Genetic interactions of Drosophila melanogaster arrest reveal roles for translational repressor bruno in accumulation of gurken and activity of delta

Nan Yan, Paul M. Macdonald

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

arrest mutants have pleiotropic phenotypes, ranging from an early arrest of oogenesis to irregular embryonic segmentation defects. One function of arrest is in translational repression of oskar mRNA; this biochemical activity is presumed to be involved in other functions of arrest. To identify genes that could provide insight into how arrest contributes to translational repression or that may be targets for arrest-dependent translational control, we screened deficiency mutants for dominant modification of the arrest phenotype. Only four of the many deficiencies tested, which cover ∼30% of the genome, modified the starting phenotype. One enhancer, identified fortuitously, is the Star gene. Star interaction with arrest results in excess Gurken protein, supporting the model that gurken is a target of repression. Two modifiers were mapped to individual genes. One is Lk6, which encodes a protein kinase predicted to regulate the rate-limiting initiation factor eIF4E. The second is Delta. The interaction between arrest and Delta mimics the phenotype of homozygous Delta mutants, suggesting that arrest could positively control Delta activity. Indeed, arrest mutants have significantly reduced levels of Delta protein at the interface of germline and follicle cells.

Original languageEnglish (US)
Pages (from-to)1433-1442
Number of pages10
JournalGenetics
Volume168
Issue number3
DOIs
StatePublished - Nov 2004

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Drosophila melanogaster
Phenotype
Genes
Oogenesis
Peptide Initiation Factors
Protein Kinases
Genome
Messenger RNA
Proteins

ASJC Scopus subject areas

  • Genetics
  • Genetics(clinical)

Cite this

Genetic interactions of Drosophila melanogaster arrest reveal roles for translational repressor bruno in accumulation of gurken and activity of delta. / Yan, Nan; Macdonald, Paul M.

In: Genetics, Vol. 168, No. 3, 11.2004, p. 1433-1442.

Research output: Contribution to journalArticle

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