FB2024_03 , released June 25, 2024
Allele: Dmel\Handko
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General Information
Symbol
Dmel\Handko
Species
D. melanogaster
Name
FlyBase ID
FBal0196563
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Progenitor genotype
Associated Insertion(s)
Cytology
Description

The Hand coding region has been replaced by a w[+] marker.

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

Hand173/Handko and Handko/Df(2L)J1 adults suffer a high rate of premature mortality.

Visceral mesoderm development appears normal in homozygous Handko embryos.

40% of Handko mutants die as embryos and the remaining 60% die as first instar larvae. Handko larvae are smaller and less active than wild-type larvae. About ~3% of mutants survive for a few days after hatching, but are sluggish and remain as small as first instar larvae.

Approximately 20% of Handko mutant embryos show a range of cardiac morphological defects, including misalignment of cardioblasts and reduced numbers of pericardial nephrocytes. Additionally, the number of lymph gland

hematopoietic cells is reduced in more than half of Handko mutant embryos and lymph gland cell clusters are often missing completely. Severely affected embryos (about 3%) show a significant reduction of all three cell types. However, neither the ring gland nor somatic muscles are affected.

Handko mutants that survive to the first instar larval stage show cardiac and lymph gland defects. At 18 hours after egg laying (AEL), the majority of Handko mutants have cardioblasts and pericardial cells that are well aligned at the dorsal midline. However, the number of lymph gland hematopoietic cells flanking the anterior aorta is largely reduced at this stage. By 20 hours AEL a subset of Handko mutants start to show a reduced number of pericardial cells and thinner heart tube. The cardiac morphological defects become more significant around 24 hours AEL as mutants show a hypoplastic heart with an abnormally thin heart tube and further reduced numbers of pericardial cells, as well as gaps in the posterior heart tube. By 26 hours AEL the three-dimensional chamber-like structure of the posterior heart is dramatically disrupted and most pericardial nephrocytes are missing. The lymph gland is absent or largely reduced by 24 hours AEL in the majority of Handko first instar larvae. TUNEL labelling shows that more than 30% of Handko larvae show increased apoptosis in regions normally occupied by lymph gland hematopoietic progenitors and pericardial cells and that a subset of mutants show increased apoptosis of the cardioblasts.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement
Reference
NOT suppressed by
Statement
Reference
Phenotype Manifest In
Suppressed by
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference
Xenogenetic Interactions
Statement
Reference

Expression of BacA\p35Scer\UAS.cHa under the control of Scer\GAL4HCH.Hand in Handko mutant embryos prevents ectopic apoptosis. These mutants no longer show reduced lymph gland hematopoietic progenitors and pericardial nephrocytes during the late stage embryonic stage. Larval lethality is not prevented but is delayed. At 18 hours AEL, Scer\GAL4HCH.Hand>BacA\p35Scer\UAS.cHa; Handko larvae start to display an abnormal appearance. At 24 hours AEL, these larvae develop thin hypoplastic hearts and reduced lymph gland hematopoietic progenitors, although this phenotype is less severe than that seen at the same stage in Handko larvae.

Expression of Hsap\HAND2Scer\UAS.cHa, under the control of Scer\GAL4HCH.Hand, in Handko mutant embryos rescues the cardiac and lymph gland defects of these mutants, such that almost all embryos hatch and develop into first instar larvae with nearly normal hearts and lymph glands. These larvae survive for up to 6 days.

Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer

Separable from: a second-site lethal mutation.

The occasional embryonic dorsal vessel defects observed in FBrf0190292 for the Handko chromosome are attributable to a linked lethal mutation on the chromosome and not due to the loss of Hand function caused by the Handko allele itself.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (3)