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Relevant bibliographies by topics / Drosophila Troponin I

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Journal articles

Academic literature on the topic 'Drosophila Troponin I'

Author: Grafiati

Published: 6 September 2023

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Journal articles on the topic "Drosophila Troponin I"

1

QIU, Feng, Anne LAKEY, Bogos AGIANIAN, et al. "Troponin C in different insect muscle types: identification of two isoforms in Lethocerus, Drosophila and Anopheles that are specific to asynchronous flight muscle in the adult insect." Biochemical Journal 371, no. 3 (2003): 811–21. http://dx.doi.org/10.1042/bj20021814.

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The indirect flight muscles (IFMs) of Lethocerus (giant water bug) and Drosophila (fruitfly) are asynchronous: oscillatory contractions are produced by periodic stretches in the presence of a Ca2+ concentration that does not fully activate the muscle. The troponin complex on thin filaments regulates contraction in striated muscle. The complex in IFM has subunits that are specific to this muscle type, and stretch activation may act through troponin. Lethocerus and Drosophila have an unusual isoform of the Ca2+-binding subunit of troponin, troponin C (TnC), with a single Ca2+-binding site near t

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2

Terami, Hiromi, Benjamin D. Williams, Shin-ichi Kitamura, et al. "Genomic Organization, Expression, and Analysis of the Troponin C Gene pat-10 of Caenorhabditis elegans." Journal of Cell Biology 146, no. 1 (1999): 193–202. http://dx.doi.org/10.1083/jcb.146.1.193.

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We have cloned and characterized the troponin C gene, pat-10 of the nematode Caenorhabditis elegans. At the amino acid level nematode troponin C is most similar to troponin C of Drosophila (45% identity) and cardiac troponin C of vertebrates. Expression studies demonstrate that this troponin is expressed in body wall muscle throughout the life of the animal. Later, vulval muscles and anal muscles also express this troponin C isoform. The structural gene for this troponin is pat-10 and mutations in this gene lead to animals that arrest as twofold paralyzed embryos late in development. We have s

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3

Mas, José-Antonio, Elena García-Zaragoza, and Margarita Cervera. "Two Functionally Identical Modular Enhancers in Drosophila Troponin T Gene Establish the Correct Protein Levels in Different Muscle Types." Molecular Biology of the Cell 15, no. 4 (2004): 1931–45. http://dx.doi.org/10.1091/mbc.e03-10-0729.

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The control of muscle-specific expression is one of the principal mechanisms by which diversity is generated among muscle types. In an attempt to elucidate the regulatory mechanisms that control fiber diversity in any given muscle, we have focused our attention on the transcriptional regulation of the Drosophila Troponin T gene. Two, nonredundant, functionally identical, enhancer-like elements activate Troponin T transcription independently in all major muscles of the embryo and larvae as well as in adult somatic and visceral muscles. Here, we propose that the differential but concerted intera

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4

Beall, C. J., and E. Fyrberg. "Muscle abnormalities in Drosophila melanogaster heldup mutants are caused by missing or aberrant troponin-I isoforms." Journal of Cell Biology 114, no. 5 (1991): 941–51. http://dx.doi.org/10.1083/jcb.114.5.941.

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We have investigated the molecular bases of muscle abnormalities in four Drosophila melanogaster heldup mutants. We find that the heldup gene encodes troponin-I, one of the principal regulatory proteins associated with skeletal muscle thin filaments. heldup3, heldup4, and heldup5 mutants, all of which have grossly abnormal flight muscle myofibrils, lack mRNAs encoding one or more troponin-I isoforms. In contrast, heldup2, an especially interesting mutant wherein flight muscles are atrophic, synthesizes the complete mRNA complement. By sequencing mutant troponin-I cDNAs we demonstrate that the

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5

Nongthomba, Upendra, Mark Cummins, Samantha Clark, Jim O. Vigoreaux, and John C. Sparrow. "Suppression of Muscle Hypercontraction by Mutations in the Myosin Heavy Chain Gene of Drosophila melanogaster." Genetics 164, no. 1 (2003): 209–22. http://dx.doi.org/10.1093/genetics/164.1.209.

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Abstract The indirect flight muscles (IFM) of Drosophila melanogaster provide a good genetic system with which to investigate muscle function. Flight muscle contraction is regulated by both stretch and Ca2+-induced thin filament (actin + tropomyosin + troponin complex) activation. Some mutants in troponin-I (TnI) and troponin-T (TnT) genes cause a “hypercontraction” muscle phenotype, suggesting that this condition arises from defects in Ca2+ regulation and actomyosin-generated tension. We have tested the hypothesis that missense mutations of the myosin heavy chain gene, Mhc, which suppress the

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6

Marín, María-Cruz, José-Rodrigo Rodríguez, and Alberto Ferrús. "Transcription of Drosophila Troponin I Gene Is Regulated by Two Conserved, Functionally Identical, Synergistic Elements." Molecular Biology of the Cell 15, no. 3 (2004): 1185–96. http://dx.doi.org/10.1091/mbc.e03-09-0663.

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The Drosophila wings-up A gene encodes Troponin I. Two regions, located upstream of the transcription initiation site (upstream regulatory element) and in the first intron (intron regulatory element), regulate gene expression in specific developmental and muscle type domains. Based on LacZ reporter expression in transgenic lines, upstream regulatory element and intron regulatory element yield identical expression patterns. Both elements are required for full expression levels in vivo as indicated by quantitative reverse transcription-polymerase chain reaction assays. Three myocyte enhancer fac

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7

Chechenova, Maria B., Sara Maes, Sandy T. Oas, et al. "Functional redundancy and nonredundancy between two Troponin C isoforms inDrosophilaadult muscles." Molecular Biology of the Cell 28, no. 6 (2017): 760–70. http://dx.doi.org/10.1091/mbc.e16-07-0498.

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We investigated the functional overlap of two muscle Troponin C (TpnC) genes that are expressed in the adult fruit fly, Drosophila melanogaster: TpnC4 is predominantly expressed in the indirect flight muscles (IFMs), whereas TpnC41C is the main isoform in the tergal depressor of the trochanter muscle (TDT; jump muscle). Using CRISPR/Cas9, we created a transgenic line with a homozygous deletion of TpnC41C and compared its phenotype to a line lacking functional TpnC4. We found that the removal of either of these genes leads to expression of the other isoform in both muscle types. The switching b

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8

Vicente-Crespo, Marta, Maya Pascual, Juan M. Fernandez-Costa, et al. "Drosophila Muscleblind Is Involved in troponin T Alternative Splicing and Apoptosis." PLoS ONE 3, no. 2 (2008): e1613. http://dx.doi.org/10.1371/journal.pone.0001613.

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9

Naimi, Benyoussef, Andrew Harrison, Mark Cummins, et al. "A Tropomyosin-2 Mutation Suppresses a Troponin I Myopathy inDrosophila." Molecular Biology of the Cell 12, no. 5 (2001): 1529–39. http://dx.doi.org/10.1091/mbc.12.5.1529.

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A suppressor mutation, D53, of theheld-up 2 allele of the Drosophila melanogaster Troponin I (wupA) gene is described. D53, a missense mutation, S185F, of the tropomyosin-2,Tm2, gene fully suppresses all the phenotypic effects ofheld-up 2, including the destructive hypercontraction of the indirect flight muscles (IFMs), a lack of jumping, the progressive myopathy of the walking muscles, and reductions in larval crawling and feeding behavior. The suppressor restores normal function of the IFMs, but flight ability decreases with age and correlates with an unusual, progressive structural collapse

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10

Montana, Enrico S., and J. Troy Littleton. "Characterization of a hypercontraction-induced myopathy in Drosophila caused by mutations in Mhc." Journal of Cell Biology 164, no. 7 (2004): 1045–54. http://dx.doi.org/10.1083/jcb.200308158.

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The Myosin heavy chain (Mhc) locus encodes the muscle-specific motor mediating contraction in Drosophila. In a screen for temperature-sensitive behavioral mutants, we have identified two dominant Mhc alleles that lead to a hypercontraction-induced myopathy. These mutants are caused by single point mutations in the ATP binding/hydrolysis domain of Mhc and lead to degeneration of the flight muscles. Electrophysiological analysis in the adult giant fiber flight circuit demonstrates temperature-dependent seizure activity that requires neuronal input, as genetic blockage of neuronal activity suppre

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