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Homologous association of the Bithorax-Complex during embryogenesis: consequences for transvection in Drosophila melanogaster

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Gemkow,  M. J.
Department of Molecular Biology, MPI for biophysical chemistry, Max Planck Society;

Verveer,  P. J.
Max Planck Society;

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Arndt-Jovin,  D. J.
Department of Molecular Biology, MPI for biophysical chemistry, Max Planck Society;

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Citation

Gemkow, M. J., Verveer, P. J., & Arndt-Jovin, D. J. (1998). Homologous association of the Bithorax-Complex during embryogenesis: consequences for transvection in Drosophila melanogaster. Development, 125, 4541-4552.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0012-FCD7-2
Abstract
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 post-gastrulating embryos, and is not perturbed by the transcriptional state of the genes throughout embryogenesis. Pairing frequencies never reach 100% indicative 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. Surprisingly, the pairing of homologous alleles was reduced, albeit only to 20 - 30%, by 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 although trans-regulation of the Ultrabithorax gene was abolished. A zeste protein null mutation neither delayed the onset of pairing nor led to unpairing of the homologous alleles. These data are discussed in 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.