Area:
Drosophila Neurobiology
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High-probability grants
According to our matching algorithm, Thomas L. Schwarz is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
1989 — 1991 |
Schwarz, Thomas L. |
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. |
Localization and Structure of a Cloned K+ Channel
K+ channels are essential for nerve, muscle, endocrine, and immune cells. An understanding of these channels is vital for understanding the basic properties of electrically excitable cells and for understanding the manner in which those properties are varied to give a cell its individual character. The regulation of K+ channels has been shown to be a mechanism by which the plasticity underlying simple forms of learning can take place. The biochemical study of these channels has recently been facilitated by the cloning of the Shaker locus of Drosophila melanogaster. This gene, through alternative splicing of mRNA, gives rise to a family of proteins that can form K+ channels of the type known as A-channels. This application proposes a continuation of that research and will be directed to two questions about the Shaker products. 1) How are different subtypes of a channel distributed within an organism and within a single neuron in order to produce the appropriate physiological properties of a cell? Antibodies to common regions and to sequences that characterize particular splicing variants will be used for immunocytochemistry. Do these variants have s differential tissue distribution? Are variants targeted to particular subcellular locations such as terminals, axons, or post-synaptic membranes? 2) What structural properties of an ion channel permit ions to cross the membrane and account for the selectivity of the channel for a particular species of ion? By mutating particular residues of the cloned gene and expressing the mutant channels in oocytes we will ask how these changes influence function. A region whose sequence suggests that it may line the pore of the channel will be targeted. Can alterations within this region alter permeation or the selectivity of the channel for potassium? Together, these studies aim to elucidate the cell biology of an important class of channels and the mechanism by which these channels work.
|
0.964 |
1992 — 2003 |
Schwarz, Thomas L. |
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. |
Structure, Localization and Cloning of Channels |
0.964 |
1996 — 2000 |
Schwarz, Thomas L. |
P50Activity Code Description: To support any part of the full range of research and development from very basic to clinical; may involve ancillary supportive activities such as protracted patient care necessary to the primary research or R&D effort. The spectrum of activities comprises a multidisciplinary attack on a specific disease entity or biomedical problem area. These grants differ from program project grants in that they are usually developed in response to an announcement of the programmatic needs of an Institute or Division and subsequently receive continuous attention from its staff. Centers may also serve as regional or national resources for special research purposes. |
Genetic Dissection of Transmitter Release
Learning and memory are likely to involve changes in the efficacy of synaptic transmission. In many cases, these changes are thought to involve modulation of the mechanism by which transmitter is released from the nerve terminal. This proposal attempts to illuminate some of the fundamental cellular mechanisms by which synapses release transmitter, on the presumption that understanding these mechanisms is a precondition to fully understanding how release is altered by learning or by disease states. The approach of this proposal is to use Drosophila genetics to explore two proteins appear to be central to this process: synaptotagmin and synaprobrevin. Both proteins are on synaptic vesicles and Drosophila mutations have been isolated in both genes. Mutations will be characterized by a combination of electrophysiology, electron microscopy, and the use of a fluorescent dye to monitor membrane trafficking. To probe the actions of these proteins more closely, engineered alteration in these proteins will be reintroduced into the mutant files. Drosophila will also be used to screen for novel mutations that may reveal previously unknown components of the synaptic machinery. Specifically, this project will: 1. Create alterations in particular domains of synaptotagmin for biochemical and genetic experiments. 2. By examining the phenotype of these altered synaptotagmins to test the hypotheses that synaptotagmin is the Ca2+ -sensor for triggering vesicle fusion, a regulator of vesicle docking, and involved in vesicle recycling. 3. Use Drosophila that lack synaprobrevin and use cloned genes encoding additional members of the v-SNARE family to identify sequences essential for targeting synaptobrevin to vesicles and targeting vesicles to their appropriate release sites. 4. Use altered synaptobrevins to determining which regions are essential for vesicle fusion with the plasma membrane. 5. Screen for enhancers and suppressors of known synaptic mutations and characterize those mutations. 6. Screen physiologically for mutations in synaptic transmission and characterize those mutations.
|
0.964 |