Print by Debbie Covarrubias
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Puerto Vallarta Beach


The Glaunsinger lab studies the creative strategies viruses use to manipulate gene expression in host cells.  Our primary focus is RNA-based regulation of gene expression, including both transcriptional and posttranscriptional control.  We are interested in viral factors that directly target RNA, as well as how viruses interface with and usurp cellular pathways to control gene expression.  We study these events using gamma-herpesviruses such as Kaposi's sarcoma-associated herpesvirus, which is a major cause of AIDS-associated cancers. We anticipate that these studies will enhance our understanding of virus-host interactions, as well as provide insight into how gene expression pathways are normally regulated in human cells.

Glaunsinger lab celebrates 10 years at Berkeley!

A fantastic decade of research, friendship, and fun...capped by plenty of champagne and a surprise party for Britt. :-) Check out pictures of the celebration!

Britt Named 2015 HHMI Investigator!!

HHMI celebration
Read about our work, and that of the other new HHMI investigators here:

Research Highlight #1

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Nearly half of the mammalian genome is composed of transposable elements, which are silent—at least most of the time. However, a subset of these elements that do not encode for any proteins, termed short interspersed nuclear repeats, or SINEs, can get activated in response to viral infection. Postdoc John Karijolich (now a new PI of his own lab at Vanderbilt!) recently reported that these SINE RNAs might have been co-opted by cells as an early warning system to alert the cell of a potential incoming virus. We now describe a technique to profile activated murine B2 SINEs, revealing that tens of thousands of these elements are de-repressed during gamma-herpesvirus infection. Given that SINE elements are present in many cellular mRNAs, we show that these virus-induced noncoding RNAs can base pair with complementary sequences in RNA Pol2 transcripts and impede mRNA export.

Research Highlight #2

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Most of us think about gene expression as a linear series of events starting with mRNA synthesis in the nucleus and ending with mRNA degradation after translation in the cytoplasm. However, by manipulating mRNA abundance in the cytoplasm--something herpesviruses do very efficiently--we are finding surprising interconnectivity in the gene expression cascade. In a paper recently published in Cell Host & Microbe (with an accompanying preview article), Emma Abernathy and Sarah Gilbertson discover an mRNA degradation-synthesis feedback loop in mammalian cells. They show that cells in which mRNA decay in the cytoplasm is accelerated send a signal to the nucleus to reduce transcription, indicating that overall mRNA abundance is somehow "sensed" in cells. In mammals, large changes in mRNA abundance appear to be interpreted as a stress or threat, leading the cell to further restrict gene expression at the level of transcription. In a clever twist of fate, viral genes (which use the same transcription machinery as the cell) somehow manage to escape this repression, and thus likely benefit from the feedback mechanism.

TWiV Comes to Berkeley!

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Vincent Racaniello, the host of the awesome This Week in Virology (TWiV) podcast, visited UC Berkeley! Check out the live podcast at the Microbiology Student Symposium featuring our research~

Come visit us...

Li Ka Shing Building photo
Our lab is located in the UC Berkeley Li Ka Shing Center for Biomedical Sciences, on a floor dedicated to infectious disease research. Check out our awesome new space, which includes amazing views of the bay and the beautiful Berkeley campus!
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