Homologous association of the Bithorax-Complex during embryogenesis: consequences for transvection in Drosophila melanogaster.
Transvection is the phenomenon by which the expression of a gene can be controlled by its homologous counterpart in trans, presumably due to pairing of alleles in diploid interphase cells. Transvection or trans-sensing phenomena have been reported for several loci in Drosophila, the most thoroughly studied of which is the Bithorax-Complex (BX-C). It is not known how early trans-sensing occurs nor the extent or duration of the underlying physical interactions. We have investigated the physical proximity of homologous genes of the BX-C during Drosophila melanogaster embryogenesis by applying fluorescent in situ hybridization techniques together with high-resolution confocal light microscopy and digital image processing. The association of homologous alleles of the BX-C starts in nuclear division cycle 13, reaches a plateau of 70% in postgastrulating embryos, and is not perturbed by the transcriptional state of the genes throughout embryogenesis. Pairing frequencies never reach 100%, indicating that the homologous associations are in equilibrium with a dissociated state. We determined the effects of translocations and a zeste protein null mutation, both of which strongly diminish transvection phenotypes, on the extent of diploid homologue pairing. Although translocating one allele of the BX-C from the right arm of chromosome 3 to the left arm of chromosome 3 or to the X chromosome abolished trans-regulation of the Ultrabithorax gene, pairing of homologous alleles surprisingly was reduced only to 20-30%. A zeste protein null mutation neither delayed the onset of pairing nor led to unpairing of the homologous alleles. These data are discussed in the light of different models for trans-regulation. We examined the onset of pairing of the chromosome 4 as well as of loci near the centromere of chromosome 3 and near the telomere of 3R in order to test models for the mechanism of homologue pairing.
Department of Molecular Biology, Max Planck Institute for Biophysical Chemistry, FRG.
M J
MJ
Gemkow
P J
PJ
Verveer
D J
DJ
Arndt-Jovin
D000483:Alleles; D000818:Animals; D002874:Chromosome Mapping; D020223:Chromosome Painting; D003433:Crosses, Genetic; D004268:DNA-Binding Proteins / Q000235:genetics*; D029721:Drosophila Proteins; D004331:Drosophila melanogaster / Q000196:embryology / Q000235:genetics*; D005786:Gene Expression Regulation; D015321:Gene Rearrangement; D017344:Genes, Insect; D018398:Homeodomain Proteins / Q000235:genetics*; D017404:In Situ Hybridization, Fluorescence; D019476:Insect Proteins / Q000235:genetics*; D008938:Mitosis / Q000235:genetics*; D009687:Nuclear Proteins; D017384:Sequence Deletion; D014157:Transcription Factors; D014158:Transcription, Genetic; D014178:Translocation, Genetic
C062393:Abd-B proteins, Drosophila; D004268:DNA-Binding Proteins; D029721:Drosophila Proteins; D018398:Homeodomain Proteins; D019476:Insect Proteins; D009687:Nuclear Proteins; D014157:Transcription Factors; C066177:Ubx protein, Drosophila; C060849:z protein, Drosophila; C066591:abd-A protein, Drosophila