Print by Debbie Covarrubias
picture of student examining plaque assay
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Puerto Vallarta Beach
Glaunsinger lab-2014


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.

Britt Named 2015 HHMI Investigator!!

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

Research Highlight #1

graphical abstract
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.

Research Highlight #2

IFA image of NCL staining
During lytic Kaposi’s sarcoma-associated herpesvirus (KSHV) infection, the viral endonuclease SOX promotes widespread degradation of cytoplasmic messenger RNA (mRNA). However, select mRNAs escape SOX-induced cleavage and remain robustly expressed. Prominent among these is interleukin-6 (IL-6), a growth factor important for survival of KSHV infected B cells. IL-6 escape is notable because it contains a sequence within its 3’ untranslated region (UTR) that can confer protection when transferred to a SOX-targeted mRNA, and thus overrides the endonuclease targeting mechanism. Postdoc Mandy Muller pursued how this protective RNA element functions to maintain mRNA stability, and identified a set of proteins that associate specifically with the protective element. Remarkably, she found that the IL-6 3’ UTR was also protected against mRNA degradation by the vhs endonuclease encoded by herpes simplex virus, despite the fact that its mechanism of mRNA targeting is distinct from SOX--suggesting that the IL-6 sequence may function as a more broad-acting nuclease escape element. These findings highlight how a network of RNA-protein interactions can impact endonuclease targeting, and identify new features underlying the regulation of the IL-6 mRNA.

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~

Lab Location

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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