greg mullen

 greg mullen

greg P. mullen

  • Courses1
  • Reviews14

Biography

Oklahoma City University - Biology


Resume

  • 1991

    PhD

    Genetics

    The University of British Columbia

  • 1987

    BSc

    Biology

    The University of British Columbia

    Preparing Future Faculty

  • Western Blotting

    qPCR

    Protein Expression

    Cell

    Molecular Biology

    Cell Biology

    Molecular Genetics

    Teaching

    Genetics

    Developmental Biology

    Laboratory

    Scientific Writing

    Confocal Microscopy

    Molecular Cloning

    Fluorescence Microscopy

    Genetic interactions between UNC-17/VAChT and a novel transmembrane protein in Caenorhabditis elegans.

    James B. Rand

    Janet S. Duerr

    Jonathon Hodgkin

    Eleanor A. Mathews

    The unc-17 gene encodes the vesicular acetylcholine transporter (VAChT) in Caenorhabditis elegans. unc-17 reduction-of-function mutants are small

    slow growing

    and uncoordinated. Several independent unc-17 alleles are associated with a glycine-to-arginine substitution (G347R)

    which introduces a positive charge in the ninth transmembrane domain (TMD) of UNC-17. To identify proteins that interact with UNC-17/VAChT

    we screened for mutations that suppress the uncoordinated phenotype of UNC-17(G347R) mutants. We identified several dominant allele-specific suppressors

    including mutations in the sup-1 locus. The sup-1 gene encodes a single-pass transmembrane protein that is expressed in a subset of neurons and in body muscles. Two independent suppressor alleles of sup-1 are associated with a glycine-to-glutamic acid substitution (G84E)

    resulting in a negative charge in the SUP-1 TMD. A sup-1 null mutant has no obvious deficits in cholinergic neurotransmission and does not suppress unc-17 mutant phenotypes. Bimolecular fluorescence complementation (BiFC) analysis demonstrated close association of SUP-1 and UNC-17 in synapse-rich regions of the cholinergic nervous system

    including the nerve ring and dorsal nerve cords. These observations suggest that UNC-17 and SUP-1 are in close proximity at synapses. We propose that electrostatic interactions between the UNC-17(G347R) and SUP-1(G84E) TMDs alter the conformation of the mutant UNC-17 protein

    thereby restoring UNC-17 function; this is similar to the interaction between UNC-17/VAChT and synaptobrevin.

    Genetic interactions between UNC-17/VAChT and a novel transmembrane protein in Caenorhabditis elegans.

    James B. Rand

    Eleanor A. Mathews

    John R. McManus

    John A. Crowell

    Robert J. Hobson

    Shigeki Watanabe

    Mingyu Gu

    Kiely Grundahl

    The recycling of synaptic vesicles requires the recovery of vesicle proteins and membrane. Members of the stonin protein family (Drosophila Stoned B

    mammalian stonin 2) have been shown to link the synaptic vesicle protein synaptotagmin to the endocytic machinery. Here we characterize the unc-41 gene

    which encodes the stonin ortholog in the nematode Caenorhabditis elegans. Transgenic expression of Drosophila stonedB rescues unc-41 mutant phenotypes

    demonstrating that UNC-41 is a bona fide member of the stonin family. In unc-41 mutants

    synaptotagmin is present in axons

    but is mislocalized and diffuse. In contrast

    UNC-41 is localized normally in synaptotagmin mutants

    demonstrating a unidirectional relationship for localization. The phenotype of snt-1 unc-41 double mutants is stronger than snt-1 mutants

    suggesting that UNC-41 may have additional

    synaptotagmin-independent functions. We also show that unc-41 mutants have defects in synaptic vesicle membrane endocytosis

    including a ∼50% reduction of vesicles in both acetylcholine and GABA motor neurons. These endocytic defects are similar to those observed in apm-2 mutants

    which lack the µ2 subunit of the AP2 adaptor complex. However

    no further reduction in synaptic vesicles was observed in unc-41 apm-2 double mutants

    suggesting that UNC-41 acts in the same endocytic pathway as µ2 adaptin.

    UNC-41/stonin functions with AP2 to recycle synaptic vesicles in Caenorhabditis elegans.

    James B. Rand

    Michael W. Quick

    Robert J. Barstead

    Gary Moulder

    John R. McManus

    Stephen D. Fields

    Paurush Saxena

    Eleanor A. Mathews

    Sodium-dependent neurotransmitter transporters participate in the clearance and/or recycling of neurotransmitters from synaptic clefts. The snf-11 gene in Caenorhabditis elegans encodes a protein of high similarity to mammalian GABA transporters (GATs). We show here that snf-11 encodes a functional GABA transporter; SNF-11–mediated GABA transport is Na+ and Cl− dependent

    has an EC50 value of 168 μM

    and is blocked by the GAT1 inhibitor SKF89976A. The SNF-11 protein is expressed in seven GABAergic neurons

    several additional neurons in the head and retrovesicular ganglion

    and three groups of muscle cells. Therefore

    all GABAergic synapses are associated with either presynaptic or postsynaptic (or both) expression of SNF-11. Although a snf-11 null mutation has no obvious effects on GABAergic behaviors

    it leads to resistance to inhibitors of acetylcholinesterase. In vivo

    a snf-11 null mutation blocks GABA uptake in at least a subset of GABAergic cells; in a cell culture system

    all GABA uptake is abolished by the snf-11 mutation. We conclude that GABA transport activity is not essential for normal GABAergic function in C. elegans and that the localization of SNF-11 is consistent with a GABA clearance function rather than recycling.

    The Caenorhabditis elegans snf-11 Gene Encodes a Sodium-dependent GABA Transporter Required for Clearance of Synaptic GABA.

    I have considerable scientific expertise in genetics

    imaging

    cell biology and molecular biology. My writing is clear and well-organized

    and I have written (or co-written) many publications over the last ten years. I am a creative thinker

    who is self-disciplined

    and is capable of working independently. I have helped mentor new lab personnel

    including undergraduate and graduate students in the lab. I hold to high standards

    especially with respect to scientific rigor and ethical conduct. I have participated in a number of collaborations

    with co-workers at OMRF

    as well as colleagues elsewhere.

    Greg

    Department of Zoology

    Department of Zoology

    University of British Columbia

    Oklahoma City University

    Michael Smith Laboratories

    University of British Columbia

    University of Oklahoma Health Sciences Center

    Oklahoma Medical Research Foundation

    2501 N Blackwelder Ave Oklahoma City

    OK 73106

    I am thrilled to be teaching Genetics (Fall semester) and Cell Biology (Spring semester) as an Adjunct Instructor at Oklahoma City University! The students are wonderful

    and I am trying my very best to be a great teacher!

    Adjunct Professor

    Oklahoma City University

    Vancouver

    British Columbia

    Canada

    I worked on muscle sarcomere assembly in the nematode C. elegans with Dr. Donald Moerman. My research addressed the role of the extracellular matrix (ECM) proteoglycan Perlecan in anchoring the contractile apparatus to the underlying ECM.

    Graduate Student

    Department of Zoology

    University of British Columbia

    I am excited and honored to join the Department of Biology at Oklahoma City University as an Assistant Professor! I will be officially starting in the Fall semester of 2014. This is a wonderful opportunity for me

    and I appreciate the strong support and encouragement of all my friends and colleagues! Thank you all so much!

    Oklahoma City University

    Research Scientist

    I am a research scientist at OMRF working on nervous system development and function using a nematode (C. elegans) as a model organism. Our work has implications for human conditions such as Myasthesia gravis and Autism

    as well as providing a general framework for understanding how synaptic release is regulated.

    Oklahoma Medical Research Foundation

    Postdoctoral Fellow

    I worked in the C. elegans Gene Knockout Laboratory with Dr. Donald Moerman. Our lab provided deletion mutants (\"gene knockouts\") to the C. elegans research community. These mutants have provided considerable insight into many biological processes and human disease conditions.

    Michael Smith Laboratories

    University of British Columbia

    Department of Zoology

    University of British Columbia

    1996 – 1998: Teaching Assistant for Biology 334/335 (Introduction to Genetics) and Biology 432 (Advanced Problems in Animal Genetics).\n\n1996 – 1998: Instructor for “A Practical Introduction to Confocal Microscopy”. A one-day hands-on course for users of the BioRad MRC 600 Confocal Microscope at the Biosciences EM Facility at the University of British Columbia.

    Teaching Assistant

    Oklahoma City

    OK

    USA

    2012 – Present: Guest Lecturer for CELL 6331 (GPIBS Molecular Genetics Module) at the University of Oklahoma Health Sciences Center.\n\n2010 - Present: Guest Speaker at Wiley Post Elementary School. I give fun and informative presentations on a variety of topics

    including rocks and minerals

    and frogs and toads.\n\n2004 – Present: Guest Lecturer for CELL 6063 (Cellular and Molecular Developmental Biology) at the University of Oklahoma Health Sciences Center.\n\nIn 2010

    I successfully completed the Preparing Future Faculty course (BMSC 6202 and 6300) offered by the University of Oklahoma Health Science Center Graduate College (Melissa S. Medina

    EdD

    instructor). This course is intended to provide the necessary theoretical background and skills to be an effective educator.

    Instructor

    University of Oklahoma Health Sciences Center

    The Genetics Society of America

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