Research Topics
| M Wayne DavisSummaryAffiliation: University of Utah Country: USA Publications
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Detail Information
Publications
A mutation in the C. elegans EXP-2 potassium channel that alters feeding behaviorM W Davis
Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390 9148, USA
Science 286:2501-4. 1999....
Rapid single nucleotide polymorphism mapping in C. elegansM Wayne Davis
Department of Biology, University of Utah, Salt Lake City, Utah 84112 0840, USA
BMC Genomics 6:118. 2005..In C. elegans, single nucleotide polymorphisms (SNPs) can function as silent genetic markers, with applications ranging from classical two- and three-factor mapping to measuring recombination across whole chromosomes...- Gene activation using FLP recombinase in C. elegansM Wayne Davis
Howard Hughes Medical Institute, University of Utah, Salt Lake City, Utah, United States of America
PLoS Genet 4:e1000028. 2008..We show that we can use this to inactivate synaptic transmission in all neurons or a subset of neurons in a FLP-dependent manner... - Protons act as a transmitter for muscle contraction in C. elegansAsim A Beg
Neuroscience Program, University of Utah, Salt Lake City, UT 84112 0840, USA
Cell 132:149-60. 2008..8. The identification of the mechanisms for release and reception of proton signals establishes a highly unusual mechanism for intercellular communication... - Single-nucleotide polymorphism mappingM Wayne Davis
Department of Biology, University of Utah, Salt Lake City, USA
Methods Mol Biol 351:75-92. 2006..This chapter presents a detailed procedure for generating recombinant animals, for assaying SNPs using restriction enzymes, and for analyzing mapping data... - Heterozygous insertions alter crossover distribution but allow crossover interference in Caenorhabditis elegansMarc Hammarlund
Department of Biology, University of Utah, Salt Lake City, Utah 84112-0840, USA
Genetics 171:1047-56. 2005..However, because crossovers are not completely eliminated distal to insertions, we propose that alignment can be reestablished after a megabase-scale gap in sequence homology... - Single-copy insertion of transgenes in Caenorhabditis elegansChristian Frøkjaer-Jensen
Department of Biology and Howard Hughes Medical Institute, University of Utah, 257 South 1400 East, Salt Lake City, Utah 84112, USA
Nat Genet 40:1375-83. 2008..We have successfully inserted transgenes as long as 9 kb and verified that single copies are inserted at the targeted site. Single-copy transgenes are expressed at endogenous levels and can be expressed in the female and male germlines... - Targeted gene deletions in C. elegans using transposon excisionChristian Frøkjaer-Jensen
Howard Hughes Medical Institute, Department of Biology, University of Utah, Salt Lake City, Utah, USA
Nat Methods 7:451-3. 2010..Repair can delete up to 25 kb of DNA and simultaneously insert a positive selection marker... - Protein localization in electron micrographs using fluorescence nanoscopyShigeki Watanabe
Department of Biology and Howard Hughes Medical Institute, University of Utah, Salt Lake City, Utah, USA
Nat Methods 8:80-4. 2011..Fluorescence correlated with organelles imaged in electron micrographs from the same sections. We used these methods to localize histones, a mitochondrial protein and a presynaptic dense projection protein in electron micrographs... - UNC119 is required for G protein trafficking in sensory neuronsHoubin Zhang
Department of Ophthalmology, University of Utah Health Science Center, Salt Lake City, Utah, USA
Nat Neurosci 14:874-80. 2011..UNC119 deletion in both mouse and C. elegans led to G protein mislocalization. Thus, UNC119 is a Gα subunit cofactor essential for G protein trafficking in sensory cilia... - Induction and repair of zinc-finger nuclease-targeted double-strand breaks in Caenorhabditis elegans somatic cellsJason Morton
Department of Biochemistry, University of Utah School of Medicine, 15 North Medical Drive East, Salt Lake City, UT 84112, USA
Proc Natl Acad Sci U S A 103:16370-5. 2006..DNA ligase IV is required for efficient end joining, particularly of blunt ends. In its absence, a secondary end-joining pathway relies more heavily on microhomologies in producing deletions... - A conserved metalloprotease mediates ecdysis in Caenorhabditis elegansM Wayne Davis
Department of Biology, University of Utah, Salt Lake City, UT 84112 0840, USA
Development 131:6001-8. 2004..NAS-37 degradation of the Haemonchus cuticle suggests that the metalloproteases and the cuticle substrates involved in exsheathment of parasitic nematodes are conserved in free-living nematodes... - Mobilization of a Drosophila transposon in the Caenorhabditis elegans germ lineJ L Bessereau
Department of Biology, University of Utah, Salt Lake City 84112-0840, USA
Nature 413:70-4. 2001..Fourth, these insertions can subsequently be remobilized to generate deletion and frameshift mutations by imperfect excision... - Mutations in the Caenorhabditis elegans Na,K-ATPase alpha-subunit gene, eat-6, disrupt excitable cell functionM W Davis
Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas 75235 9038, USA
J Neurosci 15:8408-18. 1995..To explain these abnormalities, we propose that a reduction of Na,K-ATPase activity in eat-6 mutants leads to a reduction of the ion concentration gradients that power membrane potential changes... - Gene conversion and end-joining-repair double-strand breaks in the Caenorhabditis elegans germlineValérie J Robert
Ecole Normale Superieure, Biologie Cellulaire de la Synapse, Paris, France
Genetics 180:673-9. 2008..Surprisingly, expression of the transposase using an intestine-specific promoter can induce repair, raising the possibility that activation of transposase expression in somatic cells can lead to transposition of Mos1 in the germline... - Social feeding in Caenorhabditis elegans is induced by neurons that detect aversive stimuliMario de Bono
Howard Hughes Medical Institute, Department of Anatomy, UCSF, California 94143 0452, USA
Nature 419:899-903. 2002..Our data suggest a model for regulation of social feeding by opposing sensory inputs: aversive inputs to nociceptive neurons promote social feeding, whereas antagonistic inputs from neurons that express osm-3 inhibit aggregation...