iBiology Videos

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?

Squamous cell carcinomas (SCCs) are commonly occurring, dangerous cancers that may originate from skin stem cells. By developing methods to identify the stem cells that will lead to cancer, Fuchs’ lab has been able to study how these cells differ from normal skin stem cells. They found that the gene expression profile in normal versus cancer stem cells is very different and is likely the result of differences in the cancer stem cell niche. The tumor microenvironment may include immune cells and greater proximity to TGF-beta secreting blood vessels. Fuchs’ lab showed that cancer stem cells exposed to TGF-beta had increased expression of proteins in the glutathione metabolism pathway; the same pathway which is involved in the breakdown of chemotherapy drugs. Further studies in SCC patients, showed a strong correlation between increased mRNA levels for glutathione pathway proteins and decreased survival. These results suggest that drugs which block TGF-beta activity, in combination with other chemotherapeutics, may be an effective therapy for some SCC.

In her second talk, Fuchs focuses primarily on studies of adult skin stem cells.  Adult stem cells have the ability to make more stem cells and to generate the cells of a differentiated tissue. Skin stem cells can replenish the epidermis and make hair follicle cells. Skin grown in culture from just a few skin stem cells can be used to treat burn patients or replace damaged corneal epithelium.  Stem cells reside in specific niches or microenvironments and signals from the niche determine whether a stem cell is going to be quiescent or make tissue. Fuchs’ lab has studied hair follicle stem cells for many years and has identified the signals that activate hair follicle stem cells as well as the specific set of transcription factors that are upregulated in the activated stem cells. They have shown that many of the genes turned on during stem cell activation are regulated by super enhancers which sense the niche environment.

Dr. Fuchs begins her talk with a brief history of stem cells including the discovery in the 1970s that adult skin stem cells could be cultured in vitro indefinitely.  This early work provided the foundation for later advances in embryonic stem cell (ESC) culture. ESCs are special because they can generate all the different tissues of the body, thus providing great potential for use in regenerative medicine. The use of ESCs is controversial, however, so scientists have developed ways of generating pluripotent stem cells that do not use embryonic tissue.  Fuchs reviews methods such as nuclear transfer and the generation of induced pluripotent stem cells (iPSCs) by reprogramming adult somatic cells. Cells generated by these methods may be used for drug and therapy screening and they may provide treatments for human diseases such as macular degeneration, Parkinson’s and other degenerative diseases.

A horrific fungal disease called White Nose Syndrome began to cause massive mortality of small brown bats in the Northeastern United States in 2006. Dr. Frick explains that she and her colleagues used historical data from bat censuses and recent mortality data to model possible outcomes for bat populations in this region. Sadly, their data indicate almost certain regional extinction for the bats unless this disease can be stopped. This work was done in Dr. Thomas Kunz’s lab at Boston University. Dr. Frick is currently an Assistant Adjunct Professor of Ecology and Evolutionary Biology at the University of California, Santa Cruz.

This talk is a supplement to the annotated primary literature paper found in the American Association for the Advancement of Science’s (AAAS) Science in the Classroom Project.

A horrific fungal disease called White Nose Syndrome began to cause massive mortality of small brown bats in the Northeastern United States in 2006. Dr. Frick explains that she and her colleagues used historical data from bat censuses and recent mortality data to model possible outcomes for bat populations in this region. Sadly, their data indicate almost certain regional extinction for the bats unless this disease can be stopped. This work was done in Dr. Thomas Kunz’s lab at Boston University. Dr. Frick is currently an Assistant Adjunct Professor of Ecology and Evolutionary Biology at the University of California, Santa Cruz.

In their final talk, Walther and Farese explain how proteins are targeted specifically to the surface of lipid droplets.  This has functional consequences since proteins at the surface of lipid droplets govern lipid droplet growth and hydrolysis, and some of these proteins are associated with diseases. Farese and Walther end their talk by describing a number of diseases or physiological conditions that are now recognized as resulting from mutations in genes encoding proteins involved in lipid droplet formation. 

In Part 2, Walther and Farese explain in more depth how lipid droplets form in cells in an organized manner.  Triglycerides and other neutral lipids are made in the ER membrane.  They accumulate in localized regions of the membrane that grow towards the cytosol and eventually bud off into lipid droplets.  Farese and Walther describe experiments from their lab and others that have identified a protein complex in the ER membrane called LDAF1/Seipin that regulates where triglycerides localize and grow into mature lipid droplets.