Molecular analysis of the Adh region of the genome of Drosophila melanogaster

Chia, William; Karp, Robert L.; McGill, S; Ashburner, Michael

doi:10.1016/0022-2836(85)90389-4

Cited by 47 publications

(42 citation statements)

References 29 publications

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“…The probe hybridized to a single site on the left arm of chromosome 2 at cytological position 35A4-B1. This region of the Drosophila genome has been the focus of much attention including extensive screens for recessive lethal or sterile mutants (45,46). We obtained a clone from the Ashburner lab to determine the sequence of the spel1 genomic DNA and the…”

Section: Resultsmentioning

confidence: 99%

Microsatellite instability in Drosophila spellchecker1 (MutS homolog) mutants

Flores

Engels

1999

Proc. Natl. Acad. Sci. U.S.A.

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We have cloned a mutS homolog from Drosophila melanogaster called spellchecker1 (spel1) and have constructed spel1 mutant f lies. MutS proteins promote the correction of DNA mismatches and serve important roles in DNA replication, recombination, and repair. The spel1 gene belongs to a subfamily of mutS first characterized by the MSH2 gene of yeast and which also includes hMSH2, one of the two major hereditary nonpolyposis colon cancer loci of humans. Like msh2 mutants in other species, we find that f lies lacking the spel1 gene suffer a highly increased rate of instability in long runs of dinucleotide repeats when analyzed after 10-12 f ly generations. Using a new assay, we have also discovered that mutations in spel1 decrease the stability of a dinucleotide repeat when it is copied into the site of a double-strand break during gene conversion. Contrary to the case in mammalian cells, spel1 deficiency does not affect tolerance of f lies to a methylating agent nor does it affect resistance to ␥-irradiation.

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Section: Resultsmentioning

confidence: 99%

Microsatellite instability in Drosophila spellchecker1 (MutS homolog) mutants

Flores

Engels

1999

Proc. Natl. Acad. Sci. U.S.A.

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“…Adh nLA248 is an X-ray induced Adh null allele, which produces an Adh transcript 250 bp longer than normal (Chia et al, 1985b). The chromosome bearing Adh nLA248 also carries the markers cn and bw (Lindsley & Grell, 1968) and when homozygous gives white-eyed flies.…”

Section: Drosophila Melanogaster Stocksmentioning

confidence: 99%

A Tirant insertion in the alcohol dehydrogenase locus of Drosophila melanogaster

Gibson

1998

Heredity

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An alcohol dehydrogenase allele Adh AAS44 isolated from an Australian natural population of Drosophila melanogaster is associated with low activity in adult flies. A 5.0 kb insertion in the first intron between the distal and proximal promoters has been partially sequenced and shown to be homologous to the retrotransposon Tirant. The insertion is the major change in the transcriptional unit of Adh AAS44 , but there is also a single nucleotide change in the adult Adh enhancer. The main phenotypic effect associated with the Tirant insertion is a reduction in alcohol dehydrogenase activity and transcript level in adult flies. There is a very much smaller reduction in 3rd instar larvae. The data indicate that Tirant affects transcription from the distal promoter. The possible mechanisms for this differential effect on transcription are discussed.

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“…In addition to saturation mutagenesis, which has resulted in the recovery of all of the lethal and many of the visible complementation groups, approximately 400 kb of this region has been isolated on overlapping genomic clones and physically mapped. In the course of correlating the physical map to the genetic map, a number of interesting genetic interactions between genes located in this region have been described (7,11). Here, we consider the relationship between no ocelli (nocA) and 1(2)35Ba and describe the nature of the 1(2)35Ba gene product, its expression pattern, and its function.…”

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“…These mutants when homozygous or when heterozygous with deletions which include nocA, exhibit a complete or partial loss of the ocelli, adult photosensory organs located between the compound eyes on the vertex of the head. All of the nocA alleles associated with aberrations that can be physically mapped are located approximately 110 to 120 kb distal to Adh (7,25). The lethal complementation group which maps immediately distal to nocA is 1(2)35Ba.…”

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confidence: 99%

“…First, the nocA allele nocATE3SA is caused by the insertion of a large, cytologically visible transposable element, TE35A, which contains two functional copies each of the white and roughest genes (19). Many of the nocATE35A revertant 0, isolated on the basis of loss of the white genes carried by TE35A, retain up to 7 to 8 kb of the transposable element sequence at the insertion site; these flies nevertheless exhibit wild-type ocelli, indicating that the noc phenotype associated with the TE35A insertion is caused by some type of position effect and is not due to the disruption of a coding region (8 (7,11). A summary of these results, shown in Fig.…”

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