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High-probability grants
According to our matching algorithm, Peter G. Fuerst is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2010 — 2014 |
Fuerst, Peter Gerard |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Role of Molecular Recognition in Retinal Patterning and Synaptic Organization
DESCRIPTION (provided by applicant): Candidate and Environment: Dr. Peter Fuerst will conduct the research contained within this proposal at Washington State University. Washington State University is an ideal environment in which to conduct advanced biomedical research using mouse models and in which to advance a research program. Research Proposal: The research we propose will use mouse models to identify the molecular mechanisms underpinning development of the retina. The mouse models, all developed by the applicant, include a conditional allele of the Down syndrome cell adhesion molecule, Dscam, as well as an allelic series of mouse mutant Dscam strains and a null allele of the Dscam homologue Dscam-like1 (Dscaml1). Dscam and Dscam- Like1 are essential for normal development of the nervous system and Dscam is proposed to contribute to the pathology of Down syndrome. In the retina, Dscam is required for soma mosaic spacing, regulation of cell number and neurite arborization and lamination. Our published results concerning Dscam and Dscaml1 are the first demonstrations of mutations found to ablate mosaic patterning and the first genes shown to mediate isoneuronal and heteroneuronal repulsion in vertebrates. Specific Aims: We propose to use the Dscam and Dscaml1 mutant mouse models to discover mechanisms underpinning development of the retina and to probe the function of Dscam in the mammalian nervous system. This will be accomplished by testing the following hypotheses detailed in this research proposal. Hypotheses: 1) We will test the hypothesis that DSCAM mediates multiple distinct functions using an allelic series and conditional allele of Dscam mouse mutant lines to genetically and temporally isolate Dscam-dependent developmental processes. 2) We will test the hypothesis that DSCAM mediates adhesion between cell types and repulsion within cell types and that DSCAM activity in the retina is mediated by homophillic interactions and not by a ligand-receptor mechanism by using a conditional allele coupled to cell type specific deletion. 3) We will test the hypothesis that Dscam and Dscaml1 regulate normal developmental cell death. Long-term goals: This research will uncover fundamental aspects of neural organization and provide the funding necessary for Dr. Fuerst to establish a successful academic career focused on hypothesis driven biomedical research. Significance: Neurite arborization, regulation of cell number and soma mosaic spacing are fundamental aspects of neurodevelopment that are not currently well understood at the molecular level in vertebrates. Our preliminary research indicates that DSCAM plays a vital role in mediating these processes in the mammalian nervous system. Identifying mechanisms by which DSCAM functions using a series of mouse mutant alleles and a conditional allele will contribute to our understanding of nervous system development and the causation of disorders associated with neural dysgenesis and also contribute valuable research models to the neuroscience community. PUBLIC HEALTH RELEVANCE: The primary goal of the proposed work is to understand how molecular recognition cues facilitate neural patterning. Research will focus on discovering the mechanisms by which two recognition cues;the Down Syndrome Cell Adhesion Molecule (Dscam) and its homologue Dscam-like1 (Dscaml1), mediate circuit formation within the retina. Both Dscam and Dscaml1 are required for neurite lamination, neurite arborization and regulation of cell number. Therefore, understanding the mechanism by which these molecules function will advance scientific understanding of neural development on multiple fronts. Furthermore, decreasing Dscam dosage decreases the incidence of retinal developmental cell death suggesting that the retina may provide an excellent system in which to model enhanced developmental cell death of neurons that occurs in Down syndrome patients, who overexpress Dscam as a result of Chromosome 21 trisomy.
|
0.955 |
2017 — 2018 |
Borghuis, Bart Gerard (co-PI) [⬀] Fuerst, Peter Gerard |
R21Activity Code Description: To encourage the development of new research activities in categorical program areas. (Support generally is restricted in level of support and in time.) |
Off Bipolar Cell Receptive Field Development and Plasticity
Candidates and Environment: Dr. Fuerst will conduct anatomical, genetic and morphological experiments related to Aims 1 and 2 at the University of Idaho. Dr. Fuerst's expertise is centered in developmental biology and genetics of retinal development. Fuerst identified the first molecules that regulate retinal mosaics and developed the genetic reagents for use in these experiments. Dr. Borghuis will carry out the electrophysiological and 2-photon fluorescence imaging experiments of Aims 1 and 2 at the University of Louisville. Borghuis discovered that OFF bipolar cells primarily utilize kainate type glutamate receptors and developed the iGluSnFR method to monitor bipolar cell synaptic output. Dr. Borghuis has also developed the computational tools for analyzing imaging data, an established strength of his lab. Research Proposal: Developing neurons readily extend axons and dendrites and make novel synaptic connections, but this ability is severely limited in the adult brain. In our preliminary studies we find evidence that synaptogenesis by retinal bipolar cells is controlled by regulating axons and dendrite growth: while new synapses appear to form, they are restricted to the territory occupied by the bipolar cells' axons and dendrites. We have identified two genes that regulate bipolar cell axonal and dendritic arbor tiling, the Down syndrome cell adhesion molecule (Dscam) and Bcl-2 associated X protein (BAX). Deletion of either gene results in continuous growth and overlap of the axonal and dendritic arbors of OFF bipolar cells. Based on the continuous ability of OFF bipolar cells to make novel anatomical contacts in the wild type retina, and their ability to connect with previously untargeted cells in the Dscam and Bax null retinas, we hypothesize that activating axon and dendrite outgrowth in OFF bipolar cells is sufficient to induce synaptogenesis with targets that would not otherwise be contacted. We test this hypothesis in two specific Aims. Aim 1: we will map normal connectivity patterns of OFF bipolar cells in the developing and aging wild type retina and measure how histological changes during OFF bipolar cell synapse maturation and aging impact functional synaptic connectivity. Aim 2: we will inducibly delete Dscam in adult mice using the Cre:ER system to test if activating dendrite and axon outgrowth in a retina that developed normally is sufficient to induce synaptogenesis. We will determine if the expanding axonal and dendritic arbors that are observed Dscam or Bax null mice establish functional synapses using electrophysiology and 2-photon glutamate imaging. Long-term goals: Our long-term goal is to understand how to activate adult neurons to make novel synapses for use in human therapies. Significance: Understanding why adult mammalian neurons lose the ability to make novel synapses is important because reactivating adult neurons to make new synaptic connections will be critical for regeneration and repair in neurological disease. We will test if activation of dendrite and axon outgrowth is sufficient for OFF bipolar cells to establish synaptic connections with targets they would not otherwise encounter.
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0.955 |