FlyBase Allele Report: Dmel\msk[5]

General Information

Symbol

Dmel\msk⁵

Species

D. melanogaster

Name

FlyBase ID

FBal0122948

Feature type

allele

Associated gene

Dmel\msk

Associated Insertion(s)

Carried in Construct

Key Links

Genomic Maps

JBrowse

Allele class

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

Mutagen

ethyl methanesulfonate

(Baker et al., 2002)

Progenitor genotype

Cytology

Description

Amino acid replacement: E2term.

(Baker et al., 2002)

Nucleotide substitution: G4T.

(Baker et al., 2002)

Amino acid replacement: ?2term.

(Lorenzen et al., 2001)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

3L:8,116,443..8,116,443 [+]

Nucleotide change:

G8116443T

Reported nucleotide change:

G4T

Amino acid change:

E2term | msk-PA

Reported amino acid change:

E2term

(Baker et al., 2002)

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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

abnormal cell death | larval stage | somatic clone

(Vrailas et al., 2006)

lethal | embryonic stage | recessive

(Baker et al., 2002)

lethal | larval stage | recessive

(Baker et al., 2002)

lethal | recessive

(Lorenzen et al., 2001)

visible | recessive | somatic clone

(Pepple et al., 2007)

Phenotype Manifest In

Detailed Description

Statement

Reference

msk⁴/msk⁵ embryos show a muscle detachment phenotype.

(Liu et al., 2013)

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.

(Pepple et al., 2007)

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.

(Vrailas et al., 2006)

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 msk^Scer\UAS.cLa is expressed under the control of Scer\GAL4^en-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.

(Baker et al., 2002)

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

(Johnson Hamlet and Perkins, 2001)

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

(Lorenzen et al., 2001)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

NOT suppressed by

Statement

Reference

msk⁵ has abnormal cell death | somatic clone | larval stage phenotype, non-suppressible by BacA\p35^GMR.PH

(Vrailas et al., 2006)

Enhancer of

Statement

Reference

msk[+]/msk⁵ is an enhancer of visible phenotype of Dg^RNAi.UAS, Scer\GAL4^Tub.PU

(Kucherenko et al., 2008)

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

(Lorenzen et al., 2001)

Suppressor of

Statement

Reference

msk[+]/msk⁵ is a suppressor of visible phenotype of Dys^RNAi.NH2.UAS, Scer\GAL4^Act.PU

(Kucherenko et al., 2008)

msk[+]/msk⁵ is a suppressor of visible phenotype of Dys^RNAi.C.UAS, Scer\GAL4^Tub.PU

(Kucherenko et al., 2008)

msk[+]/msk⁵ is a suppressor of visible phenotype of Scer\GAL4^c684, if^m8.UAS

(Baker et al., 2002)

msk[+]/msk⁵ is a suppressor of visible phenotype of rl^Sem

(Lorenzen et al., 2001)

NOT Suppressor of

Statement

Reference

msk⁵ is a non-suppressor of visible phenotype of Egfr^E1

(Baker et al., 2002)

msk⁵ is a non-suppressor of visible phenotype of rl^Sem

(Baker et al., 2002)

Phenotype Manifest In

Enhanced by

Statement

Reference

msk⁴/msk⁵ has visceral muscle fiber | embryonic stage phenotype, enhanceable by mbc^D11.2/mbc[+]

(Liu et al., 2013)

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

(Liu et al., 2013)

Enhancer of

Statement

Reference

msk[+]/msk⁵ is an enhancer of posterior crossvein phenotype of Dg^RNAi.UAS, Scer\GAL4^Tub.PU

(Kucherenko et al., 2008)

msk⁵ is an enhancer of wing vein phenotype of rho^Stg

(Marenda et al., 2006)

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

(Lorenzen et al., 2001)

Suppressor of

Statement

Reference

msk[+]/msk⁵ is a suppressor of posterior crossvein phenotype of Dys^RNAi.C.UAS, Scer\GAL4^Tub.PU

(Kucherenko et al., 2008)

msk[+]/msk⁵ is a suppressor of posterior crossvein phenotype of Dys^RNAi.NH2.UAS, Scer\GAL4^Act.PU

(Kucherenko et al., 2008)

msk[+]/msk⁵ is a suppressor of eye phenotype of Scer\GAL4^lz-gal4, sens^UAS.cNa

(Pepple et al., 2007)

msk[+]/msk⁵ is a suppressor of wing phenotype of Scer\GAL4^c684, if^m8.UAS

(Baker et al., 2002)

msk[+]/msk⁵ is a suppressor of mesoderm phenotype of Scer\GAL4^twi.PG, csw^{UAS.Tag:Myr(Src64B)}

(Johnson Hamlet and Perkins, 2001)

msk[+]/msk⁵ is a suppressor of wing vein | ectopic phenotype of rl^Sem

(Lorenzen et al., 2001)

NOT Suppressor of

Statement

Reference

msk⁵ is a non-suppressor of wing vein | ectopic phenotype of Egfr^E1

(Baker et al., 2002)

msk⁵ is a non-suppressor of wing vein | ectopic phenotype of rl^Sem

(Baker et al., 2002)

Other

Statement

Reference

dpp^hr4, msk[+]/msk⁵ has embryo | maternal effect phenotype

(Quijano et al., 2016)

Dys^RNAi.C.UAS, msk[+]/msk⁵ has wing vein | ectopic phenotype

(Kucherenko et al., 2008)

Additional Comments

Genetic Interactions

Statement

Reference

The progeny from msk⁵/+ mothers and dpp^hr4/+ fathers present embryo ventralization, as compared to controls.

(Quijano et al., 2016)

The presence of mbc^D11.2/+ or Ced-12^KO/+ increases the severity of muscle attachment defects in msk⁴/msk⁵ embryos.

(Liu et al., 2013)

One copy of msk⁵ weakly suppresses the detached posterior crossvein phenotype seen when Dys^{dsRNA.NH2.Scer\UAS} is expressed under the control of Scer\GAL4^Act.PU.

One copy of msk⁵ moderately suppresses the detached posterior crossvein phenotype seen when Dys^{dsRNA.C.Scer\UAS} is expressed under the control of Scer\GAL4^tub.PU but produces extra wing vein material.

One copy of msk⁵ enhances the posterior crossvein phenotype seen when Dg^{dsRNA.Scer\UAS} is expressed under the control of Scer\GAL4^tub.PU.

(Kucherenko et al., 2008)

The wing blistering caused by expression of if^m8.Scer\UAS under the control of Scer\GAL4^337Y is suppressed by msk⁵/+.

(Baker et al., 2002)

msk⁵ dominantly suppresses the formation of extra eve-positive mesodermal cells seen in embryos expressing csw::Src64B^{src90.Scer\UAS} under the control of Scer\GAL4^twi.PG.

(Johnson Hamlet and Perkins, 2001)

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

(Lorenzen et al., 2001)

Xenogenetic Interactions

Statement

Reference

Expression of BacA\p35^GMR.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.

(Vrailas et al., 2006)

Complementation and Rescue Data

Partially rescued by

msk⁵ is partially rescued by Scer\GAL4^ey.PH/msk^UAS.cLa

(Pepple et al., 2007)

Comments

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

23879

y¹ w^*; mwh¹ msk⁵ P{neoFRT}80B/TM3, P{ftz-lacZ.ry⁺}TM3, Sb¹ ry^*

Notes on Origin

Discoverer

Selected as: a dominant suppressor of the wing blister phenotype caused by if^m8.Scer\UAS expressed under the control of Scer\GAL4^c684.

(Baker et al., 2002)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (1)

Reported As

Symbol Synonym

msk⁵

(Restrepo et al., 2022, Quijano et al., 2016, Liu et al., 2013, Kucherenko et al., 2008, Pepple et al., 2007, Xu et al., 2007, Vrailas et al., 2006)

Name Synonyms

Secondary FlyBase IDs

References (11)

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