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  • richardmitnick 1:03 pm on January 3, 2017 Permalink | Reply
    Tags: , Harvard Medical School, , Metformin   

    From Harvard Medical: “Diabetes Drug vs. Cancer” 

    Harvard University
    Harvard University

    harvard-medical-school-bloc

    Harvard Medical School

    December 20, 2016
    SUE McGREEVEY

    1
    Image: Getty Images

    Considerable evidence has indicated that a drug used for more than 50 years to treat Type 2 diabetes can also prevent or slow the growth of certain cancers. But the mechanism behind metformin’s anticancer effects has been unknown.

    Now, a team of Harvard Medical School investigators at Massachusetts General Hospital has identified a pathway that appears to underlie metformin’s ability both to block the growth of human cancer cells and to extend the lifespan of the C. elegans roundworm. Their findings imply that this single genetic pathway plays an important role in a wide range of organisms.

    “We found that metformin reduces the traffic of molecules into and out of the nucleus—the ‘information center’ of the cell,” said Alexander Soukas, HMS assistant professor of medicine at Mass General and senior author of the study published in Cell.

    “Reduced nuclear traffic translates into the ability of the drug to block cancer growth and, remarkably, is also responsible for metformin’s ability to extend lifespan,” Soukas said. “By shedding new light on metformin’s health-promoting effects, these results offer new potential ways that we can think about treating cancer and increasing healthy aging.”

    Metformin appears to lower blood glucose in patients with Type 2 diabetes by reducing the liver’s ability to produce glucose for release into the bloodstream. Evidence has supported the belief that metformin blocks the activity of mitochondria, the powerhouses of the cell. But, Soukas said, more recent information suggests the mechanism is more complex.

    Several studies have shown that individuals taking metformin have a reduced risk of developing certain cancers and of dying from cancers that do develop. Current clinical trials are testing the impact of metformin on cancers of the breast, prostate and pancreas. Several research groups are working to identify its molecular targets.

    Soukas’ team had observed that, just as it blocks the growth of cancer cells, metformin slows growth in C. elegans, suggesting that the roundworm could serve as a model for investigating the drug’s effects on cancer.

    Their experiments found that metformin’s action against cancer relies on two elements of a single genetic pathway: the nuclear pore complex, which allows the passage of molecules into and out of the nucleus, and an enzyme called ACAD10. Basically, metformin’s suppression of mitochondrial activity reduces cellular energy, restricting the traffic of molecules through the nuclear pore. This shuts off an important cellular growth molecule called mTORC1, resulting in activation of ACAD10, which both slows the growth and extends the lifespan of C. elegans.

    In human melanoma and pancreatic cancer cells, the investigators confirmed that drugs in the metformin family induced ACAD10 expression, an effect that depended on the function of the nuclear pore complex. Without the complete signaling pathway—from mitochondrial suppression through nuclear pore restriction to ACAD10 expression—cancer cells were no longer sensitive to the effects of metformin-like drugs.

    “Amazingly, this pathway operates identically, whether in the worm or in human cancer cells,” said Soukas. “Our experiments showed two very important things: If we force the nuclear pore to remain open or if we permanently shut down ACAD10, metformin can no longer block the growth of cancer cells. That suggests that the nuclear pore and ACAD10 may be manipulated in specific circumstances to prevent or even treat certain cancers.”

    The essential contribution of ACAD10 to metformin’s anticancer action is intriguing, Soukas added, because the only published study on ACAD10 function tied a variant in the gene to the increased risk of Type 2 diabetes in Pima Indians, suggesting that ACAD10 also has a role in the drug’s antidiabetes action.

    “What ACAD10 does is a great mystery that we are greatly interested in solving,” he said. “Determining exactly how ACAD10 slows cell growth will provide additional insights into novel therapeutic targets for cancer and possibly ways to manipulate the pathway to promote healthy aging.”

    Support for this study includes National Institutes of Health grants R03DK098436, K08DK087941, R01DK072041 and R01CA166717; a Broad Institute SPARC Grant; and the Ellison Medical Foundation New Scholar in Aging Award.

    See the full article here .

    Please help promote STEM in your local schools.

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    harvard-medical-school-campus

    The Harvard Medical School community is dedicated to excellence and leadership in medicine, education, research and clinical care. To achieve our highest aspirations, and to ensure the success of all members of our community, we value and promote common ideals that center on collaboration and service, diversity, respect, integrity and accountability, lifelong learning, and wellness and balance. To be a citizen of this community means embracing a collegial spirit that fosters inclusion and promotes achievement.

    Harvard University campus

    Harvard is the oldest institution of higher education in the United States, established in 1636 by vote of the Great and General Court of the Massachusetts Bay Colony. It was named after the College’s first benefactor, the young minister John Harvard of Charlestown, who upon his death in 1638 left his library and half his estate to the institution. A statue of John Harvard stands today in front of University Hall in Harvard Yard, and is perhaps the University’s best known landmark.

    Harvard University has 12 degree-granting Schools in addition to the Radcliffe Institute for Advanced Study. The University has grown from nine students with a single master to an enrollment of more than 20,000 degree candidates including undergraduate, graduate, and professional students. There are more than 360,000 living alumni in the U.S. and over 190 other countries.

     
  • richardmitnick 10:16 am on December 15, 2016 Permalink | Reply
    Tags: Gene osteocrin, Genetic Repurposing, Harvard Medical School, Mammalian bone gene may be repurposed to fuel cognition in humans   

    From Harvard: “Genetic Repurposing” 

    Harvard University
    Harvard University

    harvard-medical-school-bloc

    Harvard Medical School

    Mammalian bone gene may be repurposed to fuel cognition in humans

    12.15.16
    Ekaterina Pesheva

    1
    Image: Vivian Budnik, University of Massachusetts Medical School

    A gene that regulates bone growth and muscle metabolism in mammals may take on an additional role as a promoter of brain maturation, cognition and learning in human and nonhuman primates, according to a new study led by neurobiologists at Harvard Medical School.

    Describing their findings in the Nov. 10 issue of Nature, researchers say their work provides a dramatic illustration of evolutionary economizing and creative gene retooling—mechanisms that contribute to the vast variability across species that share nearly identical set of genes yet differ profoundly in their physiology.

    The research reveals that osteocrin—a gene found in the skeletal muscles of all mammals and well-known for its role in bone growth and muscle function—is completely turned off in rodent brains yet highly active in the brains of nonhuman primates and humans.

    Notably, osteocrin was found predominantly in cells of the neocortex—the most evolved part of the primate brain, which regulates sensory perception, spatial reasoning and higher-level thinking and language in humans.

    The gene’s marked presence in an area of the brain responsible for higher-level function and thought, the researchers said, suggests a possible role in the development of cognition, a cardinal feature that distinguishes the brains of human and nonhuman primates from those of other mammals.

    Brain development in humans and other primates is profoundly affected by sensory experience and social interactions. Scientists have long sought to unravel genes in the brain that are turned on and off by experiences to fuel the rise of brain functions unique to such complex species.

    The HMS team’s findings—part of an ongoing quest to elucidate the mechanisms that underlie human brain development, function and disease—reveal that osteocrin is precisely one such gene, activated by sensory stimulation. Furthermore, the team added, this is the first illustration of evolutionary gene repurposing in the brain.

    “We have uncovered what we believe is a critical clue into the evolution of the human brain, one that gives us a glimpse into the genetic mechanisms that may account for differences in cognition between mice and humans,” said senior investigator Michael Greenberg, the Nathan Marsh Pusey Professor of Neurobiology and chair of the HMS Department of Neurobiology.

    For their experiments, the team analyzed RNA levels—the molecular footprints of gene activity—in the brain cells of mice, rats and humans. Although many of the same genes were activated in both mouse and human brain cells, the scientists observed, a small subset of genes was activated solely in human brain cells. Much to the scientists’ surprise, the bone gene osteocrin was most highly expressed in the human brain, yet completely shut off in the brain cells of mice.

    Going a step further, the scientists placed brain cells from all three species in lab dishes and chemically re-created conditions that mimic sensory stimulation. Chemical stimulation activated osteocrin selectively in excitatory neurons, so called for their role in stimulating rather than dampening nerve signaling. But researchers noted something even more intriguing: The activity of the gene was most intense in neurons of the neocortex, the topmost layer of cells covering the brain and responsible for higher-level cognition, such as long-term memory, thought and language. At the same time, osteocrin was noticeably absent from other parts of the brain responsible for noncognitive functions such as spatial navigation, balance, breathing, heart rate and temperature control.

    When researchers compared osteocrin levels to levels of another brain protein, BDNF, well known for its role in neuronal growth and repair, they noticed another striking difference. While BDNF was present throughout the brain, osteocrin was restricted to the neocortex and, to a lesser extent, the amygdala, an area of the brain thought to play a role in memory formation, decision making and emotional responses. Osteocrin was also markedly expressed in cells of the temporal lobe, which houses functions such as learning, memory and audio-visual processing—and the occipital lobe, which houses the visual cortex, the area of the brain responsible for the processing of visual information.

    Further analysis revealed that in the primate brain, sensory stimulation appears to switch on osteocrin through a previously unknown DNA enhancer. Enhancers—snippets of DNA that act as the genome’s regulators—are the “handles” that turn on some genes while shutting off others. In doing so, enhancers can profoundly alter genetic expression, fueling dramatic differences between organisms with nearly identical DNA. The rodent versions of osteocrin lacked the stimulation-activated DNA enhancer, the analysis showed.

    In yet another critical observation, researchers found the osteocrin enhancer was, in turn, switched on by a protein called MEF2. Mutations in MEF2 are a well-established cause of intellectual disability and neurodevelopmental disorders, so the link between the two begs further study, the researchers said, as it may portend a role for osteocrin in such developmental anomalies.

    “Humans share many genes with rodents and as much as 90 percent of their DNA in some parts of the genome,” says co-first author Gabriella Boulting, a neurobiologist at HMS. “In this case we see how turning up the expression of the same gene in a different location may precipitate dramatic differences in the function of brain cells.”

    Further analysis revealed that osteocrin’s activation curbed the growth of neuronal dendrites—branchlike projections responsible for transmitting signals from one brain cell to the next.

    “Restricting dendritic growth is a precision-enhancing mechanism, essential to ensuring that neuronal wires don’t get crossed and compromise signal transmission from one cell to the next,” says study first co-author Bulent Ataman, a neurobiologist at HMS.

    This observation, Ataman added, suggests that osteocrin’s activity may help enhance nerve cell agility and proper signal transmission to ensure robust communication across neurons.

    To confirm that the activity-induced gene expression observed in nerve cells in the lab also occurred in the functioning, intact brain, researchers temporarily blocked vision in one eye of a macaque, a common technique to study activity-triggered brain plasticity and visually-induced gene activation in the visual cortex. This proof-of-concept experiment, they surmised, would reveal whether osteocrin is, indeed, awakened by visual stimulation and shut off by its absence. A day later, the researchers observed that osteocrin expression was markedly higher in cells from the visually intact parts of the macaque brain, compared with cells in vision-deprived areas.

    The findings illustrate a foundational principle in neurobiology—abnormal visual experiences can interfere with the development and function of brain cells in the visual cortex, a phenomenon first described more than 50 years ago by David Hubel and Torsten Wiesel, two of the founding members of the Department of Neurobiology at HMS. The two shared the 1981 Nobel Prize in Physiology or Medicine for their discoveries on visual information processing in the brain.

    “Nature and nurture interact to wire up the brain, and abnormal vision can alter that wiring,” said Margaret Livingstone, the Takeda Professor of Neurobiology at HMS. “Our observations reveal the molecular basis for what Hubel and Wiesel observed more than half a century ago.”

    Researchers say their findings have sparked more questions, including exactly how osteocrin interacts with neurons, precisely what factors regulate its expression and, most importantly, how it can alter brain physiology in disease and health.

    The research was funded by the National Institutes of Health grants RC2MH089952 and P50MH106933 with additional support from the Ellen R. and Melvin J. Gordon Center for the Cure and Treatment of Paralysis at Spaulding Rehabilitation Hospital and by the NIH’s Ruth L. Kirschstein National Research Service Award 5F32NS086270.

    See the full article here .

    Please help promote STEM in your local schools.

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    Stem Education Coalition

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    The Harvard Medical School community is dedicated to excellence and leadership in medicine, education, research and clinical care. To achieve our highest aspirations, and to ensure the success of all members of our community, we value and promote common ideals that center on collaboration and service, diversity, respect, integrity and accountability, lifelong learning, and wellness and balance. To be a citizen of this community means embracing a collegial spirit that fosters inclusion and promotes achievement.

    Harvard University campus

    Harvard is the oldest institution of higher education in the United States, established in 1636 by vote of the Great and General Court of the Massachusetts Bay Colony. It was named after the College’s first benefactor, the young minister John Harvard of Charlestown, who upon his death in 1638 left his library and half his estate to the institution. A statue of John Harvard stands today in front of University Hall in Harvard Yard, and is perhaps the University’s best known landmark.

    Harvard University has 12 degree-granting Schools in addition to the Radcliffe Institute for Advanced Study. The University has grown from nine students with a single master to an enrollment of more than 20,000 degree candidates including undergraduate, graduate, and professional students. There are more than 360,000 living alumni in the U.S. and over 190 other countries.

     
  • richardmitnick 12:19 pm on December 5, 2016 Permalink | Reply
    Tags: , Harvard Medical School, , ,   

    From Harvard Medical School: “Zika’s Entry Points” 

    Harvard University
    Harvard University

    harvard-medical-school-bloc

    Harvard Medical School

    December 1, 2016
    HANNAH ROBBINS
    ERIC BENDER

    Fast-spreading virus can take multiple routes into the growing brain.

    1
    Zika virus (light blue) spreads through a three-dimensional model of a developing brain. Image: Max Salick and Nathaniel Kirkpatrick/Novartis

    Around the world, hundreds of women infected with the Zika virus have given birth to children suffering from microcephaly or other brain defects, as the virus attacks key cells responsible for generating neurons and building the brain as the embryo develops.

    Studies have suggested that Zika enters these cells, called neural progenitor cells or NPCs, by grabbing onto a specific protein called AXL on the cell surface. Now scientists at the Harvard Stem Cell Institute (HSCI) and Novartis have shown that this is not the only route of infection for NPCs.

    The scientists demonstrated that the Zika virus infected NPCs even when the cells did not produce the AXL surface receptor protein that is widely thought to be the main vehicle of entry for the virus.

    “Our finding really recalibrates this field of research, because it tells us we still have to go and find out how Zika is getting into these cells,” said Kevin Eggan, principal faculty member at HSCI, professor of stem cell and regenerative biology at Harvard University’s Faculty of Arts and Sciences and Harvard Medical School, and co-corresponding author on a paper reporting the research in Cell Stem Cell.

    “It’s very important for the research community to learn that targeting the AXL protein alone will not defend against Zika,” agreed Ajamete Kaykas, co-corresponding author and a senior investigator in neuroscience at the Novartis Institutes for Biomedical Research (NIBR).

    Previous studies have shown that blocking expression of the AXL receptor protein does defend against the virus in a number of human cell types. Given that the protein is highly expressed on the surface of NPCs, many labs have been working on the hypothesis that AXL is the entry point for Zika in the developing brain.

    “We were thinking that the knocked-out NPCs devoid of AXL wouldn’t get infected,” said Max Salick, a NIBR postdoctoral researcher and co-first author on the paper. “But we saw these cells getting infected just as much as normal cells.”

    Working in a facility dedicated to infectious disease research, the scientists exposed two-dimensional cell cultures of AXL-knockout human NPCs to the Zika virus. They followed up by exposing three-dimensional mini-brain “organoids” containing such NPCs to the virus. In both cases, cells clearly displayed Zika infection. This finding was supported by an earlier study that knocked out AXL in the brains of mice.

    “We knew that organoids are great models for microcephaly and other conditions that show up very early in development and have a very pronounced effect,” said Kaykas. “For the first few months, the organoids do a really good job in recapitulating normal brain development.”

    Historically, human NPCs have been difficult to study in the lab because it would be impossible to obtain samples without damaging brain tissue. With the advancements in induced pluripotent stem cell (iPS cell) technology, a cell reprogramming process that allows researchers to coax any cell in the body back into a stem cell-like state, researchers can now generate these previously inaccessible human tissues in a petri dish.

    The team was able to produce human iPS cells and then, using gene-editing technology, modify the cells to knock out AXL expression, said Michael Wells, a Harvard postdoctoral researcher in the Eggan Lab and co-first author. The scientists pushed the iPS cells to become NPCs, building the two-dimensional and three-dimensional models that were infected with Zika.

    The Harvard and NIBR collaborators started working with the virus in mid-April 2016, only six months before they published their findings. This unusual speed of research reflects the urgency of Zika’s global challenge, as the virus has spread to more than 70 countries and territories.

    “At the genesis of the project, my wife was pregnant,” Eggan remarked. “One can’t read the newspapers without being concerned.”

    The collaboration grew out of interactions at the Broad Institute of Harvard and MIT’s Stanley Center for Psychiatric Research, where Eggan directs the stem cell program. His lab already had developed cell culture systems for studying NPCs in motor neuron and psychiatric diseases. The team at Novartis had created brain organoids for research on tuberous sclerosis complex and other genetic neural disorders.

    “Zika seemed to be a big issue where we could have an impact, and we all shared that interest,” Eggan said. “It’s been great to have this public/private collaboration.”

    The researchers are studying other receptor proteins that may be open to Zika infection in hopes that their basic research eventually will help in the quest to develop vaccines or other drugs that defend against the virus.

    See the full article here .

    YOU CAN HELP FIND A CURE FOR THE ZIKA VIRUS.

    There is a new project at World Community Grid [WCG] called OpenZika.
    Zika
    Zika depiction. Image copyright John Liebler, http://www.ArtoftheCell.com
    Rutgers Open Zika

    WCG runs on your home computer or tablet on software from Berkeley Open Infrastructure for Network Computing [BOINC]. Many other scientific projects run on BOINC software.Visit WCG or BOINC, download and install the software, then at WCG attach to the OpenZika project. You will be joining tens of thousands of other “crunchers” processing computational data and saving the scientists literally thousands of hours of work at no real cost to you.

    This project is directed by Dr. Alexander Perryman a senior researcher in the Freundlich lab, with extensive training in developing and applying computational methods in drug discovery and in the biochemical mechanisms of multi-drug-resistance in infectious diseases. He is a member of the Center for Emerging & Re-emerging Pathogens, in the Department of Pharmacology, Physiology, and Neuroscience, at the Rutgers University, New Jersey Medical School. Previously, he was a Research Associate in Prof. Arthur J. Olson’s lab at The Scripps Research Institute (TSRI), where he ran the day-to-day operations of the FightAIDS@Home project, the largest computational drug discovery project devoted to HIV/AIDS, which also runs on WCG. While in the Olson lab, he also designed, led, and ran the largest computational drug discovery project ever performed against malaria, the GO Fight Against Malaria project, also on WCG.

    Rutgers smaller

    Please help promote STEM in your local schools.

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    The Harvard Medical School community is dedicated to excellence and leadership in medicine, education, research and clinical care. To achieve our highest aspirations, and to ensure the success of all members of our community, we value and promote common ideals that center on collaboration and service, diversity, respect, integrity and accountability, lifelong learning, and wellness and balance. To be a citizen of this community means embracing a collegial spirit that fosters inclusion and promotes achievement.

    Harvard University campus

    Harvard is the oldest institution of higher education in the United States, established in 1636 by vote of the Great and General Court of the Massachusetts Bay Colony. It was named after the College’s first benefactor, the young minister John Harvard of Charlestown, who upon his death in 1638 left his library and half his estate to the institution. A statue of John Harvard stands today in front of University Hall in Harvard Yard, and is perhaps the University’s best known landmark.

    Harvard University has 12 degree-granting Schools in addition to the Radcliffe Institute for Advanced Study. The University has grown from nine students with a single master to an enrollment of more than 20,000 degree candidates including undergraduate, graduate, and professional students. There are more than 360,000 living alumni in the U.S. and over 190 other countries.

     
  • richardmitnick 2:23 pm on September 9, 2016 Permalink | Reply
    Tags: , , , , Harvard Medical School,   

    From AAAS: “Scientists Build Giant Petri Dish to Film Bacteria Resistance” 

    AAAS

    AAAS

    8 September 2016
    Meagan Phelan

    Researchers have developed a large plate on which to film bacteria as they mutate in the presence of higher and higher concentrations of antibiotics, providing unprecedented insights into the phenomenon of antibiotic resistance.

    “Our device allows us to systematically map the different ways by which bacteria can become resistant to a range of antibiotics and antibiotic combinations,” said co-author Roy Kishony, a professor in the department of systems biology at Harvard Medical School and a principal investigator at Technion-Israel Institute of Technology.

    The ultimate goal, Kishony added, is to develop tools “that can predict the evolution of pathogens under different treatments, and better guide treatment choice.”

    “With our plate device, the evolutionary paths that the bacteria follow to achieve antibiotic resistance appear clearly and visually,” said co-author Michael Baym, a postdoctoral fellow in the Kishony Lab at Harvard Medical School, “and will hopefully let us start tailoring our approaches to treating resistance to different evolutionary modes.”

    The 2-by-4 foot petri dish used by the researchers to grow the bacteria contains nine bands at its base that can support varying concentrations of antibiotic. The results are reported in the 9 September issue of Science.

    Antibiotics have been used to treat patients since the 1940s, greatly reducing illness and death. However, these drugs have been used so frequently that the bacteria they are designed to kill have adapted to them in many cases, making the drugs less effective. At least 2 million people become infected with bacteria resistant to antibiotics each year in the United States, according to the Centers for Disease Control and Prevention, and at least 23,000 of these die as a result.

    “We know quite a bit about the internal defense mechanisms bacteria use to evade antibiotics,” Baym said, “but we don’t really know much about their physical movements across space as they adapt to survive in different environments.”

    To better understand how antibiotic resistance evolves in space and time, Baym and his colleagues developed a device called the microbial evolution growth arena plate, or MEGA-plate. The researchers used the antibiotics trimethoprim and ciprofloxacin in the MEGA plate in concentrations from zero to 10,000 times the original dose.

    On the right side of the plate where antibiotic levels were zero, Baym, Kishony, and colleagues grew Escherichia coli bacteria, which appeared white on the inky black background. Over two weeks, a camera mounted on the ceiling above the plate took periodic snapshots of the bacteria mutating.

    In the band with no antibiotic, the bacteria spread up until the point where they could no longer survive as they mingled with the first traces of antibiotic. Then, a small group of bacteria developed genetic mutations that allowed them to persist.

    1
    Researchers traced the branching patterns of bacterial evolution on the MEGA plate. | Katharine Sutliff/ Science

    As these drug-resistant mutants arose, their descendants migrated to areas of higher and higher antibiotic concentration, developing further mutations to compete with other mutants around them. As they continued their journey to the highest antibiotic concentration level, all remaining bacterial mutants had to evolve further still.

    Through this process of cumulative, successive mutations, the researchers could visualize how bacteria that are normally sensitive to antibiotics can evolve resistance to extremely high concentrations — those up to 100,000-fold higher than the one that killed their predecessors — in just over ten days.

    The bacteria were unable to adapt directly from zero antibiotic to the highest concentrations, for both drugs tested, revealing that exposure to intermediate concentrations of antibiotics is essential for the bacteria to evolve resistance.

    Initial mutations at each new band on the plate led to slower growth, hinting that bacteria adjusting to the antibiotic aren’t able to grow at ideal speed while developing mutations. Once fully resistant, however, such bacteria regained normal growth rates.

    “One of our main objectives in the lab is to reveal such evolutionary tradeoffs,” said Kishony, “whereby a bacterium becoming resistant to a drug confers a cost we might be able to exploit. We might potentially use other drugs to enhance such resistance-associated weakness.”

    Intriguingly, the researchers also found that the location of bacterial species played a role in their success in developing resistance. For example, when the researchers moved the trapped mutants — those behind their fast-moving, fit counterparts — to the “frontlines” of the growing bacteria, they were able to grow into new regions where the frontline bacteria could not.

    “What we saw suggests that evolution is not always led by the most resistant mutants,” said Baym. “The strongest mutants are, in fact, often moving behind more vulnerable strains.”

    This overturns the assumption that mutants that survive the highest concentration of a drug drive the fitness of bacterial populations; rather, it is those mutants that are both sufficiently fit and arise sufficiently close to the advancing front that lead the evolutionary road.

    The work of Baym, Kishony, and colleagues was inspired by Hollywood wizardry, the authors say. Kishony saw a digital billboard advertising the 2011 film Contagion, a grim narrative about a deadly viral pandemic. The marketing tool was built using a giant lab dish to show hordes of painted, glowing microbes creeping slowly across a dark backdrop to spell out the title of the movie.

    “This project was fun and joyful throughout,” Kishony said. “Seeing the bacteria spread for the first time was a thrill. Our MEGA-plate takes complex, often obscure, concepts in evolution, such as mutation selection, lineages, parallel evolution and clonal interference, and provides a visual seeing-is-believing demonstration of these otherwise vague ideas. It’s also a powerful illustration of how easy it is for bacteria to become resistant to antibiotics.”

    See the full article here .

    The American Association for the Advancement of Science is an international non-profit organization dedicated to advancing science for the benefit of all people.

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