Britt A. Glaunsinger

The paper identifies two clusters of residues in the SARS-CoV-2 nsp1 N-terminal domain that are critical for distinguishing between host and viral mRNA targets and mediating mRNA decay.

Pol III occupies TATA-enriched, TBP-dependent inflammatory gene promoters, primes basal expression, then restrains Pol II induction during MHV68, HSV-1 and influenza A infection.

The paper shows that stress-induced cleavage of TFIIB by caspases-3 and 7 reduces its ability to form promoter complexes, restricting expression of stimulus-responsive genes during stress.

The paper models and validates the DNA binding structure of KSHV ORF24, revealing a non-canonical binding mode and cooperative pre-assembly with RNA polymerase II for promoter recognition.

This study shows that RNase L, an antiviral nuclease, represses transcription by reducing RNA polymerase II elongation, particularly affecting immune-related genes.

This study identifies SP140's role in regulating IFN-β mRNA stability through RESIST, revealing a dual antiviral and interferon regulatory function.

The paper identifies polyadenylation as a mechanism driving SINE RNA accumulation during gammaherpesvirus infection, linking Pol III transcription to mRNA-like processing.

The paper identifies TFIIB as a target for degradation during cellular stress and viral infection, showing two pathways for its depletion and how KSHV counteracts this to support viral transcription.

The paper identifies and characterizes viral transcriptional effector domains from coronaviruses and herpesviruses using high-throughput assays and perturbations.

The paper identifies ORF29 as a viral DNA packaging motor subunit that potentiates late gene expression in KSHV, linking transcription and packaging processes.

This study investigates how HSV-1 manipulates RNA Polymerase III by increasing tRNA expression and altering transcriptional machinery interactions.

The paper uses a CRISPR/Cas9 screen to identify KSHV transcriptional modifiers, finding ORF46's DNA binding domain is essential for viral DNA replication.

This study identifies key residues in SARS-CoV-2 nsp1 that regulate host and viral mRNA translation, revealing functional differences between these mRNA types.

The paper shows that mRNA decay during early apoptosis represses RNA polymerase II transcription, creating positive feedback that amplifies gene expression shutdown.

This study shows that gammaherpesvirus MHV68 infection alters the tRNAome by increasing pre-tRNA expression and affecting tRNA processing.

This paper identifies how herpesviral TBP mimics interact with RNA polymerase II to drive late gene transcription, distinguishing viral from cellular TBP function.

This study identifies MHV68 ORF36 kinase as a key factor in B2 SINE ncRNA activation during gammaherpesvirus infection, linking it to chromatin modification changes.

This paper identifies conserved CxnC motifs in KSHV ORF66 essential for its interaction with ORF34 and late gene expression.

This study identifies the critical role of the ORF18-ORF30 interaction in KSHV late gene expression through mutational analysis.

The paper shows that changes in mRNA decay alter RNA binding protein localization, linking cytoplasmic RNA degradation to transcription.

This study identifies KSHV ORF68 as a DNA-binding protein essential for viral DNA cleavage and packaging, revealing its role in capsid formation and infectious virion production.

The paper identifies RNA elements that protect mRNAs from viral endonuclease cleavage, showing they are specific to viral enzymes and not cellular ones.