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Medical Biochemistry Commons

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Articles 1 - 5 of 5

Full-Text Articles in Medical Biochemistry

2-Heptyl-4-Quinolone, A Precursor Of The Pseudomonas Quinolone Signal Molecule, Modulates Swarming Motility In Pseudomonas Aeruginosa, Dae-Gon Ha, Judith H. Merritt, Thomas H. Hampton, James T. Hodgkinson, Matej Janecek, David R. Spring, Martin Welch, George A. O'Toole Sep 2011

2-Heptyl-4-Quinolone, A Precursor Of The Pseudomonas Quinolone Signal Molecule, Modulates Swarming Motility In Pseudomonas Aeruginosa, Dae-Gon Ha, Judith H. Merritt, Thomas H. Hampton, James T. Hodgkinson, Matej Janecek, David R. Spring, Martin Welch, George A. O'Toole

Dartmouth Scholarship

Pseudomonas aeruginosa is an opportunistic pathogen capable of group behaviors, including biofilm formation and swarming motility. These group behaviors are regulated by both the intracellular signaling molecule c-di-GMP and acylhomoserine lactone quorum-sensing systems. Here, we show that the Pseudomonas quinolone signal (PQS) system also contributes to the regulation of swarming motility. Specifically, our data indicate that 2-heptyl-4-quinolone (HHQ), a precursor of PQS, likely induces the production of the phenazine-1-carboxylic acid (PCA), which in turn acts via an as-yet-unknown downstream mechanism to repress swarming motility. We show that this HHQ- and PCA-dependent swarming repression is apparently independent of changes in global …


Mediator Influences Telomeric Silencing And Cellular Life Span, Xuefeng Zhu, Beidong Liu, Jonas O. P. Carlsten, Jenny Beve, Thomas Nyström, Lawrence C. Myers, Claes M. Gustafsson Jun 2011

Mediator Influences Telomeric Silencing And Cellular Life Span, Xuefeng Zhu, Beidong Liu, Jonas O. P. Carlsten, Jenny Beve, Thomas Nyström, Lawrence C. Myers, Claes M. Gustafsson

Dartmouth Scholarship

The Mediator complex is required for the regulated transcription of nearly all RNA polymerase II-dependent genes. Here we demonstrate a new role for Mediator which appears to be separate from its function as a transcriptional coactivator. Mediator associates directly with heterochromatin at telomeres and influences the exact boundary between active and inactive chromatin. Loss of the Mediator Med5 subunit or mutations in Med7 cause a depletion of the complex from regions located near subtelomeric X elements, which leads to a change in the balance between the Sir2 and Sas2 proteins. These changes in turn result in increased levels of H4K16 …


Chloroquine Treatment Of Arpe-19 Cells Leads To Lysosome Dilation And Intracellular Lipid Accumulation: Possible Implications Of Lysosomal Dysfunction In Macular Degeneration, Patrick M. Chen, Zoë J. Gombart, Jeff W. Chen Mar 2011

Chloroquine Treatment Of Arpe-19 Cells Leads To Lysosome Dilation And Intracellular Lipid Accumulation: Possible Implications Of Lysosomal Dysfunction In Macular Degeneration, Patrick M. Chen, Zoë J. Gombart, Jeff W. Chen

Dartmouth Scholarship

Age-related macular degeneration (AMD) is the leading cause of vision loss in elderly people over 60. The pathogenesis is still unclear. It has been suggested that lysosomal stress may lead to drusen formation, a biomarker of AMD. In this study, ARPE-19 cells were treated with chloroquine to inhibit lysosomal function. Chloroquine-treated ARPE-19 cells demonstrate a marked increase in vacuolation and dense intracellular debris. These are identified as chloroquine-dilated lysosomes and lipid bodies with LAMP-2 and LipidTOX co-localization, respectively. Dilation is an indicator of lysosomal dysfunction. Chloroquine disrupts uptake of exogenously applied rhodamine-labeled dextran by these cells. This suggests a disruption …


Rho Activation Of Mdia Formins Is Modulated By An Interaction With Inverted Formin 2 (Inf2), Hua Sun, Johannes S. Schlondorff, Elizabeth J. Brown, Henry N. Higgs, Martin R. Pollak Feb 2011

Rho Activation Of Mdia Formins Is Modulated By An Interaction With Inverted Formin 2 (Inf2), Hua Sun, Johannes S. Schlondorff, Elizabeth J. Brown, Henry N. Higgs, Martin R. Pollak

Dartmouth Scholarship

Inverted formin 2 (INF2) encodes a member of the diaphanous subfamily of formin proteins. Mutations in INF2 cause human kidney disease characterized by focal and segmental glomerulosclerosis. Disease-causing mutations occur only in the diaphanous inhibitory domain (DID), suggesting specific roles for this domain in the pathogenesis of disease. In a yeast two-hybrid screen, we identified the diaphanous autoregulatory domains (DADs) of the mammalian diaphanous-related formins (mDias) mDia1, mDia2, and mDia 3 as INF2_DID-interacting partners. The mDias are Rho family effectors that regulate actin dynamics. We confirmed in vitro INF2_DID/mDia_DAD binding by biochemical assays, confirmed the in vivo interaction of these …


Superparamagnetic Nanoparticle Capture Of Prions For Amplification, Michael B. Miller, Surachai Supattapone Jan 2011

Superparamagnetic Nanoparticle Capture Of Prions For Amplification, Michael B. Miller, Surachai Supattapone

Dartmouth Scholarship

Prion diseases are associated with the presence of PrP(Sc), a disease-associated misfolded conformer of the prion protein. We report that superparamagnetic nanoparticles bind PrP(Sc) molecules efficiently and specifically, permitting magnetic separation of prions from a sample mixture. Captured PrP(Sc) molecules retain the activity to seed protein misfolding cyclic amplification (PMCA) reactions, enabling the rapid concentration of dilute prions to improve detection. Furthermore, superparamagnetic nanoparticles clear contaminated solutions of PrP(Sc). Our findings suggest that coupling magnetic nanoparticle capture with PMCA could accelerate and improve prion detection. Magnetic nanoparticles may also be useful for developing a nontoxic prion decontamination method for biologically …