Open AccessA pairing-sensitive element that mediates trans-inactivation is associated with the Drosophila brown gene.
Author(s) -
Thomas D. Dreesen,
Steven Henikoff,
Kate Loughney
Publication year - 1991
Publication title -
genes and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.136
H-Index - 438
eISSN - 1549-5477
pISSN - 0890-9369
DOI - 10.1101/gad.5.3.331
Subject(s) - biology , genetics , position effect , variegation (histology) , ectopic expression , transposable element , gene , heterochromatin , chromosomal rearrangement , p element , allele , enhancer , drosophilidae , chromosomal inversion , gene rearrangement , transposase , chromosome , mutant , gene expression , drosophila melanogaster , karyotype
Position-effect variegation in Drosophila is the mosaic expression of a gene juxtaposed to heterochromatin by chromosome rearrangement. The brown (bw+) gene is unusual in that variegating mutations are dominant, causing "trans-inactivation" of the homologous allele. We show that copies of bw+ transposed to ectopic sites are not trans-inactivated by rearrangements affecting the endogenous gene. However, when position-effect variegation is induced on an ectopic copy by chromosome rearrangement, the allele on its paired homolog is trans-inactivated, whereas other copies of bw+ are not. This confirms that trans-inactivation is "chromosome local" and maps the responsive element to the immediate vicinity of brown. Subsequent P-transposase-induced deletions within the ectopic copy in cis to the rearrangement breakpoint caused partial suppression of trans-inactivation. Surprisingly, the amount of suppression was correlated with deletion size, with some degree of trans-inactivation persisting even when the P[bw+] transposon was completely excised. The chromosome-local nature of the phenomenon and its extreme sensitivity to small disruptions of somatic pairing leads to a model in which a regulator of the brown gene is inactivated by direct contact with heterochromatic proteins.