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High-probability grants
According to our matching algorithm, Rayla Greenberg Temin is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
1994 — 1999 |
Ganetzky, Barry [⬀] Temin, Rayla |
N/AActivity Code Description: No activity code was retrieved: click on the grant title for more information |
Genetics of Segregation Distortion in Drosophila @ University of Wisconsin-Madison
9408473 Abstract The long term goal of these studies is to elucidate the genetic and molecular structure of segregation distortion (SD) chromosomes, their mechanism of action and their evolutionary origin. The immediate aims are to (1) molecularly characterize Sd and its products, (2) isolate and analyze null mutations of Sd+, (3) cytogenetically enolase M(SD), an upward modifier of distortion and Su(SD), a strong X-linked suppressor of distortion. %%% Segregation Distorter (SD) is a naturally occurring meiotic drive system on the second chromosome of Drosophila melanogaster with the property that heterozygous SD/SD+ males transmit the SD chromosome to their offspring in vast excess over the normal homolog. The basis of this distorted transmission is the dysfunction of spermatids that receive the SD+ chromosome. Dysfunction of these spermatids is associated with a failure of chromatin condensation in the nuclei but the underlying molecular mechanisms are unknown. The long term goal of these studies is to elucidate the genetic and molecular structure of SD chromosomes. ***
|
0.915 |
1999 — 2004 |
Ganetzky, Barry [⬀] Temin, Rayla |
N/AActivity Code Description: No activity code was retrieved: click on the grant title for more information |
Genetic and Molecular Studies of Segregation Distortion in Drosophila @ University of Wisconsin-Madison
Segregation Distorter (SD) is a naturally occurring meiotic drive system on the second chromosome of Drosophila melanogaster with the property that heterozygous SD/SD+ males transmit the SD chromosome to their offspring in vast excess over the normal homolog. The basis of this distorted transmission is the dysfunction of spermatids that receive the SD+ chromosome. Dysfunction of these spermatids is associated with a failure of chromatin condensation. The SD system comprises a collection of genetic elements that act in concert to cause distortion. These loci include: Sd, E(SD), M(SD), St(SD) and Rsp.Sd is the gene primarily responsible for distortion; E(SD), M(SD) and St(SD) are strong upwards modifiers of distortion; and Rsp is the target site at which Sd and the modifiers act. SD chromosomes carry an insensitiveRsp allele whereas SD+ homologs whose transmission is affected carry a sensitive Rsp. The sd locus has been demonstrated to encode a truncated version of the nuclear transport protein, RanGAP. However, the mechanism by which this altered protein causes selective sperm dysfunction is unknown. It is hypothesized that the mutant protein has an aberrant location inside the nucleus rather than outside which could disrupt nuclear import and export leading ultimately to failure of chromatin condensation and sperm dysfunction. To explore this model the developmental changes that occur in nuclear morphology during spermatogenesis in normal and distorting males will be determined, the subcellular distribution and localization of wildtype and mutant RanGAP during spermatogenesis in distorting and non-distorting backgrounds will be characterized and the nuclear vs cytoplasmic distribution of GFP reporter constructs containing nuclear import and export signals will be observed in order to test the hypothesis that nuclear transport is defective. M(SD) and Su(SD) will be studied. Identification of the proteins encoded by these genes and a determination of their cytological location will be the initial steps in an attempt to understand their suppressor effects. Identification of the Sd gene product as a mutant RanGAP raises questions about the role in distortion of other components of the Ran system and thus, the consequences on distortion of overexpressing wildtype or dominant negative forms of Ran and RanGEF in the male germline will be explored.
Analysis of SD is significant because it represents a striking exception to the fundamental principles of genetic transmission and population genetics and may therefore provide insights into the mechanisms that normally ensure the fidelity of these processes, the perturbations that can affect these mechanisms, and the consequence of such perturbations. Furthermore, SD appears to involve disruption of basic biological processes such as spermatogenesis and the regulation of chromatin structure and function and can thus be informative about their genetic control.
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0.915 |