Other Publications (8)
- Brain Research
- Development Genes and Evolution
- Mechanisms of Development
- Journal of Undergraduate Neuroscience Education : JUNE : a Publication of FUN, Faculty for Undergraduate Neuroscience
- CBE Life Sciences Education
- Journal of Esthetic and Restorative Dentistry : Official Publication of the American Academy of Esthetic Dentistry ... [et Al.]
- Bulletin of Environmental Contamination and Toxicology
Articles by Kathleen M. Raley-Susman in JoVE
Fourier-Based Diffraction Analysis of Live Caenorhabditis elegans Jenny Magnes1, Harold M. Hastings2, Kathleen M. Raley-Susman3, Clara Alivisatos1, Adam Warner1, Miranda Hulsey-Vincent1 1Physics and Astronomy Department, Vassar College, 2 This manuscript describes how to distinguish different nematodes using far-field diffraction signatures. We compare the locomotion of 139 wild type and 108 "Roller" C. elegans by averaging frequencies associated with the temporal Fraunhofer diffraction signature at a single location using a continuous wave laser.
Other articles by Kathleen M. Raley-Susman on PubMed
Microtubule-associated Protein 2 (MAP2) Associates with the NMDA Receptor and is Spatially Redistributed Within Rat Hippocampal Neurons After Oxygen-glucose Deprivation Brain Research. Jul, 2003 | Pubmed ID: 12834896 MAP2 (microtubule-associated protein 2) is a cytoskeletal phosphoprotein that regulates the dynamic assembly characteristics of microtubules and appears to provide scaffolding for organelle distribution into the dendrites and for the localization of signal transduction apparatus in dendrites, particularly near spines. MAP2 is degraded after ischemia and other metabolic insults, but the time course and initial triggers of that breakdown are not fully understood. This study determined that MAP2 resides in a complex with the NMDA receptor, suggesting that spatially localized changes may be important in the mechanism of MAP2 redistribution and breakdown after oxygen-glucose deprivation (OGD). Using OGD in the adult rat hippocampal slice as a model system, this study demonstrated that MAP2 breakdown occurs very early after OGD, with the first statistical decrease in MAP2 levels within the first 30 min after the insult. There is a dramatic redistribution of MAP2 to the somata of pyramidal neurons, particularly neurons at the CA1-subiculum border. Free radicals and nitric oxide are not involved in the damage to MAP2. NMDA-receptor activation plays a prominent role in the MAP2 breakdown. In direct response to NMDA receptor activation, calcium influx, likely through the receptor ion channel complex, as well as release of calcium from the mitochondria through activation of the 2Na(+)-Ca(2+) exchanger of mitochondria, triggers MAP2 degradation. The proteolysis of MAP2 is limited by endogenous calpain activity, likely via the spatial access of calpain to MAP2.
The Invertebrate Microtubule-associated Protein PTL-1 Functions in Mechanosensation and Development in Caenorhabditis Elegans Development Genes and Evolution. Oct, 2008 | Pubmed ID: 18807071 PTL-1, a microtubule-associated protein of the structural MAP2/tau family, is the sole member of this gene family in Caenorhabditis elegans. Sequence analysis of available invertebrate genomes revealed a number of single, putative tau-like genes with high similarity to ptl-1. The ptl-1 gene is expressed in a number of cells, most notably mechanosensory neurons. We examined the role of ptl-1 in C. elegans in adult neurons as well as during development. A ptl-1 knockout strain of worms exhibited an egg-hatching defect, as well as a reduced sensitivity to touch stimuli. In addition, the knockout allele ptl-1(ok621) acts as a dominant enhancer of several temperature-sensitive alleles of mec-7 and mec-12, which code the isoforms of beta-tubulin and alpha-tubulin that together form the unusual 15 protofilament microtubules involved in touch sensation. These results demonstrate for the first time a functional role for this microtubule-associated protein in nematodes and suggest that PTL-1 is involved in mechanosensation as well as some aspect of embryogenesis.
Microtubules, the ER and Exu: New Associations Revealed by Analysis of Mini Spindles Mutations Mechanisms of Development. May-Jun, 2009 | Pubmed ID: 19303437 During Drosophila oogenesis, organized microtubule networks coordinate the localization of specific RNAs, the positioning of the oocyte nucleus, and ooplasmic streaming events. We used mutations in mini spindles (msps), a microtubule-associated protein, to disrupt microtubule function during mid- and late-oogenesis, and show that msps is required for these microtubule-based events. Since endoplasmic reticulum (ER) organization is influenced by microtubules in other systems, we hypothesized that using msps to alter microtubule dynamics might affect the structure and organization of the ER in nurse cells and the oocyte. ER organization was monitored using GFP-tagged versions of Reticulon-like1 and protein disulfide isomerase. Analyses of living cells indicate microtubule associations mediate the movement of ER components within the oocyte. Surprisingly, the distribution and behavior of tubular ER in the oocyte differs from general ER, suggesting these two compartments of the ER interact differently with microtubules. We find that the morphology of Exu particles is msps-dependent, and that Exu is specifically associated with tubular ER in msps mutants. Our results extend previous descriptions of sponge bodies and the fusome, suggesting both are manifestations of a dynamic structure that interacts with microtubules and persists throughout oogenesis.
Exploration of Gerontogenes in the Nervous System: a Multi-level Neurogenomics Laboratory Module for an Intermediate Neuroscience and Behavior Course Journal of Undergraduate Neuroscience Education : JUNE : a Publication of FUN, Faculty for Undergraduate Neuroscience. 2010 | Pubmed ID: 23493645 In this paper, we describe and assess a laboratory module that we introduced into an intermediate-level undergraduate course in Neuroscience and Behavior (NEUR201) in order to expose students to the new and rapidly developing neurogenomic and bioinformatics approaches to neuroscience research. The laboratory accompanies a topics-based, highly process-oriented course that explores research methodologies and integrative approaches to particular topics in the field. The laboratory comprises multi-week modules that expand upon the topics being covered in class. In the class for which this module was developed, a key topic under discussion is the role played by the nervous system in aging and/or lifespan. This laboratory module focuses on the model organism, Caenorhabditis elegans (C. elegans), which has been studied extensively. There is a large and ongoing literature elucidating a number of genes involved in determining or modulating lifespan in C. elegans. Students choose a candidate gerontogene expressed in neurons in C. elegans from a provided list for which we have mutant strains. Students use available databases to become experts on their candidate gene and design, carry out and analyze a behavioral experiment. In addition, students use available bioinformatics and genomic tools to conduct a protein sequence phylogenetic analysis of their candidate protein across at least 10 different taxa of animals. The laboratory module thus focuses on the integration of behavioral, genetic and bioinformatics approaches, as well as on the evolutionary considerations of the role played by gerontogenes in different organisms.
Mancozeb-induced Behavioral Deficits Precede Structural Neural Degeneration Neurotoxicology. Jan, 2013 | Pubmed ID: 23103283 Manganese-containing fungicides like Mancozeb have been associated with neurodegenerative conditions like Parkinson's disease. We examined the behavioral damage and differential neuronal vulnerability resulting from Mancozeb exposure using Caenorhabditis elegans, an important mid-trophic level soil organism that is also a powerful model for studying mechanisms of environmental pollutant-induced neurodegenerative disease. The dopamine-mediated swim to crawl locomotory transition behavior is exquisitely vulnerable to Mancozeb, with functional impairment preceding markers of neuronal structural damage. The damage is partially rescued in mutants lacking the divalent metal transporter, SMF-1, demonstrating that some, but not all, of the damage is mediated by manganese. Increasing concentrations of Mancozeb recruit additional behavioral dysfunction, notably serotonin-mediated egg-laying behavior, but without evident serotonergic neuronal structural damage. Thus, measurements of behavioral dysfunction are a sensitive early marker of fungicide toxicity that could be exploited to examine further mechanisms of neuron damage and possible therapeutic interventions. These results also provide important insight into the consequences of fungicide use on the ecological behavior of nematodes.
Preferences of Lay Persons and Dental Professionals Regarding the Recurring Esthetic Dental Proportion Journal of Esthetic and Restorative Dentistry : Official Publication of the American Academy of Esthetic Dentistry ... [et Al.]. Mar-Apr, 2016 | Pubmed ID: 26880426 This study evaluated the preferences of dental professionals and lay persons with respect to the Recurring Esthetic Dental (RED) Proportion, an objective mathematical tool used in treatment planning the "apparent" widths of maxillary anterior teeth.
Chronic Exposure to Perfluorooctane Sulfonate Reduces Lifespan of Caenorhabditis Elegans Through Insulin/IGF-1 Signaling Bulletin of Environmental Contamination and Toxicology. Jul, 2016 | Pubmed ID: 27095033 Perfluorooctane sulfonate (PFOS) is a persistent organic pollutant. Although multiple adverse effects of PFOS have been demonstrated, whether PFOS can accelerate aging and affect animal longevity remains unknown. In Caenorhabditis elegans, we found that a 50 h exposure to 0.2-200 µM PFOS reduced lifespan in a concentration dependent manner. In transgenic nematodes, lifespans are affected by mutations of daf-16, daf-2 or age-1 genes, which are related to the Insulin/IGF-1 Signaling pathway (IIS). PFOS exposure caused an additional reduction in average lifespan in daf-2(e1370) and daf-16b(KO) nematodes. In contrast, daf-16(mu86) nematodes showed no additional reduction with PFOS exposure and age-1(hx546) mutants did not exhibit a reduction in lifespan with PFOS exposure, compared with wildtype nematodes. Overall, our findings demonstrate that PFOS exposure accelerates aging and shortens longevity of animals. The PFOS-induced effect may involve genes of the IIS pathway, particularly daf-16 and age-1.