William G. Wadsworth - US grants
Affiliations: | University of Medicine and Dentistry of New Jersey, Piscataway Township, New Jersey, United States |
Area:
Neuroscience BiologyWe are testing a new system for linking grants to scientists.
The funding information displayed below comes from the NIH Research Portfolio Online Reporting Tools and the NSF Award Database.The grant data on this page is limited to grants awarded in the United States and is thus partial. It can nonetheless be used to understand how funding patterns influence mentorship networks and vice-versa, which has deep implications on how research is done.
You can help! If you notice any innacuracies, please sign in and mark grants as correct or incorrect matches.
High-probability grants
According to our matching algorithm, William G. Wadsworth is the likely recipient of the following grants.| Years | Recipients | Code | Title / Keywords | Matching score |
|---|---|---|---|---|
| 1995 — 1998 | Wadsworth, William G | 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. |
Extracellular Matrix and Axonal Guidance in C Elegans @ Univ of Med/Dent Nj-R W Johnson Med Sch |
0.927 |
| 2000 — 2009 | Wadsworth, William G | 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. R56Activity Code Description: To provide limited interim research support based on the merit of a pending R01 application while applicant gathers additional data to revise a new or competing renewal application. This grant will underwrite highly meritorious applications that if given the opportunity to revise their application could meet IC recommended standards and would be missed opportunities if not funded. Interim funded ends when the applicant succeeds in obtaining an R01 or other competing award built on the R56 grant. These awards are not renewable. |
Extracellular Matrix and Axonal Guidance in C. Elegans @ Univ of Med/Dent Nj-R W Johnson Med Sch DESCRIPTION (provided by applicant): Nervous systems comprise a grid-like network of longitudinal and circumferential nerves. Several molecules have been found that guide circumferential migrations in C. elegans including UNC-6, the founding member of the netrin protein family. Little is known, however, about the molecular mechanisms that govern different responses individual migrating axons have to these guidance cues. These differences are important since they allow a variety of axon migration patterns to develop and a greater number of connections to form. Two approaches are proposed to study the molecular basis of the responses that axons have to guidance cues. First, genes are being identified and studied that affect the guidance of only subsets of circumferentially migrating axons. Specifically, these genes are required for migration patterns that are different from those of other circumferential axons. In one case, a gene has been found that is expressed in only a few neurons and which encodes a conserved cytoplasmic protein. This gene genetically interacts with genes encoding components of known axon guidance signaling pathways and is therefore a strong candidate for regulating neuron-specific axon guidance responses. Second, genetic screens are being used to isolate second site mutations that suppress the phenotypes of specific unc-6 mutations. These unc-6 mutations disrupt UNC-6 structural domains that are responsible for mediating distinct UNC-6 guidance activities. By isolating mutations that can suppress the phenotypes of these unc-6 mutations, proteins that interact with UNC-6 to help mediate the different UNC-6 activities might be identified. In a pilot screen, an extragenic mutation that reverts the uncoordinated movement and axon guidance defects caused by an unc-6 mutation has been recovered. Understanding the molecular mechanisms that control axon and cell guidance could prove critical for developing therapeutic agents that treat nerves damaged by injuries or disease. |
0.927 |
| 2009 — 2013 | Wadsworth, William G | 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. |
Molecular Mechanisms Regulating Axon Guidance Receptor Activity @ Univ of Med/Dent Nj-R W Johnson Med Sch DESCRIPTION (provided by applicant): As the nervous system develops, axons are guided along specific pathways to find their targets and make functional connections. The precise pattern of connections is essential for proper nervous system function. Axon migrations are directed by guidance cues in the extracellular environment. On the surface of migrating axons, receptors detect the cues and produce signals that control cytoskeletal dynamics to direct where an axon extends. Several classes of guidance cues and receptors have been identified, including the UNC-6/netrin cue and the UNC-40/DCC receptor. The molecular mechanisms that determine the directional response when a receptor is ligated by a guidance cue are not well understood. To explore the molecular basis of axon responses, we preformed a genetic screen in C. elegans for mutations that suppress axon guidance defects caused by a specific unc-6 missense allele, rh46. Our results indicate that we uncovered mutations that enhance UNC-40 signaling when UNC-40 is ligated by UNC-6. One mutation is a loss-of-function allele of clec-38, which encodes a protein with a transmembrane and extracellular C-type lectin-like domains. Our preliminary results indicate that clec-38 negatively regulates UNC-40 signaling in several different neurons. In one case, loss of clec- 38 function causes the failure of a neuron cell body to migrate and the precocious UNC-6-dependent formation of its axon. We also uncovered a missense mutation within the unc-40 ectodomain sequence that in combination with unc-6(rh46) causes new axons migration patterns. This response is suppressed when unc- 6(rh46) is replaced with unc-6(rh46ur282) or unc-6(rh46ur301), alleles that have second site mutations that suppress the original rh46 mutation. These intragenic mutations were also recovered from the screen. These observations indicate an interaction between UNC-6 and the UNC-40 ectodomain in vivo and they suggest that the ligated confirmation of the receptor influences the nature of the axon response. We propose to further study the molecular mechanisms through which the UNC-40 signals are regulated. We plan to further characterize CLEC-38, determine other components that regulate UNC- 40 signaling, genetically dissect the signaling which controls the UNC-40 axon response, and extend our genetic screening. PUBLIC HEALTH RELEVANCE: Neurons must make the proper connections in order for a nervous system to function. Understanding the molecular mechanisms that enable molecules to direct neurons to their targets could provide new insights into disorders that affect the wiring of the nervous system and could also prove useful for developing therapeutic agents to treat nerves damaged by injuries or disease. |
0.927 |