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David Sabatini (Whitehead, MIT, HHMI) 1: Introduction to mTOR and the Regulation of Growth

https://www.ibiology.org/cell-biology/mtor-regulationDavid Sabatini outlines the critical role of mTOR in the regulation of growth. mTOR senses nutrient levels, growth factors and other signals and integrates a response to regulate cell growth.(Part 1 of 3) Growth can be defined as the increase in the size of a cell or organism, due to a gain in mass caused by nutrient uptake and assimilation. Surprisingly, how growth is regulated was not well understood until quite recently. In his first talk, David Sabatini describes how insight into this question came from an unusual direction. The small molecule drug rapamycin was known to have anti-growth effects, but its intracellular target was not known. Sabatini explains how he purified and cloned the target of rapamycin from rat brain and showed that it was a protein kinase. This protein was named mTOR in mammals and was shown to be homologous to the TOR proteins in yeast. Sabatini and others went on to show that mTOR is at the heart of two large protein complexes, mTORC1 and mTORC2, that sense upstream signals such as nutrient levels, hormones, and growth factors and direct downstream effectors to build or breakdown resources as needed for cell growth and proliferation. Speaker Biography:Dr. David M. Sabatini is a member of the Whitehead Institute for Biomedical Research, a professor of Biology at the Massachusetts Institute of Biology (MIT), an investigator of the Howard Hughes Medical Institute, a senior member of the Broad Institute of Harvard and MIT and a member of the Koch Institute for Integrative Cancer Research at MIT. His lab is interested in the regulation of growth and metabolism in mammals, with a focus on the critical mTOR pathway. Research from Sabatini’s lab has led to a better understanding of the role of the mTOR pathway in diseases such as cancer and diabetes, as well as in aging. Sabatini received his undergraduate degree in biology from Brown University. As a MD/PhD student at Johns Hopkins University School of Medicine, he did his first experiments on rapamycin and mTOR in the lab of Solomon H. Snyder. After completing his MD/PhD in 1997, Sabatini started his own lab as a Whitehead fellow at the Whitehead Institute. In 2002, he became a member of the Whitehead Institute and a faculty member at MIT.Sabatini’s groundbreaking work has been recognized with numerous awards and honors including the National Academy of Science Award in Molecular Biology (2014), the Dickson Prize in Medicine (2017), the Lurie Prize in Biomedical Sciences (2017), and the Switzer Prize (2018). Sabatini was elected to the National Academy of Sciences in 2016. Learn more about the research being done in Sabatini’s lab here: http://sabatinilab.wi.mit.eduand here:https://www.hhmi.org/scientists/david-m-sabatini

34mins

28 Nov 2018

Rank #1

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Andre Fenton (NYU) 2: Protein Kinase M zeta promotes memory and Long-Term potentiation (LTP)

Part 1: Reconstructing memory: Dr. André Fenton explains the neurobiological factors that maintain memory in our brains.Part 2: Protein Kinase M zeta is essential for storing long-term memory: Fenton describes the importance of Protein Kinase M zeta for the persistence of Long-Term potentiation and memory across days.Part 3: Preemptive cognitive training can prevent future cognitive control impairment: Fenton describes how his lab used a rat model of the neurodevelopmental origins of schizophrenia to study cognitive control in these animals.https://www.ibiology.org/ibioseminars/protein-kinase-m-zeta-essential-storing-long-term-memory.htmlTalk Overview:Dr. André Fenton explains the neurobiological factors that maintain memory in our brains.  As he describes, memory is a reconstructive process, whereby recollection of a particular experience involves the brain’s active rebuilding of the memory.  In his first lecture, Fenton outlines how scientists have been able to associate the electrical (action potential) discharge of specific neurons with particular experiences and memories.  Studying the rat hippocampus, scientists can decode information like where the rat thinks it is from the pattern of action potentials of the population of neurons.  These studies reveal that the pattern of action potentials in a network of neurons encodes aspects of the external world which define experiences, thoughts and memories.In his second lecture, Fenton provides a framework to understand the molecular mechanisms that affect acquiring and persistently storing memory.  As he explains, synapses regulate the flow of information between neurons.  The process of learning (memory acquisition) requires electrochemical communication between neurons across their synapses and this communication itself can change the synapses to subsequently make the communication easier and harder.  One of these changes, called long-term potentiation (LTP) of synaptic transmission, strengthens the communication.  An active place avoidance memory test for rodents, requires the animal to avoid uncomfortable situations (e.g. electrical shock) by learning and remembering where shocks were experienced.  Using this memory test the Fenton lab showed that Protein Kinase M zeta is essential for the persistence of LTP and memory across days.  To make adaptive decisions, animals need to evaluate information from the environment by coordinating information from multiple sources, a process known as cognitive control.  Cognitive control is impaired in diverse forms of mental illness, including schizophrenia.  Fenton’s lab used a rat model of the neurodevelopmental origins of schizophrenia to study cognitive control in these animals using variants of the active place avoidance task.  They showed that adult schizophrenia-model rats were error prone when cognitive control was needed to deal with conflicting sources of information and the patterns of electrical activity in their brains were disorganized.  Remarkably, adult schizophrenia-model animals that were trained to use cognitive control in adolescence had neither the disorganized patterns of brain electrical activity nor the cognitive control deficit, even though their brains were damaged.  These studies demonstrate that cognitive training to acquire and maintain memories reorganizes how the brain works, and this alone can inoculate against future mental dysfunction.Learn more about Dr. Fenton’s research at his lab website:https://www.fentonlab.com/the-lab

43mins

28 Mar 2017

Rank #2

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Andrew P. Nosal: Not Just on Vacation: Why Leopard Sharks Hang Out in La Jolla

Every year from June to December, hundreds to thousands of leopard sharks (Triakis semifasciata) congregate in this one particular spot along the southern California shoreline. Why are they here? Andrew Nosal answers this question and articulates why we should care. He intensely studied these sharks and their behavior over the course of several years. He discovered that most of the sharks are mature pregnant females. During the day, these pregnant females spend most of their time swimming in the warm, calm waters that are unique to the La Jolla area. At night, they forage for squid in a nearby marine canyon. Because sharks lack the ability to regulate their internal temperature (i.e., they are ectothermic), Nosal concludes the pregnant sharks are attracted to La Jolla’s warm waters to support the developing fetuses for the same reason that hens sit on their eggs. He emphasizes the importance of protecting the leopard sharks, especially considering how they carry the next generation of sharks and could easily be wiped out by careless human activity. http://www.ibiology.org/ibioseminars/andrew-p-nosal.htmlSpeaker Biography: Andrew P. Nosal is currently a postdoctoral researcher at Scripps Institution of Oceanography, where he conducts research on the behavior, ecology, and conservation of sharks and rays. Nosal is most interested in the causes and consequences of movement phenomena like aggregation (grouping) behavior, sexual segregation (spatial separation of males and females), and seasonal migration. He works closely with the Birch Aquarium and various media outlets to educate the public about sharks and rays and to dispel myths about these amazing animals. He is passionate about communicating science and, as a PhD student, received two awards for best student oral presentation at international conferences in Minneapolis, MN and Sapporo, Japan. When Nosal is not following sharks and rays, he loves hanging out and traveling with his wife and young daughter.

35mins

12 Oct 2015

Rank #3

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Megan Sykes (Columbia U.) 1: Introduction to Transplantation

https://www.ibiology.org/immunology/xenotransplantationMegan Sykes provides an introduction to the field of organ transplantation, discusses the immunological responses associated with this procedure, and explains the new onsets of xenotransplantation. Talk Overview:Dr. Megan Sykes provides an introduction to the field of organ transplantation and discusses the immunological responses associated with this procedure. Rejection is a major limitation to the success of transplantation. Sykes explains what causes rejection episodes in different types of transplantation, and outlines what we can do to prevent this from happening.As Sykes explains, the Holy grail of transplantation is tolerance, the long-term graft acceptance without the long-term use of immunosuppressants. Sykes and collaborators developed a hematopoietic cell transplantation and mixed chimerism technique that proved to induce true tolerance in humans. They showed that transient mixed chimerism, the co-existence of donor and recipient hematopoietic elements, was detected in patients where tolerance was observed. Sykes reviews the clinical trial results and explains the experimental techniques used to study the molecular features that predict tolerance and low rates of organ rejection in patients.In her third lecture, Sykes provides an overview of xenotransplantation, the use of organs or grafts from other (non-human) species. She outlines the challenges encountered with cross-species transplantation, and how scientist have been able to overcome these difficulties. Sykes and other laboratories are exploring the use of miniature pigs for xenotransplantations to humans. Sykes shows the outcome of xenotransplantations performed between different species (e.g. rat to mouse or pig to baboon), and what scientists have learned from these results.Speaker Biography:Dr. Megan Sykes is the Friedlander Professor of Medicine, a Professor of Microbiology and Immunology and a Professor of Surgical Sciences at Columbia University Medical Center, and the director of the Columbia Center for Translational Immunology. In 1982, Sykes completed her medical degree at University of Toronto and continued her medical training in Montreal and Toronto. In 1990, she joined the faculty of Massachusetts General Hospital and Harvard Medical School, where she pioneered studies to induce mixed chimerism and tolerance after organ transplantation in humans. In 2010, she moved her lab to Columbia University where she established the Columbia Center for Translational Immunology and continues her research innovating techniques in the field of allo- and xenotransplantation.For her scientific contributions, Sykes was elected member of the National Academy of Medicine (2009) and a Fellow of the AAAS (2009). Learn more about Sykes’ research at her lab website.http://www.microbiology.columbia.edu/faculty/sykes.html

32mins

31 Jul 2018

Rank #4

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Reppert 2: Neurobiology of Monarch Butterfly Migration: A Time-Compensated Sun Compass

Reppert begins by describing the amazing long-distance migration of the Eastern North American Monarch butterfly. Each fall, several hundred million Monarchs fly up to 2500 miles from the eastern United States and southern Canada to a specific over-wintering area in central Mexico. How do the butterflies know when and where to fly? Reppert explains that the migration is directed largely by an innate sun compass.In Part 2, Reppert focuses on the time-compensated sun compass system that guides the Monarch’s long migration. He describes how the butterfly eye can sense skylight cues used for directionality, including polarized UV light. This information is integrated in the central complex of the brain, which serves as the sun-compass, then is time compensated, and ultimately interacts with the motor system to control flight direction. While circadian clocks in the brain determine the seasonal migration of Monarchs, distinct circadian clocks in the antennae regulate time-compensation of the sun compass. Interestingly, work at the molecular level shows that the Monarch circadian clock mechanism is distinct and utilizes two cryptochrome (CRY) gene homologues; one previously found in Drosophila and one previously found in vertebrates.For more details of the monarch migration see http://reppertlab.org http://www.ibiology.org/ibioseminars/steven-m-reppert-part-2.htmlSpeaker Biography: Steven Reppert received both his B.S. and M.D. degrees from the University of Nebraska. He did his clinical training in pediatrics at Massachusetts General Hospital and Harvard Medical School and was a post-doctoral fellow at the NIH in the Section on Neuroendocrinology. He then joined the faculty of Harvard Medical School where he resided for 22 years before moving in 2001 to chair the Department of Neurobiology at the University of Massachusetts Medical School.For the first 23 years of his research career, Reppert’s work primarily focused on cellular and molecular mechanisms of circadian clocks in mammals. Since 2002, his research has shifted to understanding the biological basis of the long-distance migration of the Monarch butterfly with a focus on its navigational abilities and the role of its unique circadian clock. Reppert’s pioneering research has been recognized with numerous awards including an NIH MERIT award, election as a Fellow of the American Association for the Advancement of Science and the G.J. Mendel Honorary Medal for Merit in the Biological Sciences from the Academy of Sciences of the Czech Republic.

46mins

20 Jan 2015

Rank #5

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Ramanujan Hegde (MRC) 3: Recognition of Protein Localization Signals

How does the cell regulate protein localization to be sure that proteins end up where they should? Manu Hegde reviews experiments that answer this question.https://www.ibiology.org/ibioseminars/recognition-protein-localization-signals.htmlTalk Overview:Cells are organized into many different compartments such as the cytosol, nucleus, endoplasmic reticulum (ER), and mitochondria. Almost all proteins are made in the cytosol, yet each cellular compartment requires a specific set of proteins.  How does the cell regulate protein localization to be sure that proteins end up where they should? In his first lecture, Manu Hegde reviews the history of this field and highlights key experiments that have led to our current understanding of how protein localization occurs.In his second lecture, Hegde explains that although the protein localization system usually operates accurately, it does sometimes fail.  This can be due to genetic mutations, stress within an organelle, or just intrinsic inefficiencies that accompany any complex process. As a graduate student, Hegde used a cell-free in vitro system to study the translocation of prion protein into the ER. He found that a small amount of prion protein did not completely cross the ER membrane as expected, but remained in a transmembrane form. Worried that this was an artifact of the in vitro system, he designed experiments in mice to see what the effect of an increase in mislocalized, transmembrane prion protein would be. He found a striking result - even a small increase in the amount of transmembrane prion protein caused increased neurodegeneration in mice. It turns out that incomplete translocation is not unique to prion protein. Hegde tells us how, as an independent investigator, his lab went on to investigate why this happens and how the cell monitors and degrades proteins that are not properly localized.Proteins that are secreted from the cell or localized to the plasma membrane need first to be translocated into the lumen of the ER or inserted into the ER membrane. Thousands of proteins, each with a unique signal sequence, move through this pathway. How does the protein translocation machinery recognize these diverse signals and correctly localize the protein?  In his third talk, Hegde describes studies from his lab using cryo-electron microscopy to visualize the translocation machinery at different stages in the recognition and engagement of a secreted or membrane inserted protein. The structural information gleaned from these experiments helps to explain how the protein translocation machinery works with high fidelity even when it needs to recognize diverse signal sequences. Speaker Biography:As an undergraduate, Ramanujan (Manu) Hegde studied biology at the University of Chicago with the thought that he would become a doctor.  His summers and spare time were spent working in a lab, where he came to love the problem-solving of basic research. Hegde then fled Chicago winters for the sunshine of The University of California, San Francisco, where he completed an MD-PhD combined degree program. By then, he had decided to pursue basic research as a career, and moved to the National Institutes of Health where he was an investigator for 11 years. In 2011, Hegde moved to the Laboratory of Molecular Biology in Cambridge, England, where his research focuses on the mechanisms of protein biosynthesis and quality control.Hegde’s research contributions have been recognized with his election as a member of the European Molecular Biology Organization in 2013 and as a Fellow of the Royal Society in 2016.Learn more about Manu Hegde’s research here:http://www2.mrc-lmb.cam.ac.uk/groups/hegde/andhttp://www2.mrc-lmb.cam.ac.uk/group-leaders/h-to-m/ramanujan-hegde/

46mins

3 Aug 2017

Rank #6

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Zhuang 1: Super-Resolution Fluorescence Microscopy

Zhuang begins her lecture by explaining that the resolution of traditional light microscopy is about 200 nm due to the diffraction of light. This diffraction limit has long hampered the ability of scientists to visualize individual proteins and sub-cellular structures. The recent development of sub-diffraction limit, or super resolution, microscopy techniques, such as STORM, allows scientists to obtain beautiful images of individual labeled proteins in live cells.In Part 2 of her talk, Zhuang gives two examples of how her lab has used STORM; first to study the chromosome organization of E. coli and second, to determine the molecular architecture of a synapse.

50mins

3 Aug 2012

Rank #7

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Daniel Colon-Ramos (Yale/HHMI) 1: Cell biology of the synapse and behavior in C. elegans

How is the neuronal synapse assembled to produce specific behaviors and store memories?  Dr. Colon-Ramos studies C. elegans to address this fundamental question. https://www.ibiology.org/neuroscience/neuronal-synapse/Talk Overview:A fundamental question in neuroscience is how synapses are assembled in living animals to produce behaviors and store memories. Dr. Daniel Colón-Ramos and his lab address these questions by studying the cell biology of the neuronal synapse. In the first part of his seminar series, he introduces approaches his group has pioneered and implemented to image and manipulate synapses in vivo and with single-cell resolution in the nematode C.elegans. He also discusses fundamental aspects of genetics, cell biology and neuroscience which are necessary for understanding his research program and, more generally, for understanding how scientists make use of model organisms to generate new knowledge.Speaker Biography:Dr. Daniel Colón-Ramos is an associate professor in the Department of Cell Biology and Neuroscience at Yale University, adjunct professor at the Instituto de Neurobiología at the Universidad de Puerto Rico, and a Marine Biological Laboratories (MBL) fellow. His lab is interested in understanding the cell biology of the synapse--how it is established, maintained and modified to influence behavior. His group has pioneered approaches to address these questions in single cells of living animals (specifically, in nematodes called C. elegans).Born and raised in Puerto Rico, Colón-Ramos’ passion for science began at a young age. His scientific curiosity was, in part, fueled by participation in the NSF-funded Young Scholars minority research program he attended in high school. As an undergraduate at Harvard University, he pursued his love for science and social issues by conducting ethnopharmacological research in Central America with the Smithsonian Tropical Research Institute. After college, he worked as a postbac with fellow Puerto Rican scientist Dr. Mariano Garcia-Blanco at Duke University to understand the cell biology of transcription in the nuclei of Chlamydomonas reinhardtii, and to explore his interests in a career in scientific research. He pursued a PhD at Duke University with Dr. Sally Kornbluth studying the molecular mechanisms of programmed cell death, and his PhD work was recognized with a Gates Millennium Scholarship. He then joined the lab of Dr. Kang Shen at Stanford University as a Damon Runyon fellow and later, as a recipient of the “Pathways to Independence” (NIH K99/R00) award. Always striving to combine his social and science interests, in 2006, he founded the nonprofit, Ciencia Puerto Rico (CienciaPR). CienciaPR’s work was recognized in 2015 by the White House as a Bright Spot in Science Education of Hispanics.He started as an independent investigator at Yale University in 2008. His lab’s scientific work has been recognized by the Klingenstein Fellowship Award in Neurosciences in 2009, a Sloan Research Fellowship in 2010, an AAAS Early Career Award for Public Engagement with Science in 2012 and an HHMI Faculty Scholar award in 2016. His lab’s work was also recognized with the 2016 American Society for Cell Biology “E.E. Just Lecture Award”.Learn more about Colón-Ramos’ research here: http://medicine.yale.edu/lab/colon_ramos/

34mins

13 Dec 2017

Rank #8

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Prather 1: Synthetic Biology and Metabolic Engineering: Introduction

Lecture OverviewIn the first part of her lecture, Dr. Prather explains that synthetic biology involves applying engineering principles to biological systems to build “biological machines”. The key material in building these machines is synthetic DNA. Synthetic DNA can be added in different combinations to biological hosts, such as bacteria, turning them into chemical factories that can produce small molecules of choice. In Part 2, Prather describes how her lab used design principles to engineer E. coli that produce glucaric acid from glucose. Glucaric acid is not naturally produced in bacteria, so Prather and her colleagues “bioprospected” enzymes from other organisms and expressed them in E. coli to build the needed enzymatic pathway. Prather walks us through the many steps of optimizing the timing, localization and levels of enzyme expression to produce the greatest yield. Speaker Bio: Kristala Jones Prather received her S.B. degree from the Massachusetts Institute of Technology and her PhD at the University of California, Berkeley both in chemical engineering. Upon graduation, Prather joined the Merck Research Labs for 4 years before returning to academia. Prather is now an Associate Professor of Chemical Engineering at MIT and an investigator with the multi-university Synthetic Biology Engineering Reseach Center (SynBERC). Her lab designs and constructs novel synthetic pathways in microorganisms converting them into tiny factories for the production of small molecules. Dr. Prather has received numerous awards both for her innovative research and for excellence in teaching.

26mins

6 Feb 2014

Rank #9

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Lalita Ramakrishnan (Cambridge) 1: An Introduction to Tuberculosis: The Pathogenic Personality of the Tubercle bacillus

Lalita Ramakrishnan gives an introduction to tuberculosis (TB) pathogenesis, gives an overview of Mycobacterium tuberculosis’ life cycle, and explains how the TB bacteria gain entry into the host. https://www.ibiology.org/ibioseminars/introduction-tuberculosis-pathogenic-personality-tubercle-bacillus.htmlTalk Overview:In this seminar, Dr. Lalita Ramakrishnan gives an introduction to tuberculosis (TB) pathogenesis, and gives an overview of Mycobacterium tuberculosis’ life cycle. She explains how the TB bacteria gain entry into the host by using specific lipids to avoid microbicidal macrophages and recruit growth-permissive ones. Once inside the macrophage, the bacteria use multiple virulence genes to survive intracellularly. In particular, Ramakrishnan discusses bacterial efflux pumps that, in addition to promoting intracellular survival, also induce tolerance to multiple antibiotics. Most individuals have effective counterstrategies so that they are able to clear TB infection by a combination of innate and adaptive immunity. Yet scientists have not been able to understand these defense strategies enough to harness them and create an effective vaccine against TB. 
After the TB bacteria infect macrophages, a complex structure called a granuloma develops. Different immune cells arrive at the granuloma to surround the bacterial infection and fight the disease. In her second lecture, Ramakrishnan explains how her laboratory used a zebrafish model of TB to study the involvement of granulomas in TB progression. Although granulomas were thought to constrain infection, her laboratory showed that the bacteria hijack the granulomas to spread the disease. For example, Ramakrishnan showed that TB bacteria promote the recruitment of new macrophages to the granuloma that engulf dying infected macrophages to expand infection. 
Ramakrishnan’s laboratory has studied the molecular pathogenesis of TB using the power of forward genetics in the zebrafish. They discovered that mutations in LTA4H, a key enzyme in the eicosanoid pathway that alters the levels of the cytokine tumor necrosis factor (TNF), affect tuberculosis pathogenesis by regulating the inflammatory response. This work showed that a balance of TNF is required for good TB prognosis, and neither high nor low inflammation was favorable. Correspondingly, they showed that genetic variation in LTA4H in humans helps explain patterns of TB meningitis survival when patients were exposed to a treatment that suppresses the inflammatory response.Speaker Biography:Dr. Lalita Ramakrishnan is a professor of immunology and infectious diseases at the University of Cambridge, UK. She received her medical degree from the Baroda Medical College in India, and her PhD in Immunology from Tufts University in Boston. After completing her medical residency at Tufts and a fellowship in Infectious Diseases at the University of California, San Francisco, she joined the lab of Dr. Stanley Falkow at Stanford University as a postdoctoral fellow.  There she developed Mycobacterium marinum as a model for to study tuberculosis pathogenesis. She then joined the faculty at the University of Washington, where her laboratory developed the zebrafish infected with M. marinum as a model for tuberculosis. In 2014, she moved to the University of Cambridge, where her laboratory continues to unravel the molecular underpinnings of TB pathogenesis. Ramakrishnan’s work has been recognized with several awards and honors, including the NIH Director’s Pioneer Award, the Wellcome Trust Principal Research Fellowship and election to the US National Academy of Sciences (2015). Learn more about Ramakrishnan’s research here: https://www.med.cam.ac.uk/ramakrishnan/

34mins

23 Aug 2017

Rank #10

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James Spudich (Stanford) 3: Ca2+ regulation of muscle contraction

James Spudich begins his talk with an early history of muscle biology, and through parts 2-4 of his talk, he moves forward to our current understanding of the molecular basis of muscle contraction and disease. https://www.ibiology.org/ibioseminars/ca2-regulation-muscle-contraction.htmlTalk Overview:In this, his third talk, Spudich recounts his first foray into muscle research as a postdoctoral fellow. He was interested in understanding how Ca2+ regulates muscle contraction by binding to the troponin/tropomyosin complex.  Using electron micrographs and X-ray diffraction, Spudich showed that tropomyosin, which forms a long filament, lies along actin filaments and blocks the myosin binding sites on actin.  When muscle is stimulated to contract, Ca2+ is released from intracellular stores and binds to troponin.  The binding of Ca2+ to troponin causes the tropomyosin molecules to move, allowing myosin to bind to actin, and the muscle to contract.  While explaining these experiments, Spudich gives a very nice explanation of how a diffraction pattern is obtained and how to think about real and reciprocal space. More recent improvements in X-ray beam strength and electron microscopy, have confirmed this model and filled in more details. Please also check out parts 1, 2, and 4!Speaker Biography:James (Jim) Spudich is the Douglass M. and Nola Leishman Professor of Cardiovascular Disease in the Department of Biochemistry at Stanford University School of Medicine.  For the past several decades, his lab has studied the structure and function of the myosin family of motor proteins.  More recently Spudich’s lab has focused on human cardiac muscle myosin and the molecular basis of hypertrophic cardiomyopathy.  Spudich received his B.S. in chemistry from the University of Illinois and his Ph.D. in biochemistry from Stanford University. He was a post-doctoral fellow at Stanford University and then at the MRC Laboratory in Cambridge where he worked with Hugh Huxley.  Spudich joined the faculty of the University of California, San Francisco from 1971-1977.  In 1977, he moved to Stanford University where he was first a professor in the Department of Structural Biology and, since 1992, has been a professor in the Department of Biochemistry.  Spudich is also an Adjunct Professor at the Institute of Stem Cell Biology and Regenerative Medicine (inStem) and the National Center for Biological Sciences (NCBS) in Bangalore, India.Spudich serves on numerous editorial and scientific advisory boards.  His research contributions have been recognized with many honors and prizes including the Albert Lasker Basic Medical Research Award in 2012, the E.B. Wilson Award from the American Society for Cell Biology in 2011, and the Biophysics Society Award for Outstanding Investigator in 2005.  He is an elected fellow of the American Association for the Advancement of Science and the American Academy of Arts and Sciences, and an elected member of the US National Academy of Sciences.Learn more about Spudich’s research here: http://spudlab.stanford.edu/

32mins

1 Nov 2017

Rank #11

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Shiv Pillai (Harvard) 1: Early B Cell Development: A Look at the Defining Questions in Immunology

Shiv Pillai provides a historical perspective on the steps that led to formulate today’s model on how the immune system works and outlines the underpinnings of B cell development.https://www.ibiology.org/immunology/b-cell-developmentTalk Overview:Dr. Shiv Pillai provides a historical perspective on the steps that led to formulate today’s model on how the immune system works. Scientists observed that the body produces molecules (antibodies) that recognize the entry of foreign particles (antigens). He outlines the different models of the structure and functions of antibodies and explains the process by which antibody diversity is generated during B cell development (VDJ recombination). B cell development also involves two checkpoints to ensure the generation of functional antibodies and prevent the recognition of self-structures.In his second lecture, Pillai explains how earlier in his career he discovered that two surrogate light chains bind to the heavy chain in pre-B cells to create the pre-B cell receptor (pre-BCR). He showed that binding of the surrogate chains facilitates the formation of the pre-BCR that is needed for B cell development. Pillai demonstrated that the pre-BCR signals through Bruton Tyrosine Kinase (Btk). Patients with non-functional Btk manifest signs of immunodeficiency and deficiency of B-cells in the blood, which shows the importance pre-BCR signaling for proper B-cell development.In his third lecture, Pillai explains IgG4-Related Disease (IgG4-RD), a chronic inflammatory condition characterized by elevated numbers of T cells and IgG4 secreting plasma cells in the affected tissue. Using tissue samples from patients with the disease, his laboratory isolated and characterized the CD4+ T cells associated with IgG4-RD. Furthermore, he explains how the crosstalk between these CD4+ T cells and B cells is important for IgG4-RD development, and showed that depletion of B cells improves the outcome of the disease.  Speaker Biography:Dr. Shiv Pillai is a professor of medicine and health sciences and technology at Harvard Medical School, and a Ragon Institute investigator. Pillai completed his medical studies at Christian Medical College Vellore, India (1976), and subsequently obtained his doctorate in biochemistry at Calcutta University, India. He continued his postdoctoral training at David Baltimore’s lab at MIT (1984-1988). It was at Baltimore’s lab where Pillai discovered the existence and importance of surrogate light chains for B cell development. The surrogate light chains bind the antibody heavy chain in pre-B cells (immature B cells), and form the pre-B cell receptor (pre-BCR). The signaling of pre-BCR is crucial for proper B-cell development. In 1988, he joined the faculty of Massachusetts General Hospital and Harvard Medical School. Today, his lab continues to study the basis of the immune system in order to provide further understanding to human disease. Learn more about Pillai’s research at his lab website:http://www.ragoninstitute.org/portfolio-item/pillai

37mins

4 Jun 2018

Rank #12

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David Sabatini (Whitehead, MIT, HHMI) 2: Regulation of mTORC1 by Nutrients

https://www.ibiology.org/cell-biology/mtor-regulationDavid Sabatini outlines the critical role of mTOR in the regulation of growth. mTOR senses nutrient levels, growth factors and other signals and integrates a response to regulate cell growth.(Part 2 of 3) In his second talk, Sabatini explains that mTORC1 responds to many different upstream signals including a variety of growth factors, nutrients, and types of stress. How does mTORC1 sense all these different signals and integrate them to produce a response that regulates cell growth? Sabatini’s lab found that the first step in sensing nutrients such as amino acids is the movement of mTORC1 from a diffuse localization in the cytosol to the lysosomal surface. The lab then spent many years identifying the large number of proteins that regulate the movement of mTORC1 to the lysosome and allow it to sense nutrients and modulate the downstream processes that control cell growth. In particular, the lab identified several proteins that serve as direct sensors of metabolites or amino acids like leucine and arginine. Interestingly, mutations in several of the proteins in the nutrient sensing pathway upstream of mTORC1 are now known to cause human disease, including epilepsy. This suggests that modulation of mTOR, by inhibitors such as rapamycin, might provide a treatment for these conditions. In his final talk, Sabatini focuses on a lysosomal membrane protein that his lab had found to interact with mTORC1 and to sense arginine levels inside the lysosome. In some cell types, the amino acids needed to build new proteins are not taken up as free amino acids but instead come from the breakdown of proteins in the lysosome. This led the lab to ask which arginine-rich proteins are being degraded in the lysosome, which led to the realization that ribosomal proteins are amongst the most arginine-rich proteins in mammalian cells. After many more experiments, they showed that mTORC1 regulates a balance between the biogenesis of ribosomes, and the breakdown of ribosomes (known as ribophagy), dependent on the nutritional state of the cell. Ribophagy seems to be particularly important for supplying the cell with nucleosides during nutrient starvation.Speaker Biography:Dr. David M. Sabatini is a member of the Whitehead Institute for Biomedical Research, a professor of Biology at the Massachusetts Institute of Biology (MIT), an investigator of the Howard Hughes Medical Institute, a senior member of the Broad Institute of Harvard and MIT and a member of the Koch Institute for Integrative Cancer Research at MIT. His lab is interested in the regulation of growth and metabolism in mammals, with a focus on the critical mTOR pathway. Research from Sabatini’s lab has led to a better understanding of the role of the mTOR pathway in diseases such as cancer and diabetes, as well as in aging. Sabatini received his undergraduate degree in biology from Brown University. As a MD/PhD student at Johns Hopkins University School of Medicine, he did his first experiments on rapamycin and mTOR in the lab of Solomon H. Snyder. After completing his MD/PhD in 1997, Sabatini started his own lab as a Whitehead fellow at the Whitehead Institute. In 2002, he became a member of the Whitehead Institute and a faculty member at MIT.Sabatini’s groundbreaking work has been recognized with numerous awards and honors including the National Academy of Science Award in Molecular Biology (2014), the Dickson Prize in Medicine (2017), the Lurie Prize in Biomedical Sciences (2017), and the Switzer Prize (2018). Sabatini was elected to the National Academy of Sciences in 2016. Learn more about the research being done in Sabatini’s lab here: http://sabatinilab.wi.mit.eduand here:https://www.hhmi.org/scientists/david-m-sabatini

30mins

28 Nov 2018

Rank #13

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Hoekstra 3: Genetics of Behavior

OverviewIn Part 1, Hoekstra explains that her lab is working to understand how changes in an organism’s DNA result in adaptations that allow the organism to better survive or reproduce in the wild. She uses wild mice in the genus Peromyscus (commonly referred to as deer mice) as a model system because they are found in large numbers in many different habitats, allowing for many examples of adaptation to local environments, and they also thrive in a lab environment.In Part 2, Hoekstra explains how members of her lab studied the effects of a phenotypic adaptation, in this case coat color, on the ability of mouse populations to survive in different habitats. By crossing mice with light and dark coats and analyzing the genomes of the offspring, Hoekstra and her colleagues were able to identify several genes, and specific mutations in those genes, that determine coat color. Amazingly, one of the same mutations may have determined coat color in ancient mammoths!The link between genes and behavior is the focus of Hoekstra’s third talk. By studying burrowing behavior in two species of mice, both in the lab and in the wild, Hoekstra showed that burrowing is not strictly a learned behavior and is, in fact, controlled by a small number of genes. Find out more about Dr. Hoekstra’s research at her lab website at http://www.oeb.harvard.edu/faculty/hoekstra/publications.htmlAdditional ReadingPart 2:Hoekstra, H.E. 2010. From mice to molecules: the genetic basis of color adaptation. In In the Light of Evolution: Essays from the Laboratory and Field. (Ed. J.B. Losos). Roberts and Co. Publishers, Greenwood Village, CO.Manceau, M., V.S Domingues, C.R. Linnen, E.B. Rosenblum and H.E. Hoekstra. 2010. Convergence in pigmentation at multiple levels: mutations, genes and function. Philosophical Transactions of the Royal Society 365:2439-2450.Hoekstra, H.E., Hirschmann, R.J., Bundey, R.J., Insel, P. and J.P. Crossland. 2006. A single amino acid mutation contributes to adaptive color pattern in beach mice. Science 313:101-104.Steiner, C.C., J.N. Weber and H.E. Hoekstra. 2007. Adaptive variation in beach mice caused by two interacting pigmentation genes. PLoS Biology 5(9):1880-1889.Vignieri, S.N., J. Larson and H.E. Hoekstra. 2010. The selective advantage of cryptic coloration in mice. Evolution 64:2153-2158.Part 3:Weber, J.N., B.K. Peterson and H.E. Hoekstra. 2013. Discrete genetic modules are responsible for the evolution of complex burrowing behaviour in deer mice. Nature 493:402-405. Hoekstra, H.E. 2010. In search of the elusive behavior gene. In Search of the Causes of Evolution: From Field Observations to Mechanisms. (Eds. P. Grant and R. Grant). Princeton University Press, Princeton, NJ.Weber, J.N. and H.E. Hoekstra. 2009. The evolution of burrowing behavior in deer mice. Animal Behavior 77:603-609.

38mins

22 Feb 2013

Rank #14

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Paul E. Turner (Yale) 3: Phage Therapy

Part 1: Introduction to Virus Ecology and Evolution: Dr. Paul Turner describes the fundamental biology of viruses, how they interact with their host organisms, and how they might have originally evolved long ago. Part 2: Virus Adaptation to Environmental Change: Turner’s laboratory uses experimental evolution to study how viruses adapt to environmental changes.  Part 3: Phage Therapy: Turner provides an introduction to phage therapy, and how it can be improved by applying ‘evolution thinking’.https://www.ibiology.org/ibioseminars/phage-therapy.htmlTalk Overview:In his first lecture, Dr. Paul Turner describes the fundamental biology of viruses, how they interact with their host organisms, and how they might have originally evolved long ago. He provides an overview of the many reasons why viruses might be considered the most biologically successful inhabitants of earth, including their ability to rapidly reproduce, and adapt to environmental challenges. Turner explains how viruses have impacted human history, as well as earth’s history, due to their prevalent interactions with other species.       Viruses have an incredible capacity to adapt to environmental challenges, but sometimes, the environment constraints viral adaptation. Turner’s laboratory uses experimental evolution to study how viruses adapt to environmental changes (e.g. temperature changes), and the mechanisms by which viruses jump to novel host species. Turner’s work suggests that viruses with greater capacities to block the innate immune systems of their hosts, also have a greater likelihood of emerging on new host species. Also, he describes how virus adaptation to environmental change may be constraints by trade-offs: viruses can evolve either greater reproduction or greater survival, but not both simultaneously.Before antibiotics were discovered, scientists were using viruses of bacteria, bacteriophages, to treat bacterial infections in humans. Given the rise of antibiotic-resistant bacteria, scientists are revisiting the idea of using phage therapy to treat infections. In his third lecture, Turner provides an introduction to phage therapy, and how it can be improved by applying ‘evolution thinking’. His laboratory discovered phage OMKO1 that can treat multi-drug resistant bacteria in human patients while causing these bacteria to evolve greater sensitivity to antibiotics.Speaker Biography:Dr. Paul Turner is Professor of Ecology and Evolutionary Biology at Yale University, and holds an appointment in the Microbiology Program at Yale School of Medicine. His laboratory studies how viruses evolutionarily adapt to overcome environmental challenges, such as temperature changes or infection of novel host species. Turner received his bachelor’s degree in Biology from the University of Rochester in 1988, and completed his graduate studies in microbial ecology and evolution at Michigan State University in 1995. Learn more about Dr. Turner’s research here:http://turnerlab.yale.edu

22mins

28 Jun 2017

Rank #15

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Jurgen Knoblich (IMBA) 1: Asymmetric Cell Division; From Drosophila to Humans

Asymmetric cell division (in which two different daughter cells are formed) is critical during human brain development. Dr. Knoblich explains how the fate of each daughter cell is determined. Part 1: Asymmetric Cell Division: From Drosophila to Humans: Asymmetric cell division is critical during embryogenesis, including for human brain development. How is this important process determined? Part 2: Modeling Human Brain Development in 3D Organoid Culture: Knoblich’s lab has developed cerebral organoids that mimic early human brain development and can be used to model brain development and disease.https://www.ibiology.org/ibioseminars/asymmetric-cell-division-drosophila-humans.htmlTalk Overview:Dr. Knoblich begins his talk by explaining the key role that asymmetric cell division plays in development of the human brain.  During mammalian brain development, neuronal progenitor cells initially divide symmetrically to increase their numbers.  Later they divide asymmetrically to produce one progenitor cell and one (or two) cells which will terminally differentiate to become neurons.  What determines which daughter cell will become which? Working in Drosophila, Knoblich and others elucidated a signaling pathway in which Par proteins are asymmetrically localized before cell division. This recruits a complex of proteins which defines the orientation of the mitotic spindle and causes the localization of Numb protein at one pole of the cell. Upon cell division, only one daughter cell will inherit Numb protein and this ultimately will determine the fate of the daughter cells.  Interestingly, this signaling pathway is conserved from insects to mammals, however, Knoblich found an important difference that may explain why humans have many more cortical neurons than mice.  In his second talk, Knoblich describes experiments in his lab to develop 3 dimensional brain organoids from human pluripotent stem cells. While studying the development of rodent brains has proved extremely useful, there are some important developmental differences that require human tissue for investigation.  In addition, some diseases such as microcephaly cannot be modeled in mice.  Knoblich and his colleagues have developed cerebral organoids that mimic early human brain development and can be used to model neurodevelopmental disorders.  They have also been able to generate separate organoids from various regions of the human brain and then fuse them and follow the migration of live neurons between these parts, opening the path to many more studies of neuronal development. Speaker Biography:Jürgen Knoblich is a senior scientist and deputy director of the Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA) and an Adjunct Professor at the Medical University of Vienna.  Knoblich’s lab is interested in understanding how the complexity of the human brain is generated from progenitor and stem cells during development. To address this question, they study brain development in Drosophila, mice and in 3D human stem cell derived brain organoids.Knoblich completed his PhD studies in the Friedrich Miescher Laboratory of the Max Planck Institute in Tubingen, Germany.  He was a post-doctoral fellow at the University of California, San Francisco before returning to Europe in 1997 to join the Institute for Molecular Pathology in Vienna.  In 2004, Knoblich moved to the IMBA, becoming Deputy Director in 2005.Knoblich is an elected member of the Austrian Academy of Sciences and the EMBO Council.  He has received numerous awards for his research including the Wittgenstein Prize, the Schroedinger Award and the Sir Hans Krebs Medal.  Learn more about Knoblich’s research here: http://www.imba.oeaw.ac.at/research/juergen-knoblich/

32mins

20 Sep 2017

Rank #16

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Paul E. Turner (Yale) 1: Introduction to Virus Ecology and Evolution

Part 1: Introduction to Virus Ecology and Evolution: Dr. Paul Turner describes the fundamental biology of viruses, how they interact with their host organisms, and how they might have originally evolved long ago. Part 2: Virus Adaptation to Environmental Change: Turner’s laboratory uses experimental evolution to study how viruses adapt to environmental changes.  Part 3: Phage Therapy: Turner provides an introduction to phage therapy, and how it can be improved by applying ‘evolution thinking’.https://www.ibiology.org/ibioseminars/introduction-virus-ecology-evolution.htmlTalk Overview:In his first lecture, Dr. Paul Turner describes the fundamental biology of viruses, how they interact with their host organisms, and how they might have originally evolved long ago. He provides an overview of the many reasons why viruses might be considered the most biologically successful inhabitants of earth, including their ability to rapidly reproduce, and adapt to environmental challenges. Turner explains how viruses have impacted human history, as well as earth’s history, due to their prevalent interactions with other species.       Viruses have an incredible capacity to adapt to environmental challenges, but sometimes, the environment constraints viral adaptation. Turner’s laboratory uses experimental evolution to study how viruses adapt to environmental changes (e.g. temperature changes), and the mechanisms by which viruses jump to novel host species. Turner’s work suggests that viruses with greater capacities to block the innate immune systems of their hosts, also have a greater likelihood of emerging on new host species. Also, he describes how virus adaptation to environmental change may be constraints by trade-offs: viruses can evolve either greater reproduction or greater survival, but not both simultaneously.Before antibiotics were discovered, scientists were using viruses of bacteria, bacteriophages, to treat bacterial infections in humans. Given the rise of antibiotic-resistant bacteria, scientists are revisiting the idea of using phage therapy to treat infections. In his third lecture, Turner provides an introduction to phage therapy, and how it can be improved by applying ‘evolution thinking’. His laboratory discovered phage OMKO1 that can treat multi-drug resistant bacteria in human patients while causing these bacteria to evolve greater sensitivity to antibiotics.Speaker Biography:Dr. Paul Turner is Professor of Ecology and Evolutionary Biology at Yale University, and holds an appointment in the Microbiology Program at Yale School of Medicine. His laboratory studies how viruses evolutionarily adapt to overcome environmental challenges, such as temperature changes or infection of novel host species. Turner received his bachelor’s degree in Biology from the University of Rochester in 1988, and completed his graduate studies in microbial ecology and evolution at Michigan State University in 1995. Learn more about Dr. Turner’s research here:http://turnerlab.yale.edu

33mins

28 Jun 2017

Rank #17

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Catterall 1: Electrical Signaling: Life in the Fast Lane

How does a baseball player react quickly enough to hit a 90 mph fastball or a tennis player to hit a 60 mph serve? All of the fast events in our bodies, such as vision, hearing, nerve conduction and muscle contraction, involve electrical signals. In Part 1 of his talk, Dr. Catterall explains how the flow of sodium and potassium ions, through specific channels in the cell membrane, creates an electrical signal in nerve and muscle cells. He describes the structure and function of the sodium channel and its important role in physiology and pharmacology.In Part 2 of his talk, Catterall describes how voltage gated sodium channels function at an atomic level. Bacterial Na+ channels in the NaChBac family contain many of the elements of mammalian Na+ channels but in a much simpler form. Using X-ray crystallography to study NaChBac proteins, Catterall and his colleagues determined which domains of sodium channels are responsible for sensing voltage differences across the cell membrane and how these domains trigger the opening of the channel pore. It was also possible to identify the structural changes leading to the slow inactivation of channels after multiple rounds of opening and closing and to understand how NaChBac establishes its specificity for Na+ ions.In his third talk, Catterall switches his focus to voltage gated calcium channels. Na+ and Ca2+ channels share a common ancestor and consequently, much of the overall structure of the voltage sensing domain and the central pore is conserved. In spite of this homology, the calcium channel selects specifically for Ca2+ ions, even in the presence of an excess of Na+. Upon entry into the cell, Ca2+ ions regulate numerous intracellular processes. Catterall explains how his group was able to engineer a bacterial calcium channel that allowed them to identify the residues required for Ca2+ selectivity. He also describes experiments demonstrating that Ca2+ ions act locally within the cell, allowing for targeted regulation of cellular functions such as learning and memory in the brain and contraction in skeletal and cardiac muscle. http://www.ibiology.org/ibioseminars/william-catterall-part-1.htmlSpeaker Bio:Bill Catterall is Professor and Chair of the Department of Pharmacology at the University of Washington where he has been a faculty member since 1977. Catterall received his BA in Chemistry from Brown University and his PhD in Physiological Chemistry from Johns Hopkins University. He was a post-doctoral fellow with Dr. Marshall Nirenberg and a staff scientist at the NIH for a few years before moving to the University of Washington.Catterall and his colleagues discovered the voltage-gated sodium and calcium channels responsible for generating the electrical impulses necessary for most physiological functions. His lab continues to study the structure and function of these channels, their physiological regulation, and their interaction with medically important drugs. Catterall is also interested in understanding how impaired channel function may lead to human disease.Catterall has been recognized with numerous awards and honors for his contributions to the fields of electrophysiology, pharmacology, neuroscience, and cell biology. These include receiving The Bristol-Myers Squibb Award for Distinguished Research in neuroscience in 2003, The Gairdner International Award of Canada in 2010, election to the U.S. National Academy of Sciences in 1989, the Institute of Medicine and the American Academy of Arts and Sciences in 2000, and as a Foreign Member of the Royal Society of London in 2008.

26mins

25 Sep 2014

Rank #18

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Catterall 2: Voltage-gated Na+ Channels at Atomic Resolution

How does a baseball player react quickly enough to hit a 90 mph fastball or a tennis player to hit a 60 mph serve? All of the fast events in our bodies, such as vision, hearing, nerve conduction and muscle contraction, involve electrical signals. In Part 1 of his talk, Dr. Catterall explains how the flow of sodium and potassium ions, through specific channels in the cell membrane, creates an electrical signal in nerve and muscle cells. He describes the structure and function of the sodium channel and its important role in physiology and pharmacology.In Part 2 of his talk, Catterall describes how voltage gated sodium channels function at an atomic level. Bacterial Na+ channels in the NaChBac family contain many of the elements of mammalian Na+ channels but in a much simpler form. Using X-ray crystallography to study NaChBac proteins, Catterall and his colleagues determined which domains of sodium channels are responsible for sensing voltage differences across the cell membrane and how these domains trigger the opening of the channel pore. It was also possible to identify the structural changes leading to the slow inactivation of channels after multiple rounds of opening and closing and to understand how NaChBac establishes its specificity for Na+ ions.In his third talk, Catterall switches his focus to voltage gated calcium channels. Na+ and Ca2+ channels share a common ancestor and consequently, much of the overall structure of the voltage sensing domain and the central pore is conserved. In spite of this homology, the calcium channel selects specifically for Ca2+ ions, even in the presence of an excess of Na+. Upon entry into the cell, Ca2+ ions regulate numerous intracellular processes. Catterall explains how his group was able to engineer a bacterial calcium channel that allowed them to identify the residues required for Ca2+ selectivity. He also describes experiments demonstrating that Ca2+ ions act locally within the cell, allowing for targeted regulation of cellular functions such as learning and memory in the brain and contraction in skeletal and cardiac muscle. http://www.ibiology.org/ibioseminars/william-catterall-part-2.htmlSpeaker Bio:Bill Catterall is Professor and Chair of the Department of Pharmacology at the University of Washington where he has been a faculty member since 1977. Catterall received his BA in Chemistry from Brown University and his PhD in Physiological Chemistry from Johns Hopkins University. He was a post-doctoral fellow with Dr. Marshall Nirenberg and a staff scientist at the NIH for a few years before moving to the University of Washington.Catterall and his colleagues discovered the voltage-gated sodium and calcium channels responsible for generating the electrical impulses necessary for most physiological functions. His lab continues to study the structure and function of these channels, their physiological regulation, and their interaction with medically important drugs. Catterall is also interested in understanding how impaired channel function may lead to human disease.Catterall has been recognized with numerous awards and honors for his contributions to the fields of electrophysiology, pharmacology, neuroscience, and cell biology. These include receiving The Bristol-Myers Squibb Award for Distinguished Research in neuroscience in 2003, The Gairdner International Award of Canada in 2010, election to the U.S. National Academy of Sciences in 1989, the Institute of Medicine and the American Academy of Arts and Sciences in 2000, and as a Foreign Member of the Royal Society of London in 2008.

39mins

25 Sep 2014

Rank #19

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Sheng-Yang He (Michigan State U. and HHMI) 1: Introduction to Plant-Pathogen Interactions

Dr. Sheng-Yang He explores plant-pathogen interactions and provides an overview of a plant's basic immunological responses.https://www.ibiology.org/plant-biology/plant-pathogen-interactionsTalk Overview:What mechanisms do plants have to fight pathogens? In this seminar, Dr. Sheng-Yang He explores plant-pathogen interactions and provides an overview of a plant's basic immunological responses. As He explains, plants have "resistant" genes, which trigger the immune response after pathogenic infections (effector-triggered immunity). Also, plants immune system can be activated by the recognition of general patterns in pathogens (pattern-triggered immunity). Understanding these interactions could aid in the prevention of disease in plants, which would be beneficial to the agricultural industry and global food security.In his second lecture, He provides evidence on the effect of environmental factors (e.g. humidity) in the development of disease in plants. In order to understand disease susceptibility, He's laboratory studies the interaction that Arabidopsis has with the bacteria Pseudomonas syringae. He's laboratory showed that an increase in temperature and humidity increase bacterial disease severity. By genetically creating a plant that is altered in its immune system and water homeostasis, they were able to define the minimal factors that bacteria need to infect the plant. Speaker Biography:Dr. Sheng-Yang He is a University Distinguished Professor at Michigan State University and a Howard Hughes Medical Institute investigator. He obtained his bachelor's degree (1982) and a master's degree in plant protection (1991) from Zhejiang Agricultural University in China. He pursued his graduate degree in plant pathology (1991) at Cornell University and continued his post-doctoral training at this institution. He joined the faculty of the University of Kentucky (1993), and in 1995 he moved to Michigan State University. His lab investigates plant-pathogen interactions. They study the molecular mechanisms of infection, and how climate and microbiota affect disease in plants. For his scientific contributions, He was elected to the US National Academy of Sciences in 2015. Learn more about He's research at his lab website:http://www.thehelab.org

19mins

2 May 2018

Rank #20