Transcriptional Regulation by λBacteriophage Antitermination by Sean Gibbons

Transcriptional Regulation by λBacteriophage Antitermination by Sean Gibbons

Biology

As a regulator of transcription, antitermination works to allow for RNA polymerase to read through termination signals and express genes found downstream of these termination signals. The Q protein of phage λ displays this antitermination phenotype in E.coli. It works to allow for the expression of promoter distal genes by letting RNAP transcribe through termination signals that block these genes. Q function overlays the phage late gene promoter P R ’ and requires the presence of a DNA element called the Q-utilization (qut) site. The qut site must contain Q-binding sequences and a specific pause site for the Q protein to be able to modify RNAP for the antitermination phenotype. Mutations in the qut site (-13/- 15) have been shown to decrease antitermination efficiency by preventing Q protein binding. This research seeks to identify regions of the Q protein that interact with qut DNA, using a second site suppressor analysis to identify mutant Q genes that allow for antitermination phenotype on mutant (-13/- 15) qut sites.

Gibbons, Sean

Senior Showcase Oral presentation

Ripon College

April 19, 2016

The author reserves all rights

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