FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\PrmS18A.cLa
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General Information
Symbol
Dmel\PrmS18A.cLa
Species
D. melanogaster
Name
FlyBase ID
FBal0189692
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Transgenic product class
Nature of the Allele
Transgenic product class
Progenitor genotype
Carried in construct
Cytology
Description

Construct: Amino acid replacement: S18A.

Allele components
Component
Use(s)
Regulatory region(s)
Encoded product / tool
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Flies carrying the PrmS18A.cLa transgene exhibit significant defects in flight ability compared to wild-type. However, these flies do not exhibit defects in larval crawling speed. The indirect flight muscle myofibrils of these mutants are also assembled normally. There aren't any significant differences between control and mutant flies in major structural parameters such as sarcomere length, thick filament number per myofibril cross-sectional area, and percentage of myofibril area per muscle cross-sectional area. Mutant flies exhibit a 1.4-2.7% increase in myofibril cross-sectional area, although the number of thick filaments per fiber is unchanged. At peak Ca activation (pCa 5.0), over a wide range of oscillation frequencies, the magnitudes of the elastic modulus, viscous modulus, and power output from PrmS18A.cLa fibers were dramatically reduced compared to those of the control. The active elastic moduli of PrmS18A.cLa fibers is significantly less (values ranged from 23-37% at the frequencies assessed) than that of the control. The viscous moduli of active PrmS18A.cLa fibers are significantly less for most frequency values of >20Hz (values ranged from 21-59% less). Consequently, PrmS18A.cLa active fibers produce significantly less power compared with controls throughout most of the positive power-producing range (42% less at maximum power). In a relaxed condition (where no myosin crossbridges are strongly attached to actin), PrmS18A.cLa fibers exhibit a significant reduction in magnitude of elastic modulus between 2.5 and 40Hz (ranging from 25-37% less) compared with controls. In rigor conditions (no ATP, where myosin crossbridges are strongly attached), PrmS18A.cLa fibers exhibit dramatic reductions in elastic modulus (ranging from 40-49% less) over the entire frequency range and in viscous modulus (ranging from 28-51% less) at all frequencies except at 0.5 and 1000Hz. PrmS18A.cLa mutants do not exhibit any significant differences in active (pCa 5.0) muscle fiber kinetics.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

The transgene PrmS18A.cLa rescues the embryonic lethal phenotype of Prm1 to adulthood.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
Reported As
Symbol Synonym
PrmS18A.cLa
Name Synonyms
Secondary FlyBase IDs
    References (1)