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Reference
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| Citation |
Micol, J.L., Garcia-Bellido, A. (1988). Genetic analysis of 'transvection' effects involving Contrabithorax mutations in Drosophila melanogaster. Proc. Natl. Acad. Sci. USA 85(): 1146--1150. |
| FlyBase ID |
FBrf0048913 |
| Type of publication |
Research paper |
| Offprint Available |
Yes |
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External Crossreferences
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| PubMed ID |
3124114 |
| PubMed Abstract |
Contrabithorax (Cbx) alleles are dominant mutations in the Ultrabithorax (Ubx) gene of Drosophila that cause its ectopic expression
in the mesothorax. We have studied the role of the homologous chromosome in the mesothoracic phenotype in several Cbx heterozygotes.
None of the Cbx alleles studied shows variations in phenotype with extra doses of the Ubx gene. Only Cbx2 and CbxIRM (a revertant
of Cbx1) show synapsis-dependent gene expression ("transvection"). The mesothoracic phenotypes of CbxIRM and Cbx2 heterozygotes
are strongly modified when the homologous chromosome carries breakpoints proximal to or at the Ubx locus or null alleles of
this gene. These lesions in the homologous chromosome enhance the Cbx2 mutant phenotype and reduce that of CbxIRM one. The
genetic analysis of these transvection effects suggests that the transcription of the CbxIRM and Cbx2 alleles depends on RNAs
of short radius of action from the homologous Ubx gene.
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| Biosis |
85111843 |
| Zoological record |
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Associated Information
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| Comments |
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| Text of personal communication |
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Related Publications
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Also Published As
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Other Reference Information
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| Secondary IDs |
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| Language of publication |
English |
| Additional language(s) of abstract |
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| ISBN |
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| Place of publication |
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Published In
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| Abbreviation |
Proc. Natl. Acad. Sci. USA |
| Title |
Proceedings of the National Academy of Sciences of the United States of America |
| Authors |
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| Volume range |
1- |
| Year range |
1915- |
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| Publisher |
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| Place of publication |
Washington, DC |
| Language of publication |
English |
| ISBN/ISSN |
0027-8424 |
| CODEN |
PNASA6 |
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Data from Reference
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| Aberrations (14)
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| Alleles (10)
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| Balancers (4)
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| Genes (2)
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