You are here

FAU Collections » FAU Research Repository » FAU College Collections » Harriet L. Wilkes Honors College » Honors Student Theses

Devising a noncancerous model system to study multipolar spindle formation

Download pdf | Full Screen View

Date Issued:
2010
Summary:
Aneuploid tumor cells have characteristically unstable genomes which can be caused by mitotic defects such as multipolar spindles. Multipolarity relies upon the presence of extra centrosomes to form. However, some cells, both cancerous and noncancerous are able to avoid the formation of multipolar spindles through centrosomal clustering. Previous research has shown that there are a large number of genes whose activity contributes to the clustering activity, making analysis of individual components of the process difficult. In order to better understand centrosomal clustering in cancer cells, we induced supernumerary centrosomes in a genomically normal cell line, RPE, to observe how the normal cells cope with extra centrosomes. Using colcemid to induce extra centrosomes in the RPE cell line, we observed an intact clustering mechanism in fixed cells. Further manipulation of the cells has allowed us to induce multipolarity in this cell line using various disrupters of cell-cycle checkpoint and dynein function.
Title: Devising a noncancerous model system to study multipolar spindle formation.
116 views
31 downloads
Name(s): Nagarsheth, Nisha.
Harriet L. Wilkes Honors College
Type of Resource: text
Genre: Thesis
Issuance: multipart monograph
Date Issued: 2010
Publisher: Florida Atlantic University
Physical Form: electronic resource
Extent: vii, 21 p. : ill. (some col.)
Language(s): English
Summary: Aneuploid tumor cells have characteristically unstable genomes which can be caused by mitotic defects such as multipolar spindles. Multipolarity relies upon the presence of extra centrosomes to form. However, some cells, both cancerous and noncancerous are able to avoid the formation of multipolar spindles through centrosomal clustering. Previous research has shown that there are a large number of genes whose activity contributes to the clustering activity, making analysis of individual components of the process difficult. In order to better understand centrosomal clustering in cancer cells, we induced supernumerary centrosomes in a genomically normal cell line, RPE, to observe how the normal cells cope with extra centrosomes. Using colcemid to induce extra centrosomes in the RPE cell line, we observed an intact clustering mechanism in fixed cells. Further manipulation of the cells has allowed us to induce multipolarity in this cell line using various disrupters of cell-cycle checkpoint and dynein function.
Identifier: 779480861 (oclc), 3335107 (digitool), FADT3335107 (IID), fau:1405 (fedora)
Note(s): by Nisha Nagarsheth.
Thesis (B.A.)--Florida Atlantic University, Honors College, 2010.
Includes bibliography.
Electronic reproduction. Boca Raton, Fla., 2010. Mode of access: World Wide Web.
Subject(s): Centrosomes -- Research
Cancer -- Genetic aspects
Cellular signal transduction
Cell division
Held by: FBoU FAUER
Persistent Link to This Record: http://purl.flvc.org/FAU/3335107
Use and Reproduction: Copyright © is held by the author, with permission granted to Florida Atlantic University to digitize, archive and distribute this item for non-profit research and educational purposes. Any reuse of this item in excess of fair use or other copyright exemptions requires permission of the copyright holder.
Host Institution: FAU

In Collections