latheo, a new gene invloved in associative learning and memory in Drosophila melanogaster, identified from P element mutagenesis
Article Abstract:
P element mutagenesis was used to generate Drosophila melanogaster mutants deficient in learning or memory. The transposon mutagenesis resulted in the isolation of 1, 016 homozygous P element insertion mutants, which were subsequently subjected to a behavioral screen. The results showed that a new mutation, termed latheo, disrupts associative learning. The memory decay curve of latheo mutants were similar to that of flies deficient in the dopa decarboxylase gene. Mapping experiments localized the latheo locus to the second chromosome. These results imply that the latheo locus represents a new gene involved in learning (aquisition).
Publication Name: Genetics
Subject: Biological sciences
ISSN: 0016-6731
Year: 1992
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Molecular analysis of mutations induced in the vermillion gene of Drosophila melanogaster by methyl methanesulfonate
Article Abstract:
A molecular analysis of DNA alterations induced by the alkylating agent, methyl methanesulfonate (MMS) on the vermilion gene of Drosophila melanogaster was conducted. The results showed that MMS primarily induced AT-GC transitions and AT-TA transversions and deletions, with the transitions occuring primarily in the F(sub 2) and the deletions occuring in the F(sub 1). The mechanism involved in the transversions involved the formation of N-methyl DNA adducts. Comparisons with the mutational spectrum of other mutagens showed that MMS acts through a distinct spectrum, which predominantly involves the formation of nitrogen adducts.
Publication Name: Genetics
Subject: Biological sciences
ISSN: 0016-6731
Year: 1992
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Characterization of suppressor of fused, a complete suppressor of the fused segment polarity gene of Drosophila melanogaster
Article Abstract:
A study was conducted to analyze the suppressor of fused Su(fu) gene. The new gene is found in the 87C8 region of the Drosophila melanogaster's third chromosome. Su(fu) exhibited maternal effects and occured later in development. The mutation is homozygous and lacks an individual phenotype. Results show that mutation properties of Su(fu) makes it develop the same way as the Fu+ kinase.
Publication Name: Genetics
Subject: Biological sciences
ISSN: 0016-6731
Year: 1992
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