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PMID: 1334893 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

Dominant effects of suppressor of Hairy-wing mutations on gypsy-induced alleles of forked and cut in Drosophila melanogaster.

Genetics ·Vol. 132 ·No. 3 ·1992-11-00 ·Pages 691-7

Hoover KK, Gerasimova TI, Chien AJ, Corces VG

Abstract

Mutations induced by the gypsy retrotransposon in the forked (f) and cut (ct) loci render their expression under the control of the suppressor of Hairy-wing [su(Hw)] gene. This action is usually recessive, but su(Hw) acts as a dominant on the alleles fk, ctk and ctMRpN30. Molecular analysis of the gypsy element present in fk indicates that this allele is caused by the insertion of a modified gypsy in which the region normally containing twelve copies of the octamer-like repeat that interacts with the su(Hw) product is altered. Analysis of the gypsy element responsible for the ctk and ctMRpN30 mutations also reveals a correlation between the dominant action of su(Hw) and disruption of the octamer region. We propose that these disruptions alter the affinity and interaction of su(Hw) protein with gypsy DNA, thereby sensitizing the mutant phenotype to fluctuations in su(Hw) product.

Related Genes
Hw ct f<up>1</up> f<up>5</up> f<up>k</up> lz sc su(Hw) y<up>2</up>
MeSH Terms
Alleles Animals Base Sequence DNA Transposable Elements/genetics Drosophila melanogaster/anatomy & histology,genetics Genes, Dominant Genes, Suppressor Molecular Sequence Data Mutagenesis, Insertional Phenotype
Chemicals
DNA Transposable Elements
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Hoover K K
Department of Biology, Johns Hopkins University, Baltimore, Maryland 21218.
Gerasimova T I
Chien A J
Corces V G
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27 references, click to expand
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Article Info
Journal
Genetics
Abbr.
Genetics
ISSN
0016-6731
DOI
10.1093/genetics/132.3.691
Published
1992-11-00
Pages
691-7
Language
English
Region
United States
NLM ID
0374636
PMCID
PMC1205207
Subset
IM
Grants
NIGMS NIH HHS · GM35463 · United States
External Links
PubMed source DOI: 10.1093/genetics/132.3.691 PMC Full Text View journal details
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