iBiology Podcast

In his second part, Hasson explores how the ability of the storyteller to be coupled to and shape the neural responses of listeners is used as a tool to share memories across brains. Furthermore, the studies reveal the tight connections between remembering and imagining and expose the ways by which the storyteller’s perspective shape the audience point of view.

How does your brain change with each story that you hear? How can storytelling shape your memories? In this talk, Dr. Uri Hasson explores how brain activity is shared between listeners of the same story, and how those shared neural responses are coupled to and shaped by the neural activity in the storyteller’s brain. In his studies, Hasson observed higher coupling between listener’s and storyteller’s neural activity as a function of the ability of the listener to understand the story. As Hasson explains, efficient communication occurs when the storyteller’s and listeners’ brain responses are coupled.

Dr. Leland Hartwell started his scientific career studying a fundamental question in biology: how do cells know that they have everything they need in order to divide. By studying the morphology of temperature sensitive mutants in yeast, Hartwell identified many of the key regulators of the cell cycle. In this conversation, Hartwell talks to Dr. Sue Biggins about his Nobel Prize winning discoveries and the experiments that led to his seminal findings.

In his second talk, Haber explains in greater detail the molecular steps that take place during the repair of a DNA double strand break.  It turns out that the process of mating type switching in S. cerevisiae requires site-specific cutting and repair of a yeast chromosome and this is an excellent model for studying DNA DSB repair.  Working in this system and using techniques such as Southern blots, PCR and chromatin immunoprecipitation, Haber’s group was able to identify the proteins and enzymatic steps in DNA repair.

Dr. Haber begins his talk by explaining that broken chromosomes frequently arise during the process of DNA replication. In healthy cells, these double strand breaks (DSBs) are repaired by homologous recombination, an orderly process that preserves the genome.  If the homologous recombination machinery is impaired, DNA truncations, translocations, and deletions often occur, resulting in genome instability and cancer. All mechanisms of homologous recombination have one common principal; the broken ends of the DNA are repaired by base pairing with a sequence that is identical or nearly identical and acts as a template for repair enzymes.  Haber explains the general principles of homologous recombination and its critical role in maintaining genome stability.

In his second presentation, Haas shares an example of how cryocrystallography has aided structure-based drug design.

In his postdoctoral studies, David Haas set out to reduce radiation damage to protein crystals during X-ray crystallography. In 1970, he published a paper on his invention of macromolecular cryocrystallography – freezing crystals to extend their lifetime in the X-ray beam. The widespread use of the synchrotron beginning in the 1970s made cryo-cooling essential, and today nearly all protein crystal structures deposited in the international Protein Data Bank use this method.

In her second talk, Glaunsinger explores gene expression control by viruses like Kaposi’s sarcoma herpesvirus (KSHV), a frequent cause of cancer in AIDS patients.  KSHV stimulates degradation of mRNA by encoding a nuclease, SOX, which is able to target a broad set of mRNAs for degradation yet cleaves them at specific sites recognized by a combination of RNA sequence and structure. Glaunsinger then describes how widespread mRNA degradation by viral nucleases such as SOX causes redistribution of RNA binding proteins in the cell and restricts mRNA transcription by RNA polymerase II. Thus, alterations to the rate of mRNA decay can have ripple effects in the cell that influence upstream events in gene expression.

Dr. Britt Glaunsinger provides an overview of virology, and describes how the study of viruses has guided the understanding of many fundamental cellular processes, from gene expression to cancer. These insights arise from studying how viruses manipulate and hijack cellular machinery during infection and viral replication. Viruses can use the host machinery to their advantage, altering the gene expression landscape of the cell to create an environment favorable for the infection to progress. As Glaunsinger explains, one way viruses alter gene expression is by affecting the messenger RNA (mRNA) degradation process. By increasing decay of cellular messages, viruses can decrease competition for access to the translation machinery and dampen the expression of immune stimulatory elements that restrict viral replication.

Coral reefs are a vital global ecosystem: despite comprising only 1% of the world’s oceans, they support more than 25% of marine life. In addition to supporting ocean life, coral reefs also support the survival of humans by providing habitat for fish and other seafood and protecting coastlines from erosion. Corals are complex organisms that rely on a symbiotic relationship between the coral animal, zooxanthellae algae, and microbes. To date, the role of the coral microbiome in coral health and disease hasn’t been extensively studied. In this Young Scientist Seminar, Maite Ghazaleh Bucher describes her thesis research at the University of Georgia in which she characterized the microbial communities of sick and healthy corals colocalized in the Florida Keys Reef during a disease outbreak in summer 2017. Using genetic analyses, Bucher found that the coral microbiome is relatively uniform in healthy corals, even among different coral species. In contrast, she found that the microbiomes of diseased corals are dissimilar, even among corals affected by the same disease. These data support an “Anna Karenina” hypothesis for the coral microbiome. In the second stage of her research, Bucher determined that the microbial communities of apparently healthy coral tissue on diseased corals exhibited an imbalance between “healthy” and “unhealthy” microbes. This finding could lead to a quantitative way to monitor the health of corals based on their microbial signatures. Bucher ends her talk with a call to action: we all have the power to reduce our impact on the planet, so that vital ecosystems like coral reefs can be protected. What can you do to support the survival of corals?