Sahil B. Shah

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

The paper demonstrates that complex gene expression patterns can be achieved in bacteriophage genomes by adjusting promoter, terminator, and RNase cleavage site placements and strengths without dedicated regulatory genes.