Synthetic lethality of retinoblastoma mutant cells in the Drosophila eye by mutation of a novel peptidyl prolyl isomerase gene

Genetics. 2005 May;170(1):161-71. doi: 10.1534/genetics.104.036343. Epub 2005 Mar 2.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Drosophila melanogaster / embryology*
  • Drosophila melanogaster / enzymology
  • Drosophila melanogaster / genetics
  • Eye / embryology*
  • Eye / enzymology
  • Molecular Sequence Data
  • Mutation
  • Peptidylprolyl Isomerase / genetics*
  • Retinoblastoma Protein / genetics*


  • Retinoblastoma Protein
  • Peptidylprolyl Isomerase