic cell division 7 October 2008 The Stowers Institute's Rong Li Lab has better understanding of the process of meiotic characterized a mechanism that allows for divisions and how actin generates the force to asymmetrical cell division during meiosis in power intra-cellular movements." oocytes. By tracking chromosome movement in live mouse oocytes, the team discovered that Source: Stowers Institute for Medical Research chromosomes can recruit to their vicinity a protein called formin-2. This protein allows the oocyte to retain the majority of the cytoplasm – a requirement for embryonic development after fertilization – while the other daughter cell (called a polar body) resulting from the asymmetric division gets only a minimal amount and subsequently dies. The work was published this week in the advance online publication of Nature Cell Biology. Formin-2 is an actin-nucleating protein that can promote the formation of actin filaments around the chromosomes. Actin filaments undergo dynamic elongation and shortening and, in the process, push the chromosomes towards the outer edge of the oocyte. After the chromosomes reach the periphery, the actin filaments orient the cell division plane so that most of the cytoplasm required to sustain the earliest stages of development stays with the daughter cell that retains the identy of the oocyte. "This work revealed the general mechanism by which the actin cytoskeleton drives chromosome movement in mammalian meiotic oocytes," said Hongbin Li, Ph.D., Senior Research Associate and lead author on the publication. "Our findings will enable us to carry out even more detailed dissection of the molecular components and mechanisms." "Infertility and birth defects are often related to problems during oocyte meiotic cell divisions," said Rong Li, Ph.D., Investigator and senior author on the paper.
    [Show full text]
  • ASCB Member Profile
    ASCB Profile Rong Li The old joke is that biologists were science ma- Krumlauf thought Li would be a perfect fit. jors who couldn’t do the math. The new para- “Rong’s very much a lateral thinker,” Krumlauf digm in biology? Quantify, quantify and then do says. “She’s interested not only in her own the mathematical modeling. “That puts Rong Li projects but in the research of others. We need at the leading edge,” says Andrew Murray, about that synergy in an institution like ours …because the career of his very first graduate student. Li is all science is becoming interdisciplinary. To truly now an Investigator at the Stowers Institute for integrate biology, genetics, and biochemistry with Medical Research in Kansas City. “I think Rong computational science requires some uniquely is one of those ahead of the curve,” Murray says, qualified individuals,” says Krumlauf. “Even if “in her ability to interact with quantitative sci- you have teams with individual expertise, it’s not entists and biologists.” easy for them to say to another group, ‘Please “Rong Li’s been a very successful scientist solve this problem for me.’ You need someone who’s made real contributions to understanding like Rong Li who can bridge the gap just to know how the cytoskeleton is organized,” Murray what question is being asked.” Rong Li continues. He is now at Harvard University. “Rong is able to talk with mathematicians, In 1989 Murray was a newly help them understand the minted assistant professor at nature of the problem, and the University of California, then take their solutions San Francisco (UCSF).
    [Show full text]
  • Curriculum Vitae and Bibliography
    Curriculum Vitae and Bibliography Name: Rong Li Education 1984‐1988 B.S. and M.S (Combined) Yale University New Haven, Connecticut (Mol. Biochem. & Biophy.) 1988‐1992 Ph.D. University of California, San Francisco, California (Biochem. & Biophy.) San Francisco Postdoctoral Training 1993‐1994 Postdoctoral fellow University of California, Berkeley, California (Mol. Cell Biology) Berkeley Academic Appointments Dec 1994 – Assistant Professor Department of Cell Biology Dec 1999 Harvard Medical School Jan 2000 – Associate Professor Department of Cell Biology June 2005 Harvard Medical School July 2005 – Investigator Rong Li Laboratory Present Stowers Institute for Medical Research Jan 2006 – Professor (affiliated) Department of Molecular and Integrative Physiology Present University of Kansas School of Medicine Awards and Honors 1988 Phi Beta Kappa, Summa Cum Laude, Distinction in Major, Yale University 1993 – 1994 Damon Runyon‐Walter Winchell Cancer Research Fellowship 1995 – 1997 Medical Foundation New Investigator Award 1997 – 1998 The Funds for Discovery Exploratory Award 1998 – 2000 Giovanni Armenise/Harvard Foundation Award 1999 – 2001 Hoechst Marion Roussel Research Award 2000 Biological and Biomedical Sciences Mentoring Award, Harvard Medical School 2004 – 2005 The Alexander and Margaret Stewart Trust Pilot Project Program Award 2010 – 2012 William B. Neaves Award 2012 Watkins Visiting Professorship – Wichita State University Publications I. Research Papers 1. Zhou C, Slaughter BD, Unruh JR, Guo F, Yu Z, Mickey K, Narkar A, Ross TR, McClain M and Li R. Organelle‐based aggregation and retention of damaged proteins in asymmetrically dividing cells. (2014) Cell 159:530‐542 2. Li G, Li M, Zhang Y, Wang D, Li R, Guimerà R, Gao J, Zhang MQ. ModuleRole: a tool for modulization, role determination and visualization in protein‐protein interaction networks.
    [Show full text]
  • On the Role of P53 in the Cellular Response To
    ON THE ROLE OF P53 IN THE CELLULAR RESPONSE TO ANEUPLOIDY by Akshay Narkar A dissertation submitted to Johns Hopkins University in conformity with the requirements for the degree of Doctor of Philosophy Baltimore, Maryland July 2020 © 2020 Akshay Narkar All rights reserved ABSTRACT A majority of solid tumors are aneuploid and the tumor suppressor protein 53, has been implicated as the guardian of euploid genomes in animal organisms. Experiments using transformed or non-transform human cell lines showed that aneuploidy induction leads to p53 accumulation and a consequent, p21-mediated, G1 cell cycle arrest. However, it has been controversial as to whether there is a universal signal elicited by the aneuploid state that activates p53. My PhD thesis attempts to advance our understanding of the universality of the p53 response in different cell and tissue context post aneuploidy induction. In this study, we found that, whereas adherent 2-dimensional (2D) cultures of human immortalized or cancer cell lines indeed activate p53 upon aneuploidy induction as previously reported, suspension cultures of a human lymphoid cell line undergoes a p53- independent cell cycle arrest upon aneuploidy formation. To dive deeper into the molecular mechanisms regulating p53-independent arrest post aneuploidy in Nalm6 cells we performed a genome wide CRISPR/Cas9 knockout screen. This revealed previously uncharacterized functions of PDCD5 and LCMT1 in regulating chromosomal aberrations. Recent studies highlight that tissue environment plays a critical role in regulating chromosome segregation, however the role of p53 in 3D environment is not well characterized. To our surprise, 3-dimensional (3D) organotypic cultures of cells from human or mouse neural, intestinal or mammary epithelial tissues do not activate p53 or undergo G1 arrest upon aneuploidy induction.
    [Show full text]
  • Proceedings of the Fourth International Conference on the Foundations of Information Science, Beijing, August 21–24, 2010
    tripleC 9(2): 272-277, 2011 ISSN 1726-670X http://www.triple-c.at Editorial to the Special Issue: Towards a New Science of Information – Proceedings of the Fourth International Conference on the Foundations of Information Science, Beijing, August 21–24, 2010 Wolfgang Hofkirchner*, Zong-Rong Li**, Pedro C. Marijuán***, Kang Ouyang**** * [email protected], Unified Theory of Information (UTI) Research Group, Vienna, Austria ** [email protected], Social Information Science Institute (SISI), Huazhong University of Science and Tech- nology (HUST), Wuhan, P.R. of China *** [email protected], Bioinformation Group, Instituto Aragonés de Ciencias de la Salud, Zaragoza, Spain **** [email protected], Social Information Science Institute (SISI), Huazhong University of Science and Technology (HUST), Wuhan, P.R. of China In our times, an increasing number of disciplines are dealing with information in very different ways: from the information society and information technology to communication studies (and rela- ted subjects like codes, meaning, knowledge, and intelligence), as well as quantum information, bioinformation, the knowledge economy, network science, computer science and the Internet, to name but a few. At the same time, an increasing number of scientists in the East and the West have been engaged with the foundational problems underlying this development, to such an extent that it seems the time has come to integrate disciplines revolving around information. A new scien- ce of information can be envisaged that explores the possibilities of establishing a common ground around the information concept, of constructing a new scientific perspective that connects the diffe- rent information-related disciplines and provides a new framework for transdisciplinary research.
    [Show full text]