Resume

• 2004

  Ph.D

  The GPiBS program is an interdisciplinary program that combines the expertise of over 120 participating faculty from six participating departments (Biochemistry & Molecular

  Biology

  Cell Biology

  Microbiology & Immunology

  Neuroscience

  Pathology and Physiology) to provide students with the breadth of knowledge and technical acumen.

  Cell Biology (Molecular Biology

  Neuroscience

  Genetics)

• 1997

  B.S.

  Biochemistry

• Western Blotting

  ELISA

  Microsoft Office

  Microscopy

  Immunohistochemistry

  Life Sciences

  Fluorescence

  Molecular Biology

  PCR

  Confocal Microscopy

  Fluorescence Microscopy

  Genetics

  PowerPoint

  Teaching

  Problem Solving

  Research

  DNA

  Cell Biology

  Protein Purification

  Photoshop

  Neuroligin-deficient mutants of C. elegans have sensory processing deficits and are hypersensitive to oxidative stress and mercury toxicity.

  James B. Rand

  Angie Duke

  Jessica M. Heatherly

  John R. McManus

  Gregory P. Mullen

  Neuroligins are postsynaptic cell adhesion proteins that bind specifically to presynaptic membrane proteins called neurexins. Mutations in human neuroligin genes are associated with autism spectrum disorders in some families. The nematode Caenorhabditis elegans has a single neuroligin gene (nlg-1)

  and approximately a sixth of C. elegans neurons

  including some sensory neurons

  interneurons and a subset of cholinergic motor neurons

  express a neuroligin transcriptional reporter. Neuroligin-deficient mutants of C. elegans are viable

  and they do not appear deficient in any major motor functions. However

  neuroligin mutants are defective in a subset of sensory behaviors and sensory processing

  and are hypersensitive to oxidative stress and mercury compounds; the behavioral deficits are strikingly similar to traits frequently associated with autism spectrum disorders. Our results suggest a possible link between genetic defects in synapse formation or function

  and sensitivity to environmental factors in the development of autism spectrum disorders.

  Neuroligin-deficient mutants of C. elegans have sensory processing deficits and are hypersensitive to oxidative stress and mercury toxicity.

  Charles Stewart

  Heather Rice

  Min Qi

  Quentin N Pye

  Tamara Potapova

  Kim Nguyen

  Shenyun Mou

  Molina Mhatre

  Haitham Abdel-Moaty

  Kenneth Hensley

  Detailed study of glial inflammation has been hindered by lack of cell culture systems that spontaneously demonstrate the \"neuroinflammatory phenotype\". Mice expressing a glycine → alanine substitution in cytosolic Cu

  Zn-superoxide dismutase (G93A-SOD1) associated with familial amyotrophic lateral sclerosis (ALS) demonstrate age-dependent neuroinflammation associated with broad-spectrum cytokine

  eicosanoid and oxidant production. In order to more precisely study the cellular mechanisms underlying glial activation in the G93A-SOD1 mouse

  primary astrocytes were cultured from 7 day mouse neonates. At this age

  G93A-SOD1 mice demonstrated no in vivo hallmarks of neuroinflammation. Nonetheless astrocytes cultured from G93A-SOD1 (but not wild-type human SOD1-expressing) transgenic mouse pups demonstrated a significant elevation in either the basal or the tumor necrosis alpha (TNFα)-stimulated levels of proinflammatory eicosanoids prostaglandin E2 (PGE2) and leukotriene B4 (LTB4); inducible nitric oxide synthase (iNOS) and •NO (indexed by nitrite release into the culture medium); and protein carbonyl products. Specific cytokine- and TNFα death-receptor-associated components were similarly upregulated in cultured G93A-SOD1 cells as assessed by multiprobe ribonuclease protection assays (RPAs) for their mRNA transcripts. Thus

  endogenous glial expression of G93A-SOD1 produces a metastable condition in which glia are more prone to enter an activated neuroinflammatory state associated with broad-spectrum increased production of paracrine-acting substances. These findings support a role for active glial involvement in ALS and may provide a useful cell culture tool for the study of glial inflammation.

  Primary glia expressing the G93A-SOD1 mutation present a neuroinflammatory phenotype and provide a cellular system for studies of glial inflammation.

  Rand JB

  Crowell JA

  Osborne JD

  Grundahl K

  Duke A

  Frisby DL

  Vu MH

  Mathews EA

  Mullen GP

  The cho-1 gene in Caenorhabditis elegans encodes a high-affinity plasma-membrane choline transporter believed to be rate limiting for acetylcholine (ACh) synthesis in cholinergic nerve terminals. We found that CHO-1 is expressed in most

  but not all cholinergic neurons in C. elegans. cho-1 null mutants are viable and exhibit mild deficits in cholinergic behavior; they are slightly resistant to the acetylcholinesterase inhibitor aldicarb

  and they exhibit reduced swimming rates in liquid. cho-1 mutants also fail to sustain swimming behavior; over a 33-min time course

  cho-1 mutants slow down or stop swimming

  whereas wild-type animals sustain the initial rate of swimming over the duration of the experiment. A functional CHO-1GFP fusion protein rescues these cho-1 mutant phenotypes and is enriched at cholinergic synapses. Although cho-1 mutants clearly exhibit defects in cholinergic behaviors

  the loss of cho-1 function has surprisingly mild effects on cholinergic neurotransmission. However

  reducing endogenous choline synthesis strongly enhances the phenotype of cho-1 mutants

  giving rise to a synthetic uncoordinated phenotype. Our results indicate that both choline transport and de novo synthesis provide choline for ACh synthesis in C. elegans cholinergic neurons

  Choline transport and de novo choline synthesis support acetylcholine biosynthesis in Caenorhabditis elegans cholinergic neurons

  Esmon CT

  Esmon NL

  Lupu F

  Ferrell GL

  Gu J

  Zheng X

  Li W

  Previous studies have shown that blocking endothelial protein C receptor (EPCR)-protein C interaction results in about an 88% decrease in circulating activated protein C (APC) levels generated in response to thrombin infusion and exacerbates the response to Escherichia coli. To determine whether higher levels of EPCR expression on endothelial cells might further enhance the activation of protein C and protect the host during septicemia

  we generated a transgenic mouse (Tie2-EPCR) line which placed the expression of EPCR under the control of the Tie2 promoter. The mice express abundant EPCR on endothelial cells not only on large vessels

  but also on capillaries where EPCR is generally low. Tie2-EPCR mice show higher levels of circulating APC after thrombin infusion. Upon infusion with factor Xa and phospholipids

  Tie2-EPCR mice generate more APC

  less thrombin and are protected from fibrin/ogen deposition compared with wild type controls. The Tie2-EPCR animals also generate more APC upon lipopolysaccharide (LPS) challenge and have a survival advantage. These results reveal that overexpression of EPCR can protect animals against thrombotic or septic challenge.

  Overexpressing endothelial cell protein C receptor alters the hemostatic balance and protects mice from endotoxin

  Neuroligin and neurexin are cell adhesion molecules that are sufficient to induce synaptogenesis in cultured mammalian cells (Fu et al.

  2003; Nam et al.

  2005). Mutations in neuroligin are associated with a subset of cases of the developmental disorder autism (Jamain et al.

  2003). We have tested transcriptional fusion constructs using the nlg-1 regulatory sequences to drive the expression of a YFP reporter. We found that YFP expression is limited to neurons in the head

  ventral nerve cord and tail. In double reporter studies

  GABAergic neurons do not express nlg-1. Instead

  nlg-1 is expressed in a portion of cholinergic cells

  particularly in the ventral nerve cord. In addition

  many of the nlg-1 positive cells in the head are neither cholinergic nor GABAergic. Surprisingly

  neuroligin knockout animals do not exhibit obvious cholinergic defects. Instead

  they exhibit phenotypes that are similar to those of an AMPA type glutamate receptor (glr-1) knockout. The neuroligin expressing cholinergic neurons also express glr-1 glutamate receptors

  and receive input from putative glutamate-releasing interneurons. Neuroligin knockout worms have a lower frequency of spontaneous reversal

  although when these worms do reverse

  the reversal is of the same duration as wildtype worms. This phenotype is similar to that of glr-1 mutants. Another behavioral phenotype of neuroligin knockout mutants is a defect in thermotaxis. Well fed wildtype worms placed on a thermal gradient preferentially track to the temperature at which they were raised. The nlg-1 and glr-1 knockout animals do not accumulate at a specific temperature; instead

  these worms move independently of ambient temperature. Our working hypothesis is that neuroligin is required for proper localization of glr-1. We are testing this hypothesis by introducing a glr-1::GFP functional fusion into a neuroligin knockout background to assess the effect of nlg-1 on glr-1::GFP localization.\n

  Neuroligin Is Widely Expressed In The C. elegans Nervous System

  And May Effect Glutamate Receptor Localization

  https://sites.google.com/site/drjerrodhunter/\nThis is a portal website for all of my online content.

  Hunter

  Jerrod

  Gettysburg College

  University of Richmond

  J. Sargeant Reynolds Community College

  Oklahoma Medical Research Foundation

  University of Oklahoma

  US Navy

  Oklahoma School of Science and Math

  University of Oklahoma Health Sciences Center

  ECPI University

  Oklahoma Medical Research Foundation

  Designing experiments

  performing experiments and interpreting results. Maintaining lab equipment

  reagents and laboratory animals. PCR

  molecular cloning

  ELISA

  microscopy and imaging

  genetics

  behavioral analysis antibody production.

  Oklahoma Medical Research Foundation

  Biology Professor

  I teach vertebrate and invertebrate biology to gifted high school juniors and seniors.\nI try to instill an appreciation for biology

  promote intellectual engagement with biology and help students become discerning observers of the world around them as a neurobiology instructor. I develop curricula

  lesson plans and tests while maintaining alignment throughout (Sometimes on vary short notice) including genetics

  neurobiology and zoology classes.\nI instruct

  motivate and inspire students

  Oklahoma School of Science and Math

  University of Richmond

  I teach Cell Biology and Genetics. I use an active learning approach to help learners develop knowledge and acumen in the methods and thought processes employed in modern biology and bio-medical research laboratories.

  Visiting Biology Lecturer

  Richmond

  Virginia Area

  Gettysburg PA

  Visiting Assistant Professor

  Gettysburg College

  Insured personnel and reactor safety as a Lead Engineering Laboratory Technician. Provided daily operational review/quality control of education accountability as it relates to imposed government regulatory requirements in a nuclear environment. Supervised and trained 115 men in regulatory compliance. Supervised six men in documentation of regulatory compliance

  US Navy

  Graduate student

  Expanded knowledge of synaptogenesis\nDesigning experiments

  performing experiments and interpreting results. Maintaining lab equipment

  reagents and laboratory animals. PCR

  molecular cloning

  ELISA

  microscopy and imaging

  genetics

  behavioral analysis.

  University of Oklahoma Health Sciences Center

  Adjunct Professor of Neurobiology

  I teach neurobiology to upper division undergraduates and graduate students.I try to instill an appreciation for biology

  promote intellectual engagement with biology and help students become discerning observers of the world around them as a neurobiology instructor.

  University of Oklahoma

  ECPI University

  Newport News

  Anatomy and Physiology

  Biology Instructor

  Richmond

  Virginia Area

  I teach Biology and Anatomy and Physiology. I use an active learning approach to help learners develop knowledge and acumen in the methods and thought processes employed in modern biology. I try to instill an appreciation for biology

  promote intellectual engagement with biology and help students become discerning observers of the world around them. I try to instruct

  motivate and inspire students

  Assistant Professor

  J. Sargeant Reynolds Community College

  Expand knowledge of synaptogenesis \nDesigning experiments

  performing experiments and interpreting results. Maintaining lab equipment

  reagents and laboratory animals. PCR

  molecular cloning

  ELISA

  microscopy and imaging

  genetics

  behavioral analysis

  Oklahoma Medical Research Foundation