Print by Debbie Covarrubias
picture of student examining plaque assay
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Puerto Vallarta Beach

OVERVIEW

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!

champagne
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: http://www.hhmi.org/news/hhmi-selects-26-nations-top-biomedical-scientists

Research Highlight #1 (and our first BioRxiv submission!)

fish jumping to escape
The ability of viruses to control the host gene expression environment is crucial to promote viral infection. Many viruses express factors that reduce host gene expression through widespread mRNA decay. However, some mRNAs escape this fate, like the transcript encoding the immunoregulatory cytokine IL-6 during KSHV infection. IL-6 escape relies on an RNA regulatory element located in its 3’UTR and involves the recruitment of a protective protein complex. Here, we show that this escape extends beyond KSHV to a variety of related and unrelated viral endonucleases. However, the IL-6 element does not protect against cellular endonucleases, revealing for the first time a virus-specific nuclease escape element. We also identified a related escape element in the GADD45B mRNA, and hypothesize that these may be representative members of a new type of RNA regulatory element engaged during viral endonuclease-triggered mRNA decay.

Research Highlight #2

virus sign
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.

TWiV Comes to Berkeley!

TWiV logo
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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