Synthetic Lethality of Retinoblastoma Mutant Cells in the Drosophila Eye by Mutation of a Novel Peptidyl Prolyl Isomerase Gene

Mutations that inactivate the retinoblastoma (Rb) pathway are common in human tumors. Such mutations promote tumor growth by deregulating the G1 cell cycle checkpoint. However, uncontrolled cell cycle progression can also produce new liabilities for cell survival. To uncover such liabilities in Rb m...

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Bibliographic Details
Published in:Genetics (Austin) 2005-05, Vol.170 (1), p.161-171
Main Authors: Edgar, Kyle A, Belvin, Marcia, Parks, Annette L, Whittaker, Kellie, Mahoney, Matt B, Nicoll, Monique, Park, Christopher C, Winter, Christopher G, Chen, Feng, Lickteig, Kim, Ahmad, Ferhad, Esengil, Hanife, Lorenzi, Matthew V, Norton, Amanda, Rupnow, Brent A, Shayesteh, Laleh, Tabios, Mariano, Young, Lynn M, Carroll, Pamela M, Kopczynski, Casey, Plowman, Gregory D, Friedman, Lori S, Francis-Lang, Helen L
Format: Article
Language:English
Subjects:
Amino Acid Sequence
Animals
Cancer
Cell cycle
Drosophila
Drosophila melanogaster - embryology
Drosophila melanogaster - enzymology
Drosophila melanogaster - genetics
Eye - embryology
Eye - enzymology
Genetics
Investigations
Molecular Sequence Data
Mutation
Peptidylprolyl Isomerase - genetics
Retinoblastoma Protein - genetics
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Summary:Mutations that inactivate the retinoblastoma (Rb) pathway are common in human tumors. Such mutations promote tumor growth by deregulating the G1 cell cycle checkpoint. However, uncontrolled cell cycle progression can also produce new liabilities for cell survival. To uncover such liabilities in Rb mutant cells, we performed a clonal screen in the Drosophila eye to identify second-site mutations that eliminate Rbf(-) cells, but allow Rbf(+) cells to survive. Here we report the identification of a mutation in a novel highly conserved peptidyl prolyl isomerase (PPIase) that selectively eliminates Rbf(-) cells from the Drosophila eye.
ISSN:0016-6731
1943-2631
1943-2631
DOI:10.1534/genetics.104.036343