FB2024_03 , released June 25, 2024
Allele: Dmel\Dronc51
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General Information
Symbol
Dmel\Dronc51
Species
D. melanogaster
Name
FlyBase ID
FBal0193076
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Progenitor genotype
Cytology
Description

Imprecise excision of P{SUPor-P}KG02994 has deleted genomic sequence from the insertion site to codon 303 of Nc (in exon 2).

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 ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

neuron & ventral nerve cord | ectopic (with DroncI24)

Detailed Description
Statement
Reference

Nc51 mutant eye clones exhibit extra ommatidial pigment cells in the pupal retina.

NcI24/Nc51 and NcI29/Nc51 transheterozygotes exhibit a delay in vCrz neuron apoptosis. At 7 hours after puparium formation 75% vCrz neurons are still present although these all die by 48 hours after puparium formation.

S2PKG08356/S2P1, Nc51/+ and S2PKG08356/S2P1, Nc51/Nc51 mutant larvae exhibit lethality between second and third instar stages. Lethality is rescued partially by supplementing fly food with fatty acids, but viability is still reduced compared to S2PKG08356/S2P1 mutants.

Nc51 mosaic wings retain Disc\RFPhs.DsRedT4.T:nls5-positive wing epithelial cells 4-11 days after eclosion, whereas control epithelial cells undergo apoptosis moments after eclosion.

Wing blemishes are not seen in Nc51 heterozygotes.

Programmed cell death inCrz-expressing neurons in the ventral nerve cord is significantly delayed in Nc51/NcI24 mutants. Approximately 12 neurons still survive at 7 hours after pupal formation, while the number is reduced to approximately 8 at 16 hours after pupal formation, and none at 48 hours after pupal formation.

Nc51/NcI29 mutants exhibit a delay in programmed cell death in Crz-expressing neurons in the ventral nerve cord during pupation.

Dendrites of Nc51 mutant C4da neuron clones appear normal at larval stages. However, unlike wild-type, these neurons fail to properly prune their larval dendrites during metamorphosis and most display relatively intact primary and secondary larval dendritic arbors at 18 hours after puparium formation.

Nc2/Nc51 mutant third instar larvae have melanotic nodules found in the hemocoel or in association with He-positive lymph glands. They also show gut melanisation not accompanied by tissue overgrowth or hemocyte encapsulation.

Nc51 homozygous embryos hatch at the normal time, but the larvae develop more slowly than wild-type. These larvae fail to pupariate, but continue to grow for some time after controls pupariate. The resulting giant larvae die at 10-12 days after wild-type larvae pupariate. Unlike wild-type larvae, these larvae are not induced to pupariate early by feeding with ecdysone at the mid-third instar.

Nc51 homozygous larvae fail to exhibit cell death in the larval midgut ,as wild-type larvae do, at end of the third larval instar (assayed by Tunel staining) or in response to feeding with ecdysone at mid-third instar (assayed by acridine orange staining).

Nc51 homozygous embryos display head involution defects. Post-embryonic growth of these animals is slower than in wild-type and both larval moults and pupation are delayed. However, once they do reach the wandering late third instar larval stage, these larvae are generally bigger wild-type counterparts and have larger and sometimes deformed discs and brain. They also exhibit hyperplasia of the blood cells. These animals die during early pupal stages, sometimes with visible melanotic tumors.

Nc51 homozygous embryos laid by NcKG02994/Nc51 mothers do not hatch and have more severe head involution defects than Nc51 homozygotes laid by wild-type mothers. These have embryos decreased levels of cell death, as assayed by tunel staining, in the epidermis at stage 12 and the ventral nerve cord at stage 15/16. Consistent with a reduction in cell death, increases in cell number are see in multiple cases: Extra cells are associated with Bolwig's organ at stage 15 and extra cells are present in the ventral nerve cord at late embryonic stages

NcKG02994/Nc51 adults have a higher frequency of post-alar bristle duplication than NcKG02994 homozygous adults.

Adult eyes completely populated by Nc51 homozygous somatic clone cells are normal sized but rough. This is not due to supernumerary photoreceptor cells, however, ommatidial pre-clusters are irregularly spaced immediately posterior to the furrow in late third instar eye discs of this genotype.

No obvious defects are present in the wings of newly eclosed flies carrying Nc51 homozygous clones. But, the wings of these flies develop melanized blotches as they age.

Cultured hemocytes isolated from third instar Nc51 homozygous larvae are much less sensitive to induction of apoptosis by a variety of pro-apoptotic agents (cycloheximide, Actinomycin D, etoposide (Topoisomerase II inhibitor), ethanol, and smac mimetic) than wild-type controls. In addition, levels of constitutive apoptosis in these cells are significantly lower than controls.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
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Reference
Suppressed by
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Enhancer of
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Suppressor of
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Reference

Dronc51/Dronc[+] is a suppressor | partially of visible | adult stage phenotype of Scer\GAL4nub.PU, sydGLC01419

Dronc51/Nc[+] is a suppressor of abnormal neuroanatomy phenotype of ninaE17, ninaEP37H

Dronc51/Nc[+] is a suppressor of viable | conditional phenotype of S2PKG08356/S2P1

NOT Suppressor of
Statement
Reference
Phenotype Manifest In
Suppressed by
Statement
Reference

DroncI24/Dronc51 has neuron phenotype, suppressible by DreddL23

Enhancer of
Statement
Reference
Suppressor of
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Reference

Dronc51/Nc[+] is a suppressor of eye phenotype of grimGMR.PH

Dronc51/Nc[+] is a suppressor of eye phenotype of rprGMR.PH

NOT Suppressor of
Statement
Reference

Dronc51 is a non-suppressor of neuroblast | larval stage phenotype of fzy1/fzy5032

Dronc51/Nc[+] is a non-suppressor of eye phenotype of hidGMR.PG

Additional Comments
Genetic Interactions
Statement
Reference

Retinal degeneration and light-response defects are strongly suppressed in ninaEP37H, ninaE17, Nc51/+ flies.

Nc51 does not suppress the neuroblast loss seen in fzy5032/fzy1 mutant larval brains.

No viable vCrz neurons are detected at 7 hours after puparium formation in DreddL23; NcI24/Nc51 double mutants.

A Nc51 heterozygous background enhances ectopic neuroblast formation due to numbS2D.Scer\UAS expression.

A Nc51 heterozygous background enhances the melanotic blemishes found on ArkCD4 mutant wings.

Nc51/+ partially suppresses the small, rough eye phenotype caused by rprGMR.PH or grimGMR.PH but not that caused by WGMR.PG.

The melanized wing spot phenotype of ArkCD4 homozygotes is enhanced by Nc51/+.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments

Nc+t.drf rescues the partially lethality of Nc51/Nc51 homozygotes with a few animals rescued to adulthood and up to 50% reaching the pharate adult stage. The delays in larval moults seen in Nc51/Nc51 animals are also partially rescued by this transgene.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer

Associated with: CG668551

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (15)