J. Sargeant Reynolds Community College - Biology
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)
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