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General Information
Symbol
Dmel\msk5
Species
D. melanogaster
Name
FlyBase ID
FBal0122948
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

G8116443T

Reported nucleotide change:

G4T

Amino acid change:

E2term | msk-PA

Reported amino acid change:

E2term

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Amino acid replacement: E2term.

Nucleotide substitution: G4T.

Amino acid replacement: ?2term.

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

msk4/msk5 embryos show a muscle detachment phenotype.

Mosaic animals in which the whole eye is homozygous (generated using the EGUF system) have small disorganised eyes. There is a general disruption of the normal ommatidial organisation. Interommatidial bristle loss or duplication is occasionally seen. The number of cone cells per ommatidium is often decreased to three and many of these cone cells are abnormal in size. Primary pigment cells are often enlarged and abnormally shaped. The number of secondary and tertiary pigment cells is often drastically reduced compared to wild type, as shown by multiple ommatidial fusions. Ommatidia occasionally have a normal number and arrangement of rhabdomeres, but most have a decreased number of rhabdomeres, or lack them completely. 22% of ommatidia completely lack the small rhabdomeres of both R7 and R8. Rhabdomere morphology is also disrupted, with some appearing rectangular or oblong in shape.

Induction of msk5 somatic clones 48 hours before dissection at late third instar larval stage generates small homozygous msk5 null clones and homozygous wild-type twin spots, both anterior and posterior to the furrow. However, when clones are induced 72 hours before late third instar stage, there are fewer clones, and the twin spots are much larger than the msk5 null clones. At 72 hours after clone induction, msk5 clones survive posterior to the furrow in postmitotic territories, but there are no msk5 clones (only twin-spots) anterior to the furrow. Additionally, clone induction 96 hours before dissection at late third instar larval stage reveals even fewer but larger twin-spots, and no msk5 clones. Thus msk5 mutant cells are lost from proliferative domains.

msk5 eye clones do not exhibit any cell cycle defects.

msk5 eye clones are able to differentiate into neurons, and can be specified as photoreceptor cell-types, including the R8, R3 and R4 and R7 cells.

Some ommatidia no longer rotate reliably in msk5 eye clones. In these cases, the R4 cell is misplaced, although in some cases two R4 cells are specified.

Homozygotes die as late embryos or early larvae, with a normal looking cuticle. Only homozygous clones containing 8 or fewer cells are recovered in the wing. When mskScer\UAS.cLa is expressed under the control of Scer\GAL4en-e16E, homozygous msk5 clones induced in the posterior wing can grow to a typical size of more than 100 cells, whereas homozygous msk5 clones induced in the anterior wing are typically composed of 8 cells or less, indicating that msk is required for the growth of cells in the wing.

Mutant embryos develop VA2 precursor cells in nearly all of the appropriate hemisegments.

Lethality acts in the late embryo or early larval stages. Embryos are morphologically wild type.

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

msk[+]/msk5 is an enhancer of visible phenotype of DgdsRNA.UAS, Scer\GAL4Tub.PU

msk[+]/msk5 is an enhancer of visible phenotype of rl1

Suppressor of
Statement
Reference

msk[+]/msk5 is a suppressor of visible phenotype of DysdsRNA.NH2.UAS, Scer\GAL4Act.PU

msk[+]/msk5 is a suppressor of visible phenotype of DysdsRNA.C.UAS, Scer\GAL4Tub.PU

msk[+]/msk5 is a suppressor of visible phenotype of Scer\GAL4c684, ifm8.UAS

msk[+]/msk5 is a suppressor of visible phenotype of rlSem

NOT Suppressor of
Statement
Reference

msk5 is a non-suppressor of visible phenotype of EgfrE1

msk5 is a non-suppressor of visible phenotype of rlSem

Phenotype Manifest In
Enhanced by
Statement
Reference

msk4/msk5 has visceral muscle fiber | embryonic stage phenotype, enhanceable by Ced-12KO/Ced-12[+]

Enhancer of
Statement
Reference

msk5 is an enhancer of wing vein phenotype of rhoStg

msk[+]/msk5 is an enhancer of wing vein L4 phenotype of rl1

Suppressor of
Statement
Reference

msk[+]/msk5 is a suppressor of eye phenotype of Scer\GAL4lz-gal4, sensUAS.cNa

msk[+]/msk5 is a suppressor of wing phenotype of Scer\GAL4c684, ifm8.UAS

msk[+]/msk5 is a suppressor of wing vein | ectopic phenotype of rlSem

NOT Suppressor of
Statement
Reference

msk5 is a non-suppressor of wing vein | ectopic phenotype of EgfrE1

msk5 is a non-suppressor of wing vein | ectopic phenotype of rlSem

Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The progeny from msk5/+ mothers and dpphr4/+ fathers present embryo ventralization, as compared to controls.

The presence of mbcD11.2/+ or Ced-12KO/+ increases the severity of muscle attachment defects in msk4/msk5 embryos.

One copy of msk5 weakly suppresses the detached posterior crossvein phenotype seen when DysdsRNA.NH2.Scer\UAS is expressed under the control of Scer\GAL4Act.PU.

One copy of msk5 moderately suppresses the detached posterior crossvein phenotype seen when DysdsRNA.C.Scer\UAS is expressed under the control of Scer\GAL4tub.PU but produces extra wing vein material.

One copy of msk5 enhances the posterior crossvein phenotype seen when DgdsRNA.Scer\UAS is expressed under the control of Scer\GAL4tub.PU.

The wing blistering caused by expression of ifm8.Scer\UAS under the control of Scer\GAL4337Y is suppressed by msk5/+.

msk5 dominantly suppresses the formation of extra eve-positive mesodermal cells seen in embryos expressing csw::Src64Bsrc90.Scer\UAS under the control of Scer\GAL4twi.PG.

Enhancing effect of msk1 and msk2 on the rl1 phenotype is marked and that of msk5 is dramatic.

Xenogenetic Interactions
Statement
Reference

Expression of BacA\p35GMR.PH to inhibit apoptosis fails to suppress the small clone size in msk5 eye clones. msk5 null cells that survive into phase 2 eventually die in the pupal stage.

Complementation and Rescue Data
Partially rescued by
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer

Selected as: a dominant suppressor of the wing blister phenotype caused by ifm8.Scer\UAS expressed under the control of Scer\GAL4c684.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (10)