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2017
Tuesday, April 11th
2:00 PM

Immunostaining for p300 and CBP

Noah Schlenk, Whitman College

Science 159

2:00 PM - 2:15 PM

My presentation focuses on research I conducted using immunohistochemistry to identify proteins in insulin-stimulated pathways. My research contributed to our lab's ability to analyze p300 and CBP proteins for their use of acetylation. Phosphorylation has long been seen as the primary driving force of downstream signaling. Our lab examined the importance and underestimation of acetylation. Initially, the lab used Western Blotting to look for protein presence, but the results we obtained were faint and difficult to analyze. I was assigned the task of troubleshooting a protocol for the staining of these two proteins. I sliced tissue, plated it, stained it and calculated the changes between knockout- and wild-type tissue. I was ultimately successful in identifying p300 but statistically unsuccessful in identifying CBP due to a technical error.

2:15 PM

Microwave Assisted Syntheses of CB11- Carborane Derivatives

Austin Schaff, Whitman College

Science 159

2:15 PM - 2:30 PM

Derivatives of the 1-carba-closo-dodecaborane(-1) carborane anion (CB11-) have a variety of potential applications which include use as therapeutic agents, catalysts, medical imaging agents and weakly coordinating anions. A new microwave assisted synthesis of the undecachlorinated derivative (CHB11Cl11-) has been developed. This compound has synthetic application as a weakly coordinating anion for cationic catalytic processes, but currently its accessibility is limited by a lengthy synthesis. A novel synthesis of the monoesterified derivative, 12-COOCH2CH3-CHB11H10 has also been developed from the previously established carboxylic acid derivative. With this synthesis carboxylic acid derivatives can be readily converted into a variety of esterified products. Reaction with select biomolecules could be a delivery mechanism of B10 to cancer cells for Boron Neutron Capture Therapy (BNCT).

2:30 PM

Effect of SBP-1 Signaling in the Synthesis of Lipids in C. elegans

Lindsay Schwartz, Whitman College
Lizzi Wong, Whitman College

Science 159

2:30 PM - 2:45 PM

We share our study of the Epidermal Growth Factor receptor let-23 in C. elegans, an excellent model organism for examining fundamental questions in genetics. We hypothesise that an overactive EGF signaling suppresses lipid synthesis through different signaling pathways. However, the pathways are poorly understood. To better understand them, we study whole animal fat levels under different EGF signaling levels and the effect of EGF signaling on the activation of the sole C. elegans lipid transcription factor, SBP-1. We use mutant strains with different levels of EGF signaling to determine whole animal fat levels and SBP-1:Green Fluorescent Protein fusion location using phase and fluorescent microscopy. We also use this approach to look at other downstream and upstream pathways connected to lipid synthesis, which will further our understanding of the role lipid synthesis plays in human cancer development.

2:45 PM

How Does Overactive EGF Signaling Affect C.elegans Lipidome

Ally Bogisich, Whitman College

Science 159

2:45 PM - 3:00 PM

Epidermal Growth Factor signaling is critical to animal development; it is also a hallmark of many cancers. Recent research in the nematode Caenorhabditis elegans has shown a role for EGF signaling in the control of lipid synthesis, via the lipid transcription factor SBP-1. This role led us to the question: How do different levels of EGF signaling affect the spectrum of lipids produced? I used mass spectrometry to assay the entire C. elegans lipidome under normal and overactive EGF signaling. To do so, I carried out a whole fat extraction, separated the lipids by TripleTOF, then analyzed the results for distinct lipid species and their relative quantities. I found that polyunsaturated lipids are widely trending up vs. normal, while mono-/saturated lipid production is trending down. Other emerging results suggest that lipid trends in overactive EGF signaling and sbp-1 mutants aren't as tightly correlated as we had hypothesized.