FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\msn172
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General Information
Symbol
Dmel\msn172
Species
D. melanogaster
Name
FlyBase ID
FBal0061020
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Mutagen
Nature of the Allele
Allele class
Progenitor genotype
Caused by aberration
Cytology
Description

Inversion breakpoint within the coding region.

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
exacerbates  carcinoma
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Females carrying homozygous follicle cell clones can produce round eggs.

The planar organisation of basal actin filaments in the follicle cell epithelium at oogenesis stage 7 is disrupted in when the follicle epithelium is primarily composed of homozygous cells, such that the filaments no longer align perpendicular to the anterior-posterior axis. Stage 10 egg chambers containing homozygous follicle cell clones are often shorter and rounder than normal.

2% of msn172 mutant embryos display an anterior dorsal hole, 38% complete dorsal closure but show misalignment of segments and 12% show embryonic lethality without obvious defects during dorsal closure. msn172 embryos show intermittent breaks in the actin distribution at the epithelial margin, typically affecting groups of 2-4 cells. Affected cells are wider and less elongated than neighboring cells with normal actin localization. 30% of the embryos display segment misalignments during the final phase of dorsal closure. The segment misalignment defect is typically accompanied by unusual irregularities in the width of segments during the closure process. Some segments appear abnormally wide, while neighboring segments are excessively constricted.

In msn172 somatic clones in the eye ommatidia often have malformed or missing photoreceptors. Those ommatidia that have the normal complement of photoreceptors are often misrotated and display the wrong chiral form or are symmetrical. In mosaic photoreceptor R3/R4 pairs, the msn+ photoreceptor has a strong preference for adopting the R3 fate. This can often lead to chirality inversions where the msn+ R4 precursor adopts the R3 position displacing the msn172 R3 precursor. The mosaic analysis also showed that for correct 90o rotation there is no bias for any particular photoreceptor.

Homozygous or msn102/msn172 embryos show defects in dorsal closure.

Clones in the eye are externally rough. They contain elongated rhabdomeres and some ommatidia also contain missing or an extra photoreceptor. Eggs from germline clones are never laid.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
NOT Enhancer of
Statement
Reference

msn172/msn[+] is a non-enhancer of visible phenotype of Scer\GAL4en-e16E, kermitGS2053

Suppressor of
Statement
Reference

msn172/msn[+] is a suppressor | partially of visible phenotype of Rab11mo

msn172/msn[+] is a suppressor | partially of visible phenotype of Rab11N124I.UAS, Scer\GAL4GMR.PF

msn172/msn[+] is a suppressor | partially of visible phenotype of Rala35d

msn172/msn[+] is a suppressor of abnormal planar polarity phenotype of dshhs.sev.B

NOT Suppressor of
Statement
Reference

msn172/msn[+] is a non-suppressor of visible phenotype of Scer\GAL4en-e16E, kermitGS2053

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

msn172/msn[+] is a suppressor | partially of eye phenotype of Rab11N124I.UAS, Scer\GAL4GMR.PF

msn172/msn[+] is a suppressor | partially of eye phenotype of Rab11mo

msn172/msn[+] is a suppressor | partially of microchaeta phenotype of Rala35d

msn172/msn[+] is a suppressor of macrochaeta phenotype of Rala35d

msn172 is a suppressor | partially of eye phenotype of Scer\GAL4GMR.PF, egrGS9830

msn172/msn[+] is a suppressor of eye phenotype of Scer\GAL4GMR.PF, egrUAS.cMa

msn172/msn[+] is a suppressor of ommatidium phenotype of dshhs.sev.B

NOT Suppressor of
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The eye defects seen in Rab11mo homozygotes are partially suppressed by msn172/+.

The reduced eye size caused by expression of Rab11N124I.Scer\UAS under the control of Scer\GAL4GMR.PF is partially suppressed by msn172/+.

msn172, suppresses the ommatidial polarity defects seen in dshhs.sev.B flies grown at 29oC. About 80% of ommatidia are in their correct polarity compared to 55% in dshhs.sev.B alone.

The dorsal open phenotype of msn102/msn172 embryos is partially rescued by JraAsp.hs.sev expressed using heat shock or by tkvQ253D.Scer\UAS.cNb expressed under the control of Scer\GAL469B.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Rescued by
Partially rescued by
Not rescued by
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
References (19)