Winter 2014 Biomedical Seminar Series

January 10, 2013

Parkin Moderates Hypertrophy and Heart Failure Following Cardiac Pressure Overload
Eileen Gonzalez

MARC U*STAR Fellow
Summer Research Site: University of California, San Diego Summer Training Academy for Research in the Sciences (STARS) Program


Role of cagPAI in Helicobactor Pylori Pathogenesis
Oswaldo Escobar
MARC U*STAR Fellow
Summer Research Site: Center of Comparative Medicine, University of California, Davis

Abstract: Helicobactor pylori is a successful human pathogen that colonizes about 50% of the world’s population and colonizes the gastric mucosa in the stomach. H. pylori can cause chronic gastritis and has been associated with gastric cancers and ulcers. These gastric cancers and ulcers have been associated with a virulent factor the Cag Pathogenicity Island (CagPAI) which encodes for the type IV secretion system (T4SS) that acts as a molecular syringe and injects effector molecule (CagA) to induce inflammation. cagY is an essential component of the T4SS and changes in this gene may alter the functionality of the T4SS and modulate the host’s inflammatory response. To determine if inflammation may benefit H. pylori by modulating during early infection, mice were infected with 50:50 wild type (pro-inflammatory and functional cagY) and Mutant ( non-functional cagY) at 4 time points, 1, 7, 14, and 56 days. A competitive index shows that the mutant is favored very early and switches to wild type at 14 days. Changes in cagY are seen in wild type at 14 days and no change in the mutant. Levels of IL-8 from infected gastric epithelial cells (AGS cells) were measured and showed varied levels of induction in the wild type than from mutant indicating the wild type is changing its cagY to better compete with the mutant who is favored early.


Investigating Replication Restart at a Site Specific Replication Fork Barrier in Fission Yeast
Brittany Ulloa

MARC U*STAR Fellow Summer Research Site: MHIRT at the University of Oxford

ABSTRACT: The aim of this work is to establish a system for observing recombination and replication protein dynamics at a site-specific replication fork barrier. To do this, we are making use of a programmed replication fork barrier known as replication terminating sequence 1 (RTS1). RTS1 element contains four repeated motifs called region B and an enhancer motif called region A, and it is this DNA sequence that associates with several proteins, including Rtf1 and Rtf2, to enforce its replication fork barrier activity. Published work from our lab shows that when the RTS1 is positioned in an orientation that does not block the replication fork from the nearest replication origin (IO), there is virtually no recombination between the ade6 heteroalleles. When the orientation of the RTS1 if flipped around, so that it does block the replication fork from the nearest origin (AO), there is a large stimulation of recombination between ectopic homologous sequences. In order to further observe recombination and replication protein dynamics with the RTS1 system, we have designed several experiments: 1) where the nearest far origin of replication known as Ori C is deleted, and 2) where an additional block known as TER 2/3 is inserted. We hypothesize that both of these scenarios will promote an increase in replication restart.

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