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General Information
Symbol
Dmel\mid1
Species
D. melanogaster
Name
FlyBase ID
FBal0012261
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:
C5464013T
Reported nucleotide change:
C?T
Amino acid change:
Q128term | mid-PA; Q128term | mid-PB
Reported amino acid change:
Q128term
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
Nucleotide substitution: C?T.
Amino acid replacement: Q128term.
Nucleotide substitution: C659T. (Nucleotide numbering is according to cDNA clone RE27439).
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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference
mid1/mid8A69N1 embryos have disorganised and/or missing muscle fibers (lateral transverse muscles 3 and 4 and the segment border muscle). mid1/mid1 embryos have a significantly reduced percentage presence of lateral transverse muscle 4 and a significantly increased number of nuclei in transverse muscle 4 compared to controls. In hemisegments with four LT muscles, mid1/mid1 embryos show a shift in fate of the LT4 muscle towards LT1-3: the most posterior LT muscle is no longer shifted dorsally and contains an increased number of nuclei compared to controls.
midB23/mid1 mutant embryos exhibit gonad development defects that are similar in penetrance and severity to midB23 homozygotes.
An additional, ectopic eve-postive neuron is observed within the nerve cord in 35-38% of hemisegments in ~14 hour-old mutant embryos. In midlos1/mid1 embryos, the ectopic neuron is seen in 30-39% of hemisegments; in mid2/mid1 embryos, the ectopic neuron is seen in 33-34% of hemisegments; in mid1/Df(2L)Exel6012 embryos, the ectopic neuron is seen in 63-66% of hemisegments. Further experiments suggest this is an ectopic RP2 (eRP2) neuron, resulting from the transformation of a wild type neuron termed the 'M-neuron', with an ectopic GMC-1-like cell and a RP2 sib-like cell also present. This extra RP2/sib lineage is formed 2-2.5 hours after the development of the bona fide RP2 lineage.
The longitudinal tracks are interrupted and the posterior commissures are thinner than normal in mid1 embryos. The RP1 and RP3 motor axons stall or follow longitudinal axons in homozygous embryos (in wild-type embryos they exit the central nervous system towards the periphery). Sensory axons in the peripheral nervous system branch excessively or cross segment borders in mutant embryos.
mid1 and mid1/Df(2L)x528 mutant embryos show a significant loss of NB1-1 in the odd-numbered abdominal segments (77.3% and 80% loss, respectively) while the loss of NB1-1 in the even-numbered abdominal segments is minimal (6.8 and 5%).
Stage 17 mid1 embryos show a partially penetrant heart phenotype, in which some embryos show defects in the alignment of cardioblasts and pericardial cells.
Stage 16 mid1 homozygous embryos have a normal number of cells in the dorsal vessel, which has normal overall morphology. But they have increased numbers of elongated, putative ostia forming cells per hemisegment in the heart region and a corresponding decrease in numbers of dorsal vessel cells expressing cardioblast markers.
Homozygous larvae show loss of denticles predominantly in the ventral-most region of odd-numbered segments.
Denticle bands are defective in the ventral midline.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressor of
Statement
Reference
mid1/mid[+] is a suppressor of visible | dominant phenotype of gcmPyx
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference
The decreased number of ostial cardioblasts observed in edlk06602 mutant embryos is rescued by mid1 homozygosity.
mid1/Df(2L)BSC810 embryos have disorganised and/or missing muscle fibers (lateral transverse muscles 3 and 4, segment border muscle, lateral oblique 1) compared to wild type.
mid1 ptc9 larvae show complete loss of denticle belts in odd-numbered segments.
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments
Driving midScer\UAS.cLa with Scer\GAL4Mef2.PR in mid1/mid1 embryos restores Kr expressing founder cells at the lateral transverse muscle 4 position.
Expression of midScer\UAS.cBa in the mesoderm under the control of Scer\GAL4twi.PG fully rescues the lack of somatic gonadal precursor (SGP) cluster fusion and germ cell ensheathment seen in midB23/mid1 mutant embryos. The number of scattered germ cells is reduced. The SGP-related defects are also rescued in the majority of embryos when midScer\UAS.cBa is expressed under the control of Scer\GAL4Six4.PT, but not to the extent seen with Scer\GAL4twi.PG.
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (17)