Lethal(1)fibrillardysgenesis (I(1)fdg), a mutation affecting muscle development in the embryo of Drosophila melanogaster

1982 ◽  
Vol 3 (4) ◽  
pp. 329-345 ◽  
Author(s):  
Samuel M. Newman ◽  
Theodore R. F. Wright
Keyword(s):  
Drosophila Melanogaster ◽  
Muscle Development

Abnormal muscle development in the heldup3 mutant of Drosophila melanogaster is caused by a splicing defect affecting selected troponin I isoforms

1993 ◽  
Vol 13 (3) ◽  
pp. 1433-1439
Author(s):  
J A Barbas ◽  
J Galceran ◽  
L Torroja ◽  
A Prado ◽  
A Ferrús
Keyword(s):  
Drosophila Melanogaster ◽  
Splice Site ◽  
Muscle Development ◽  
Troponin I ◽  
Differential Splicing ◽  
Thin Filaments ◽  
Molecular Changes ◽  
Splicing Defect ◽  
Visible Effect ◽  
Thoracic Muscles

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.

scholarly journals Indirect flight muscles in Drosophila melanogaster as a tractable model to study muscle development and disease

2020 ◽  
Vol 64 (1-2-3) ◽  
pp. 167-173
Author(s):  
Saroj Jawkar ◽  
Upendra Nongthomba
Keyword(s):  
Drosophila Melanogaster ◽  
Muscle Development ◽  
Myoblast Fusion ◽  
Successful Development ◽  
Adult Muscle ◽  
Attachment Sites ◽  
Flight Muscles ◽  
And Function

Myogenesis is a complex multifactorial process leading to the formation of the adult muscle. An amalgamation of autonomous processes including myoblast fusion and myofibrillogenesis, as well as non-autonomous processes, such as innervations from neurons and precise connections with attachment sites, are responsible for successful development and function of muscles. In this review, we describe the development of the indirect flight muscles (IFMs) in Drosophila melanogaster, and highlight the use of the IFMs as a model for studying muscle development and disease, based on recent studies on the development and function of IFMs.

scholarly journals Abnormal muscle development in the heldup3 mutant of Drosophila melanogaster is caused by a splicing defect affecting selected troponin I isoforms.

1993 ◽  
Vol 13 (3) ◽  
pp. 1433-1439 ◽  
Author(s):  
J A Barbas ◽  
J Galceran ◽  
L Torroja ◽  
A Prado ◽  
A Ferrús
Keyword(s):  
Drosophila Melanogaster ◽  
Splice Site ◽  
Muscle Development ◽  
Troponin I ◽  
Differential Splicing ◽  
Thin Filaments ◽  
Molecular Changes ◽  
Splicing Defect ◽  
Visible Effect ◽  
Thoracic Muscles

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.

5'-flanking sequence required for regulated expression of a muscle-specific Drosophila melanogaster actin gene

1986 ◽  
Vol 6 (10) ◽  
pp. 3388-3396
Author(s):  
P K Geyer ◽  
E A Fyrberg
Keyword(s):  
Drosophila Melanogaster ◽  
Dna Sequences ◽  
Transcription Initiation ◽  
Muscle Development ◽  
Normal Function ◽  
Upstream Sequence ◽  
Actin Gene ◽  
Flanking Sequence ◽  
Mrna Accumulation ◽  
Flanking Sequences

We have functionally tested derivatives of a muscle-specific Drosophila melanogaster actin gene in which 5'-flanking sequences have been deleted or rearranged. From our results we conclude that approximately 1,000 nucleotides of 5'-flanking sequence are required for wild-type levels of mRNA accumulation during flight muscle development. Derivatives having 875 or 865 nucleotides of upstream sequence could be expressed normally, but were prone to influence by flanking foreign DNA sequences. Derivatives retaining 600 or fewer nucleotides of flanking DNA did not direct detectable levels of mRNA accumulation. The sequence residing between -919 and -640 could be inverted and yet retain normal function. Deletion of this sequence reduced mRNA accumulation markedly, but did not affect its spatial localization, suggesting that elements which confer tissue specificity reside close to the point of transcription initiation.

scholarly journals Genetic analysis of muscle development in Drosophila melanogaster

1989 ◽  
Vol 131 (2) ◽  
pp. 439-454 ◽  
Author(s):  
J.L. De la Pompa ◽  
J.R. Garcia ◽  
A. Ferrús
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Analysis ◽  
Muscle Development

scholarly journals 5'-flanking sequence required for regulated expression of a muscle-specific Drosophila melanogaster actin gene.

1986 ◽  
Vol 6 (10) ◽  
pp. 3388-3396 ◽  
Author(s):  
P K Geyer ◽  
E A Fyrberg
Keyword(s):  
Drosophila Melanogaster ◽  
Dna Sequences ◽  
Transcription Initiation ◽  
Muscle Development ◽  
Normal Function ◽  
Upstream Sequence ◽  
Actin Gene ◽  
Flanking Sequence ◽  
Mrna Accumulation ◽  
Flanking Sequences

We have functionally tested derivatives of a muscle-specific Drosophila melanogaster actin gene in which 5'-flanking sequences have been deleted or rearranged. From our results we conclude that approximately 1,000 nucleotides of 5'-flanking sequence are required for wild-type levels of mRNA accumulation during flight muscle development. Derivatives having 875 or 865 nucleotides of upstream sequence could be expressed normally, but were prone to influence by flanking foreign DNA sequences. Derivatives retaining 600 or fewer nucleotides of flanking DNA did not direct detectable levels of mRNA accumulation. The sequence residing between -919 and -640 could be inverted and yet retain normal function. Deletion of this sequence reduced mRNA accumulation markedly, but did not affect its spatial localization, suggesting that elements which confer tissue specificity reside close to the point of transcription initiation.

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