FB2025_01 , released February 20, 2025
Allele: Dmel\salm1
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General Information
Symbol
Dmel\salm1
Species
D. melanogaster
Name
FlyBase ID
FBal0015124
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
salIIA55, sal1, sal2A55, salIIA55, salIIA, salmIIA
Key Links
Nature of the Allele
Progenitor genotype
Cytology
Description
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

Homozygous loss of salm in the muscle (generated by inducing the Df(2L)salmFRT deletion in muscle using UAS-FLP under the control of Scer\GAL4Mef2.PR, in trans to salm1) results in complete tubular reversion of the indirect flight muscles.

Dorsal trunk cells are transformed into visceral branch identity in salm1 embryos. The tips of the transformed branches contain terminal cells and fusion cells, as in the lateral trunk of wild-type embryos.

Single cell class IV dendrite arborisation (da) neuron clones that are homozygous for salm1 do not show defects in the establishment or maintenance of dendritic tiling.

Extra lateral chordotonal organs are formed in mutant embryos, with the number of lateral chordotonal organs in the cluster frequently being 6 or 7 (instead of the wild type 5). The extra chordotonal organs are restricted to the lateral cluster with the other abdominal chordotonal organs (V'ch1, VchAB) remaining wild-type in number.

Homozygous salm1 clones between veins L2 and L3 have an ectopic vein L2 fork running within and along the clone boundary. Homozygous salm1 clones which intersect the wing margin are associated with ectopic islands of triple row bristles.

Clone on the dorsal surface of the wing between wing vein L2 and L3 causes branching of the wing vein L2 on the presumptive dorsal surface; forked L2 phenotype. The ectopic vein forms within and at the extreme anterior edge of the clone. When the clone extends to the margin ectopic triple row bristles are formed. Clones near the posterior wing edge cause bifurcation of wing vein L5 or the posterior crossvein.

Defects in the identity of posterior segments A8 and A9, distinct posterior spiracles are not formed.

Double mutant combinations with cnc- embryos show additive effects in the head skeleton. The strong dorsal pouch syndrome of Dfd14 embryos (labral structures are poorly involuted) is suppressed in the double mutant combination (closed oral aperture).

Anterior prothoracic pattern elements differentiate in the labial segment, two abdomen segments are replaced with thoracic segments.

embryonic lethal. Shows partial homeotic transformation of labium to prothorax and of A9 and 10 toward A8. Point mutants judged to be amorphic or nearly so judging from the phenotype of salm/Df compared with salm/salm. salm; Abd-B double mutants exhibit thoracic structures in parasegments 14 and 15; similarly, salm and Scr seem to act independently on head structures in parasegments 2 and possibly 1.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement
Reference

salm1 has visible | recessive phenotype, suppressible by kniri-1

salm1 has lethal | embryonic stage phenotype, suppressible by salaC20-sal

Phenotype Manifest In
Suppressed by
Statement
Reference

salm1 has wing vein L2 | ectopic phenotype, suppressible by kniri-1

NOT suppressed by
Enhancer of
Statement
Reference

salm1 is an enhancer of leg phenotype of Pc16

salm1 is an enhancer of sex comb phenotype of Pc16

salm1 is an enhancer of leg phenotype of ph-d2

salm1 is an enhancer of sex comb phenotype of ph-d2

salm1 is an enhancer of leg phenotype of ph-p2

salm1 is an enhancer of sex comb phenotype of ph-p2

Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

Most tracheal tip cells adopt the terminal cell fate in salm1 aopO199 double mutant embryos.

Embryos doubly mutant for rib1 and tkv4 form only the transverse connectives and visceral branches. The addition of salmScer\UAS.cKa and Scer\GAL4btl.PS to rib1 embryos does not rescue the dorsal trunk migration phenotype.

Ectopic L2 forks are not induced by homozygous salm1 clones in a kniri-1 background. Ectopic islands of triple row bristles are induced by salm1 clones in a kniri-1 background.

Embryonic lethality and the homeotic effects can be rescued by the salaC20-sal construct, individuals die as crawling larvae.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Not rescued by
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (9)
References (38)