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Research Poster PresentationsP O S T E R 4 5Asymmetric Allylation of AldehydesCatalyzed by Optically ActiveSPINOL-Based Phosphoric AcidsYimei Zhang, Monica Bassous,Chun-Hui XingFaculty Mentor: Dr. Qiao-Sheng HuDepartment of ChemistryThe asymmetric allyation of allylborons withaldehydes constitutes one of the most attractivemethods to access homoallylic alcohols. Transitionmetal-catalyzed such addition reactions have beenpreviously reported. However, reported catalystsystems suffer from relative harsh reactionconditions and/or selectivity. We are interested indeveloping “green” catalysts, i.e., organocatalysts –the use of small organic compounds as chiralcatalysts, for such addition reactions, especiallywith high enantioselectivities.1,1’-Spirodiindane-7,7’-diol (SPINOL) and itsderivatives have been demonstrated to be highlyenantioselective chiral scaffolds for a number ofuseful transformations. However, SPINOL-derivedBronsted acids, which constitute a large family ofchiral organocatalysts, remain underexplored. Inthis presentation, the use of spirodiindanediolbasedphosphoric acids as chiral catalysts forasymmetric allylation of aldehydes willbe presented.P O S T E R 4 7Analysis of MIA-Induced Keratin-6Upregulation in Mammary TissueSurendar RavindranFaculty Mentor: Dr. Jimmie FataDepartment of BiologyThe development of the mammary gland requiresco-ordinated tissue and cellular signals that directproper branching morphogenesis. Using threedimensional(3D) tissue cultures of mammary glanddevelopment we have previously found that a drugof the amiloride family, (N-Methyl, Nisobutyl)amiloride (MIA) drastically disrupts mammarydevelopment in this assay. MIA abrogates thefunction of the Na+/H exchanger type-1 (NHE-1),which is directly responsible for maintainingintracellular pH of mammary epithelial cells. Amonga number of MIA-induced tissue and cellularphenotypes, we found that associated with thisinhibited morphogenesis was an increased andectopic expression of Keratin 6 (K6), anintermediate filament protein rarely expressed inmammary epithelial cells and one that is involvedin hyper-proliferation. To determine whether K6expression occured because of increasedtranscriptional expression, I set out to measure K6mRNA levels in untreated and MIA-treatedmammary tissue using quantitative PCR. Theexperimental procedure of RT-PCR, the isolation ofmRNA, and initial results are provided here alongwith the technical hurdles we encountered.Determining whether MIA induces K6 upregulationof transcription in mammary tissue may shed lighton how co-ordinated signals become disruptedduring breast cancer.48