Clathrin is important for normal actin dynamics and progression of Sla2p-containing patches during endocytosis in yeast.
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2006-05
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Clathrin is a major vesicle coat protein involved in receptor-mediated endocytosis. In yeast and higher eukaryotes, clathrin is recruited to the plasma membrane during the early stage of endocytosis along with clathrin-associated adaptors. As coated pits undergo maturation, a burst of actin polymerization accompanies and helps drive vesicle internalization. Here, we investigate the dynamics of clathrin relative to the early endocytic patch protein Sla2p. We find that clathrin is recruited to the cortex prior to Sla2p. In the absence of clathrin, normal numbers of Sla2p patches form, but many do not internalize or are dramatically delayed in completion of endocytosis. Patches that do internalize receive Sla1p late, which is followed by Abp1, which appears near the end of Sla2p lifetime. In addition, clathrin mutants develop actin comet tails, suggesting an important function in actin patch organization/dynamics. Similar to its mammalian counterparts, the light chain (LC) subunit of yeast clathrin interacts directly with the coiled-coil domain of Sla2p. A mutant of Sla2p that no longer interacts with LC (sla2Delta376-573) results in delayed progression of endocytic patches and aberrant actin dynamics. These data demonstrate an important role for clathrin in organization and progression of early endocytic patches to the late stages of endocytosis.
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Newpher, Thomas M, and Sandra K Lemmon (2006). Clathrin is important for normal actin dynamics and progression of Sla2p-containing patches during endocytosis in yeast. Traffic (Copenhagen, Denmark), 7(5). pp. 574–588. 10.1111/j.1600-0854.2006.00410.x Retrieved from https://hdl.handle.net/10161/27391.
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Thomas Mark Newpher
I teach, mentor, and advise in Duke’s Neuroscience major, and serve as the Associate Director of Undergraduate Studies in Neuroscience. I also direct the Summer Neuroscience Program of Research, where I provide mentorship and professional development opportunities for undergraduate research fellows. I earned my B.A. in Biology from Thiel College and my Ph.D. in Molecular Biology and Microbiology from Case Western Reserve University. In addition, I received postdoctoral training in the Departments of Neurobiology and Cell Biology at Duke University, where my research focused on the molecular mechanisms that underlie learning-related synaptic plasticity.
As a faculty member in the Department of Psychology and Neuroscience I teach several courses, including Cellular and Molecular Neurobiology (NEUROSCI 223), Contemporary Neuroscience Methods (NEUROSCI 376), the Neurobiology of Learning and Memory (NEUROSCI 461S), and Neuroplasticity and Disease (NEUROSCI 353S). My courses use a variety of team-based learning activities to promote critical thinking skills, foster collaboration among students, and create an engaging, student-centered classroom experience. As a co-PI in the Duke Team-Based Learning lab, I study the impacts of collaborative learning on student performance and classroom dynamics.
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