Expansions of transgene repeats cause heterochromatin formation and gene silencing in Drosophila.
Closely linked repeats of a Drosophila P transposon carrying a white transgene were found to cause white variegation. Arrays of three or more transgenes produced phenotypes similar to classical heterochromatin-induced position-effect variegation (PEV), and these phenotypes were modified by known modifiers of PEV. This effect on the repeated transgenes was much stronger for a site near centric heterochromatin than it was for a medial site, and it strengthened with increasing copy number. Differences between variegated phenotypes could be accounted for if different topological structures were generated by pairing between closely linked repeat sequences. We propose that pairing of repeats underlies heterochromatin formation and is responsible for diverse gene silencing phenomena in animals and plants.
Dorer
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Howard Hughes Medical Institute, Basic Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98104.
Henikoff
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D000818:Animals; D030801:Animals, Genetically Modified; D002874:Chromosome Mapping; D004251:DNA Transposable Elements; D004331:Drosophila melanogaster / Q000235:genetics* / Q000648:ultrastructure; D005786:Gene Expression Regulation; D015321:Gene Rearrangement; D006570:Heterochromatin / Q000502:physiology*; D012091:Repetitive Sequences, Nucleic Acid; D015183:Restriction Mapping
D004251:DNA Transposable Elements; D006570:Heterochromatin