Gypsy retrotransposon as a tool for the in vivo analysis of the regulatory region of the optomotor-blind gene in Drosophila (original) (raw)

Genetic and molecular characterization of the optomotor-blind gene locus in Drosophila melanogaster

Genetics, 1990

The Drosophila gene optomotor-blind (omb) is involved in the development of a set of giant neurons in the optic lobes and possibly other structures in the imaginal brain. Adult flies have discrete defects in optomotor behavior. The gene has previously been mapped in chromomeres 4C5-6, together with three other genes, bifid, Quadroon and lacqueredgls. We have localized the gene in a genomic walk of 340 kb of DNA. By mapping seven chromosome breakpoints with omb phenotype we determined its minimum size to about 80 kb. From this region more than 20 RNAs of different size and temporal expression pattern are transcribed. Three of them (T3, T7 and T7') stem from primary transcripts of 40-80 kb in length. In its distal part the omb gene overlaps in at least 19 kb with four other complementation units, bifid, l(1)bifid, Quadroon and lacqueredgls. The three nonlethals affect the external appearance of the fly and seem to be unrelated to brain development.

Genetic and molecular characterization of the optomotor-blind locus in Drosophila melanogaster

Genetics

The Drosophila gene optomotor-blind (omb) is involved in the development of a set of giant neurons in the optic lobes and possibly other structures in the imaginal brain. Adult flies have discrete defects in optomotor behavior. The gene has previously been mapped in chromomeres 4C5-6, together with three other genes, bijid, Quadroon and lacqueredg'". We have localized the gene in a genomic walk of 340 kb of DNA. By mapping seven chromosome breakpoints with om6 phenotype we determined its minimum size to about 80 kb. From this region more than 20 RNAs of different size and temporal expression pattern are transcribed. Three of them (T3, T7 and T7') stem from primary transcripts of 40-80 kb in length. In its distal part the om6 gene overlaps in at least 19 kb with four other complementation units, bijid, l(I)bijid, Quadroon and lacqueredg". The three nonlethals affect the external appearance of the fly and seem to be unrelated to brain development.

The Lighten up (Lip) gene of Drosophila melanogaster, a modifier of retroelement expression, position effect variegation and white locus insertion alleles

Genetics, 1994

We are interested in identifying single gene mutations that are involved in trans-acting dosage regulation in order to understand further the role of such genes in aneuploid syndromes, various types of dosage compensation as well as in regulatory mechanisms. The Lighten up (Lip) gene in Drosophila melanogaster was identified in a mutagenic screen to detect dominant second site modifiers of white-blood (wbl), a retrotransposon induced allele of the white eye color locus. Lip specifically enhances the phenotype of wbl as well as a subset of other retroelement insertion alleles of white, including the copia-induced allele, white-apricot (wa), and six alleles caused by insertion of I elements. We isolated six alleles of Lip which are all recessive lethal, although phenotypically additive heteroallelic escapers were recovered in some combinations. Lip also suppresses position effect variegation, indicating that it may have a role in chromatin configuration. Additionally, Lip modifies the...

Molecular analysis of the yellow locus of Drosophila

The EMBO Journal, 1986

The yellow (y) locus of Drosophila controls the pattern of pigmentation of the adult cuticle and larval mouth parts. Mutations ofy belong to two phenotypic classes; typel mutants exhibit a total loss of pigmentation from all parts of the cuticle and type 2 mutants show allele-specific mosaic pigmentation patterns. We have cloned y by P-element tagging followed by chromosome walking. We demonstrate that a 2.1-kb transcript which spans 4.6 kb of genomic sequence is the y transcript. The location of this transcript and the putative protein it encodes has been defined by nuclease protection, primer extension and DNA sequencing experiments. A 12-kb genomic fragment containing this transcript along with 2.8 kb of 5'-flanking sequence and 4.6 kb of 3'-flanking sequence is sufficient for the wild-type expression of the larval and adult cuticle phenotypes in germ-line transformants. The majority (12/14) of typel mutants show structural lesions within exon coding portions of y. Most (6/7) of the type2 structural lesions map 5' to the start ofy transcription. One type2 mutant which contains an insertion within the 5'-transcribed but non-translated region appears to have resulted from the internal deletion of a P-element associated with a typel allele.

The lethal(1)optomotor-blind gene of Drosophila melanogaster is a major organizer of optic lobe development: isolation and characterization of the gene

Proceedings of the National Academy of Sciences of the United States of America, 1992

The X-chromosomal complementation unit lethal(1)optomotor-blind [l(1)omb] is defined by lack of complementation among over a dozen recessive lethal mutations that map to the omb gene locus. Mutations in l(1)omb also fail to complement viable mutations of three seemingly unrelated functions in this region: bifid (bi), manifesting defective wings, Quadroon (Qd), a semi-dominant mutation expressing abnormal tergite pigmentation, and In(1)ombH31, giving rise to a normal external morphology but with discrete defects in the optic lobes and behavior. The locus encodes a 70-kilobase primary transcript that is spliced into a 6-kilobase mature RNA. cDNAs for this transcript were isolated and sequenced and the derived amino acid sequence was analyzed. Certain features of this sequence suggest that the l(1)omb gene product is a nuclear regulatory protein. The lethal phase of various apparent null mutants was determined and found to occur mainly in the pupal stage. A large proportion of all hemi...

Somatic reversion of some copia-like induced mutations, at the white locus of drosophila melanogaster, after treatment with alkylating agents

Environmental and Molecular Mutagenesis, 1995

Batiste-Alentorn M, Xamena N, Creus A, Marcos R (1991): Genotoxicity studies with the unstable zeste-white (UZ) system of Drosophila melanogaster. Results with ten carcinogenic compounds. Environ Mol Mutagen 18:120-125. Becker HJ (1957): Uber Rontgenmosaikflecken und Defektmutationen am Auge von Drosophila und die Entwicklungsphysiologie des Auges. Z Indukt Abstammungs-Vererbungsl88:333-373. Bingham PM, Zachar Z (1989): Retrotransposons and the FB transposons from Drosophila melanogaster: In Berg DE, and Howe MM (eds): "Mobile DNA." Washington, DC: American Society for Microbiology, pp 485-502. Birchler JA, Hiebert JC (1989): Interaction of the Enhancer of whiteapricot with transposable element alleles at the white locus in Drosophila melanogaster. Genetics 122: 129-138. Birchler JA, Hiebert JC, Rabinow L (1989): Interaction of the mottler of white with transposable element alleles at the white locus in Drosophila melanogaster. Genes Dev 3:73-84. Burr B, Burr FA (1988): Activation of silent transposable elements. In Nelson 0 (ed): "Plant Transposable Elements." New York Plenum Press, pp 317-323. Cairns J (1981): The origin of human cancers. Nature 289:353-357. Carbonare BD, Gehring WJ (1985): Excision of copia element in a rever-

Induced somatic and germinal reversion of the white-spotted -1 insertional mutant phenotype in Drosophila melanogaster

Mutagenesis, 1998

The white-spotted-1 (w^1) mutant of Drosophila melanogaster is characterized by the presence of an 8.7 kb retrotransposon (B104) inserted in the regulatory region of the white locus. The frequency of reversion in both somatic tissue and the germline after exposure to three different alkylating agents has been analysed. To determine if germinal revertants were induced by precise excision of the insertional element we analysed several phenotypic revertants using PCR and Southern blot tecniques. The results indicate that, under our experimental conditions, the mutagens used did not induce excision of B104 in the white gene. In addition, the revertant phenotypes obtained were due to the existence of second site modifiers acting on expression of white. Such modifiers map near the white locus and, at least in one case, may correspond to suppressor-of-white-spotted. 'To whom correjpondence should he addressed.