Abstract
P element-induced double-strand breaks (DSBs) on the X chromosome of Drosophila melanogaster were repaired up to four times more frequently when functional Su(Hw) chromatin insulator protein was removed from all genomic binding sites. Simultaneous comparisons of interallelic gap repair frequencies at two target loci on the X chromosome confirmed that a Su(Hw) binding site nested within a template had no effect on DSB repair efficiency. The results suggest that the genome-wide homology search of broken ends for homologous template sequences is affected because it is the only step in the recombinational repair process with an apparent genome-wide interaction. We propose that the searching 3'-hydroxy ends gain a higher degree of freedom for the search in a su(Hw) mutant background.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Base Sequence
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Binding Sites / genetics
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Chromosome Breakage / genetics*
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DNA / metabolism
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DNA Repair / drug effects
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DNA Repair / genetics*
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DNA-Binding Proteins / metabolism*
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DNA-Binding Proteins / pharmacology
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Drosophila Proteins
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Drosophila melanogaster / cytology
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Drosophila melanogaster / genetics
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Drosophila melanogaster / metabolism*
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Gene Targeting
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Germ Cells / cytology
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Germ Cells / metabolism*
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Models, Genetic
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Molecular Sequence Data
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Mutation
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Nuclear Proteins / metabolism*
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Nuclear Proteins / pharmacology
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Phenotype
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Polymerase Chain Reaction
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Repressor Proteins / metabolism*
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Sequence Analysis, DNA
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X Chromosome / genetics
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X Chromosome / metabolism
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X Chromosome / ultrastructure
Substances
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DNA-Binding Proteins
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Drosophila Proteins
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Nuclear Proteins
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Repressor Proteins
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su(Hw) protein, Drosophila
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DNA