M
Miriam B. Goodman
Researcher at Stanford University
Publications - 124
Citations - 7667
Miriam B. Goodman is an academic researcher from Stanford University. The author has contributed to research in topics: Caenorhabditis elegans & Mechanotransduction. The author has an hindex of 44, co-authored 118 publications receiving 6661 citations. Previous affiliations of Miriam B. Goodman include University of Chicago & University of Illinois at Chicago.
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Journal ArticleDOI
Dissecting a circuit for olfactory behaviour in Caenorhabditis elegans
Sreekanth H. Chalasani,Nikos Chronis,Makoto Tsunozaki,Jesse M. Gray,Daniel Ramot,Miriam B. Goodman,Cornelia I. Bargmann +6 more
TL;DR: Information processing by Caenorhabditis elegans olfactory neurons and interneurons resembles information flow from vertebrate photoreceptors to ‘OFF” bipolar and ‘ON’ bipolar neurons, indicating a conserved or convergent strategy for sensory information processing.
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The MEC-4 DEG/ENaC channel of Caenorhabditis elegans touch receptor neurons transduces mechanical signals.
TL;DR: Recording from C. elegans touch receptor neurons in vivo found that external force evokes rapidly activating mechanoreceptor currents (MRCs) carried mostly by Na+ and blocked by amiloride—characteristics consistent with direct mechanical gating of a DEG/ENaC channel.
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The major α-tubulin K40 acetyltransferase αTAT1 promotes rapid ciliogenesis and efficient mechanosensation
TL;DR: It is concluded that αTAT1 is the major and possibly the sole α-tubulin K40 acetyltransferase in mammals and nematodes, and that tubulin acetylation plays a conserved role in several microtubule-based processes.
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Active Currents Regulate Sensitivity and Dynamic Range in C. elegans Neurons
TL;DR: The electrical properties of an identified sensory neuron (ASER) across four developmental stages and 42 unidentified neurons at one stage are analyzed to find that ASER is nearly isopotential and fails to generate classical Na+ action potentials, but displays a high sensitivity to input currents coupled to a depolarization-dependent reduction in sensitivity.
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MEC-2 regulates C. elegans DEG/ENaC channels needed for mechanosensation
Miriam B. Goodman,Glen G Ernstrom,Dattananda S. Chelur,Robert O'Hagan,C. Andrea Yao,Martin Chalfie +5 more
TL;DR: The findings indicate that M EC-2 regulates MEC-4/MEC-10 ion channels and raise the possibility that similar ion channels may be formed by stomatin-like proteins and DEG/ENaC proteins that are co-expressed in both vertebrates and invertebrates.