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General Information
Symbol
Dmel\Sara12
Species
D. melanogaster
Name
FlyBase ID
FBal0197108
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Cytology
Nature of the lesion
Statement
Reference

Imprecise excision of the P{EPgy2}SdcEY04602 insertion, resulting in a 5.8kb deletion that removes the complete open reading frame of Sara and a portion of the Sdc gene.

Caused by aberration
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

Sara12 escapers exhibit a midgut phenotype at 15 days after hatching. Midgut length is significantly reduced in homozygous Sara12 and Sara12/Df(2R)48 mutants with respect to wild type. The mitotic index is also decreased by half and the number of intestinal stem cells (ISCs) in the posterior midgut 15 days after hatching is significantly increased compared with wild type. Fewer Sara12 mutant clones are recovered in the adult posterior midgut than in wild type, and the clones that are recovered contain fewer cells. A higher proportion of ISC symmetric divisions occur compared to wild type. The number of enterocytes is increased at the expense of enteroendocrine cells in Sara12 mutant clones.

Sara12/Df(2R)PK1 third larval instar wing discs show an increase in the level of apoptosis compared to wild type.

9.4% of Sara12 embryos lacking both maternal and zygotic Sara+ function die as embryos with cellularization defects, 34.4% die as embryos without a gross morphological phenotype, while 56.3% survive to form mobile first instar larvae.

Zygotic Sara12 mutants die during late larval and pupal development. 5% of these homozygotes survive to adulthood, showing variable vein defects, such as delta formation at the junctions with the margin, branching of the posterior crossvein and partial vein duplications.

92.2% of Sara12 mutants lacking both maternal and zygotic Sara+ function die during embryogenesis, with various phenotypes including cellularization and dorsal/ventral patterning defects.

Targeting of endosomes to the central spindle is normal in dividing wing disc cells in Sara12 zygotic mutants.

Sara12/Df(2R)PK1 wing discs show an increase in the level of apoptosis compared to wild type.

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
Partially rescued by
Comments

Expression of SaraUbi.T:Avic\GFP largely rescues the lethality associated with homozygous Sara12.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (3)