Heterochromatic trans-inactivation of Drosophila white transgenes.
Position effect variegation of most Drosophila melanogaster genes, including the white eye pigment gene is recessive. We find that this is not always the case for white transgenes. Three examples are described in which a lesion causing variegation is capable of silencing the white transgene on the paired homologue (trans-inactivation). These examples include two different transgene constructs inserted at three distinct genomic locations. The lesions that cause variegation of white minimally disrupt the linear order of genes on the chromosomes, permitting close homologous pairing. At one of these sites, trans-inactivation has also been extended to include a vital gene in the vicinity of the white transgene insertion. These findings suggest that many Drosophila genes, in many positions in the genome, can sense the heterochromatic state of a paired homologue.
Martin-Morris
L E
LE
Howard Hughes Medical Institute, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024, USA.
Csink
A K
AK
Dorer
D R
DR
Talbert
P B
PB
Henikoff
S
S
D018528:ATP-Binding Cassette Transporters; D000818:Animals; D029721:Drosophila Proteins; D004331:Drosophila melanogaster / Q000235:genetics*; D005136:Eye Proteins; D005799:Genes, Dominant; D006570:Heterochromatin / Q000378:metabolism*; D019476:Insect Proteins / Q000235:genetics*; D015533:Transcriptional Activation; D019076:Transgenes
D018528:ATP-Binding Cassette Transporters; D029721:Drosophila Proteins; D005136:Eye Proteins; D006570:Heterochromatin; D019476:Insect Proteins; C059254:w protein, Drosophila