FB2026_02 , released June 18, 2026
Allele: Dmel\SPARCnm136
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General Information
Symbol
Dmel\SPARCnm136
Species
D. melanogaster
Name
FlyBase ID
FBal0246229
Feature type
allele
Associated gene
Dmel\SPARC
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Mutagen
Nature of the Allele
Allele class
Mutagen
Delta2-3 transposase
(Martinek et al., 2008)
Progenitor genotype
P{lacW}His2AvL1602
(Martinek et al., 2008)
Caused by aberration
Df(3R)nm136
Cytology
Description

Imprecise excision of the progenitor insertion resulting in a 1936 bp deletion within the neighbouring His2Av gene which also results in perturbation of SPARC.

(Martinek et al., 2008)
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 ( 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

      SPARCnm136 mutations (i.e. Df(3R)nm136 in combination with His2AvT:Avic\GFP-S65T) do not display embryonic VNC defects or embryonic lethality when homozygous or heterozygous with Df(3R)BSC524. Instead, these animals die during larval stages.

      Unlike wild type larvae, many SPARCnm136 mutants (i.e. Df(3R)nm136 in combination with His2AvT:Avic\GFP-S65T) crawl away from the yeast/agar and become stationary on the plate wall as 1st instars. SPARCnm136/Df(3R)BSC524 animals that survive for 72-96 hr are smaller with reduced fat bodies compared to wild type - they do not pupate and often develop necrotic bodies and have a deformed proventriculus. Processing of food appears normal in the mutants - they stop feeding prior to the emergence of proventricular defects.

      MARCM-generated fat body clones mutant for SPARCnm136 (i.e. Df(3R)nm136 in combination with His2AvT:Avic\GFP-S65T) results in adipocyte cell rounding, membrane blebbing and cortical actin reorganisation.

      SPARCMI00329/SPARCnm136 fat body from 3rd instar larvae shows a disruption of tissue morphology - adipocytes are rounded and membranes bleb. Whereas wild type adipocytes are polygonal, these mutant adipocytes are spherical with an increased number of surface pits.

      (Shahab et al., 2015)

      BM-40-SPARCnm136 mutant embryos do not display normal anterior Malpighian tubule migration, and the anterior pair of tubules project posteriorly in these animals.

      (Bunt et al., 2010)

      SPARCnm136 mutant embryos (co-expressing His2AvT:Avic\GFP-S65T to rescue defects due to disruption of His2Av) display holes in the ventral cuticles, often accompanied by a loss of anterior cuticle and head involution defects. Tracheal defects are also evident, including constricted or broken dorsal-longitudinal tracheal trunks.

      (Martinek et al., 2008)
      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
      Rescued by

      SPARCnm136 is rescued by SPARCUAS.cMa/Scer\GAL4Cg.PA

      (Shahab et al., 2015)
      Comments

      Scer\GAL4Cg.PA-mediated expression of BM-40-SPARCScer\UAS.cMa rescues SPARCnm136 mutants to adulthood.

      BM-40-SPARCCH322-97I07 rescues the larval lethality associated with SPARCnm136 mutants (i.e. Df(3R)nm136 in combination with His2AvT:Avic\GFP-S65T).

      (Shahab et al., 2015)

      Expression of SPARCScer\UAS.cMa in the haemocytes under the control of Scer\GAL4gcm-rA87.P or Scer\GAL4srp.Hemo fails to rescue embryonic lethality of SPARCnm136 embryos (co-expressing His2AvT:Avic\GFP-S65T to rescue defects due to disruption of His2Av). Ventral cuticle morphology is restored and tracheal defects are suppressed in these embryos.

      Expression of SPARCScer\UAS.cMa in neural tissues under the control of Scer\GAL4sca-109-68 fails to rescue the mutant phenotype of SPARCnm136 embryos (co-expressing His2AvT:Avic\GFP-S65T to rescue defects due to disruption of His2Av).

      (Martinek et al., 2008)
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer

      Separable from: neurnm136.

      (Shahab et al., 2015)

      The nervous system defects and embryonic lethality observed in BM-40-SPARCnm136 embryos are not due to absence of SPARC, but rather due to neurnm136, a second-site mutation on the chromosome.

      (Shahab et al., 2015)
      Comments
      Comments

      FlyBase curator comment: The lethality and ventral nerve cord phenotypes associated with SPARCnm136 in this paper have been removed as a subsequent paper (FBrf0227915) by the same group shows that these effects are caused by a second-site mutation in neur.

      (Martinek et al., 2008)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (4)
      Reported As
      Symbol Synonym
      BM-40-SPARCnm136
      Df(3R)nm136
      (Portela et al., 2010)
      SPARCnm136
      dsparc136
      (Weavers and Skaer, 2013)
      Name Synonyms
      Secondary FlyBase IDs
        References (5)