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In JoVE (1)
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Articles by Jill J. Weyers in JoVE
JoVE Clinical and Translational Medicine
प्रतिगामी और सूक्ष्म गणना टोमोग्राफी इमेजिंग के लिए तैयारी के रूप में परफ्यूज़न माउस कोरोनरी vasculature का भरना
1Department of Pathology, Center for Cardiovascular Biology, and Institute for Stem Cell and Regenerative Medicine, University of Washington, 2Departments of Bioengineering and Medicine/Cardiology, University of Washington
कोरोनरी वाहिकाओं के विज़ुअलाइज़ेशन हृदय रोगों के बारे में हमारी समझ को आगे बढ़ाने के लिए महत्वपूर्ण है. यहाँ हम एक radiopaque सिलिकॉन रबर (MICROFIL) के साथ सूक्ष्म गणना टोमोग्राफी इमेजिंग (μCT) के लिए तैयारी में murine कोरोनरी वाहिका संरचना, perfusing के लिए एक विधि का वर्णन.
Other articles by Jill J. Weyers on PubMed
The Threshold for Polyglutamine-expansion Protein Aggregation and Cellular Toxicity is Dynamic and Influenced by Aging in Caenorhabditis Elegans
Studies of the mutant gene in Huntington's disease, and for eight related neurodegenerative disorders, have identified polyglutamine (polyQ) expansions as a basis for cellular toxicity. This finding has led to a disease hypothesis that protein aggregation and cellular dysfunction can occur at a threshold of approximately 40 glutamine residues. Here, we test this hypothesis by expression of fluorescently tagged polyQ proteins (Q29, Q33, Q35, Q40, and Q44) in the body wall muscle cells of Caenorhabditis elegans and show that young adults exhibit a sharp boundary at 35-40 glutamines associated with the appearance of protein aggregates and loss of motility. Surprisingly, genetically identical animals expressing near-threshold polyQ repeats exhibited a high degree of variation in the appearance of protein aggregates and cellular toxicity that was dependent on repeat length and exacerbated during aging. The role of genetically determined aging pathways in the progression of age-dependent polyQ-mediated aggregation and cellular toxicity was tested by expressing Q82 in the background of age-1 mutant animals that exhibit an extended lifespan. We observed a dramatic delay of polyQ toxicity and appearance of protein aggregates. These data provide experimental support for the threshold hypothesis of polyQ-mediated toxicity in an experimental organism and emphasize the importance of the threshold as a point at which genetic modifiers and aging influence biochemical environment and protein homeostasis in the cell.
A Genetic Screen for Mutations Affecting Gonad Formation in Drosophila Reveals a Role for the Slit/robo Pathway
Organogenesis is a complex process requiring multiple cell types to associate with one another through correct cell contacts and in the correct location to achieve proper organ morphology and function. To better understand the mechanisms underlying gonad formation, we performed a mutagenesis screen in Drosophila and identified twenty-four genes required for gonadogenesis. These genes affect all different aspects of gonad formation and provide a framework for understanding the molecular mechanisms that control these processes. We find that gonad formation is regulated by multiple, independent pathways; some of these regulate the key cell adhesion molecule DE-cadherin, while others act through distinct mechanisms. In addition, we discover that the Slit/Roundabout pathway, best known for its role in regulating axonal guidance, is essential for proper gonad formation. Our findings shed light on the complexities of gonadogenesis and the genetic regulation required for proper organ formation.
