Key result
The heldup3 mutation in Drosophila melanogaster causes a splicing defect in the troponin I gene, leading to the selective failure to develop DLM, DVM, and TDT thoracic muscles.
A specific splicing defect in the troponin I gene of Drosophila melanogaster prevents the production of exon 6b1-containing isoforms, causing selective abortion of thoracic muscle development.
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Drosophila troponin I splicing model extends isoform-specific myogenesis insights; leaves open relevance to human sarcomeric disease.
The troponin I (TnI) gene of Drosophila melanogaster encodes a family of 10 isoforms resulting from the differential splicing of 13 exons. Four of these exons (6a1, 6a2, 6b1, and 6b2) are mutually exclusive and very similar in sequence. TnI isoforms show qualitative specificity whereby each muscle expresses a selected repertoire of them. In addition, TnI isoforms show quantitative specificity whereby each muscle expresses characteristic amounts of each isoform. In the mutant heldup3, the development of the thoracic muscles DLM, DVM, and TDT is aborted. The mutation consists of a one-nucleotide displacement of the 3' AG splice site at the intron preceding exon 6b1, resulting in the failure to produce all exon 6b1-containing TnI isoforms. These molecular changes in a constituent of the thin filaments cause the selective failure to develop the DLM, DVM, and TDT muscles while having no visible effect on other muscles wherein exon 6b1 expression is minor.
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Barbas et al. (1993) studied heldup3 mutation in Drosophila melanogaster. heldup3 mutation was evaluated on Muscle development (DLM, DVM, and TDT muscles). The heldup3 mutation in Drosophila melanogaster causes a splicing defect in the troponin I gene, leading to the selective failure to develop DLM, DVM, and TDT thoracic muscles.
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