FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Hsap\LRRK2Y1699C.UAS
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General Information
Symbol
Hsap\LRRK2Y1699C.UAS
Species
H. sapiens
Name
FlyBase ID
FBal0244981
Feature type
allele
Associated gene
Hsap\LRRK2
Associated Insertion(s)
Carried in Construct
P{UAS-hLRRK2.Y1699C}
Key Links
Transgenic product class
missense_variant
(Venderova et al., 2009)
Mutagen
Nature of the Allele
Transgenic product class
missense_variant
(Venderova et al., 2009)
Mutagen
in vitro construct
(Venderova et al., 2009)
Progenitor genotype
Carried in construct
P{UAS-hLRRK2.Y1699C}
Cytology
Description

UASt regulatory sequences drive expression of a mutant form of Hsap\LRRK2, which contains the amino acid replacement Y1699C.

(Venderova et al., 2009)
Allele components
Component
Use(s)
Regulatory region(s)
UASt
Encoded product / tool
Hsap\LRRK2
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
      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 ( 1 )
      Disease
      Evidence
      References
      model of  Parkinson's disease
      CEA
      (Godena et al., 2014, Venderova et al., 2009)
      Modifiers Based on Experimental Evidence ( 1 )
      Disease
      Interaction
      References
      model of  Parkinson's disease
      is ameliorated by Sirt2GD11528
      (Godena et al., 2014)
      is ameliorated by HDAC6KK100215
      (Godena et al., 2014)
      Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
       
      Disease-implicated variant(s)
       
      This allele represents a human variant implicated in disease.
      (Venderova et al., 2009)
      LRRK2:p.Tyr1699Cys
      (FlyBase curators, 2019-)
      Variants Synonym(s)
      Associated human disease model(s)
      External database links
      ClinVar: LRRK2_1937
      Comments concerning this variant
      Phenotypic Data
      Phenotypic Class
      Phenotype Manifest In
      Detailed Description
      Statement
      Reference

      Axonal transport of mitochondria is disrupted in larval motor neurons expressing Hsap\LRRK2Y1699C.Scer\UAS under the control of Scer\GAL4D42.

      Climbing and flight ability are reduced compared to controls in flies expressing Hsap\LRRK2Y1699C.Scer\UAS under the control of Scer\GAL4D42.

      (Godena et al., 2014)

      Expression of Hsap\LRRK2Y1699C.Scer\UAS driven by Scer\GAL4Ddc.PU causes significant locomotor deficits (reduced climbing ability) in 5 or 10 (but not 20, when all flies including controls show age-dependent locomotor deficits) day old flies, compared to controls.

      (Linhart et al., 2014)

      50 day old adults expressing Hsap\LRRK2Y1699C.Scer\UAS under the control of Scer\GAL4ple.PF at room temperature show loss of dopaminergic neurons in the dorsolateral posterior protocerebral cluster (PPL1) of the brain compared to control flies of the same age. A similar loss of neurons is seen in 20 day old adults expressing Hsap\LRRK2Y1699C.Scer\UAS under the control of Scer\GAL4ple.PF at 29[o]C.

      Expression of Hsap\LRRK2Y1699C.Scer\UAS under the control of Scer\GAL4da.G32 at room temperature significantly extends the basal lifespan of flies compared to controls, while expression of Hsap\LRRK2Y1699C.Scer\UAS under the control of Scer\GAL4elav.PU at room temperature or at 29[o]C has no significant effect on basal lifespan.

      Flies expressing Hsap\LRRK2Y1699C.Scer\UAS under the control of Scer\GAL4da.G32 at room temperature show a greater sensitivity to chronic exposure to low levels of rotenone then control flies.

      Flies expressing Hsap\LRRK2Y1699C.Scer\UAS under the control of Scer\GAL4GMR.PF at 29[o]C show loss of pigmentation in the eyes. Significantly more black lesions are seen in the mutant eyes than in controls. Ultrastructurally, severe disruption of the regular trapezoidal arrangement of the photoreceptor cells is seen. The cell lattice between photoreceptor cell arrays of different ommatidia is completely absent and the ommatidia are sometimes fused together. Large holes are often seen in the eye sections.

      (Venderova et al., 2009)
      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

      Co-expression of either HDAC6KK100215 or Sirt2GD11528 suppresses the defects in axonal transport of mitochondria seen in larval motor neurons expressing Hsap\LRRK2Y1699C.Scer\UAS under the control of Scer\GAL4D42.

      Co-expression of either HDAC6KK100215 or Sirt2GD11528 significantly rescues the defects in flight ability seen in flies expressing Hsap\LRRK2Y1699C.Scer\UAS under the control of Scer\GAL4D42.

      (Godena et al., 2014)

      Co-expression of Vps35EY14200 significantly suppresses locomotor deficits in flies with expression of Hsap\LRRK2Y1699C.Scer\UAS driven by Scer\GAL4Ddc.PU.

      (Linhart et al., 2014)
      Complementation and Rescue Data
      Comments
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (2)
      Reported As
      Symbol Synonym
      Hsap\LRRK2Y1699C.Scer\UAS
      Hsap\LRRK2Y1699C.UAS
      Name Synonyms
      Secondary FlyBase IDs
        References (5)