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General Information
Symbol
Ggal\MLCKct.UAS
Species
G. gallus
Name
FlyBase ID
FBal0141735
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-ctMLCK, UAS-MLCK
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Carried in construct
Cytology
Nature of the lesion
Statement
Reference

UASt regulatory sequences drive expression of constitutively active form of Ggal\MLCK (a truncated form in which the autoinhibitory domain has been deleted by introducing two adjacent stop codons after residue 779).

Allele components
Product class / Tool use(s)
Encoded product / tool
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

The expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4da.PU results in hyper-constriction of epidermal leading edge cells during dorsal closure, as compared to controls.

Expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4c381 results in uniform amnioserosal cell rounding.

Expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4prd.RG1 in individual amnioserosa cells induces premature apical constriction in these cells.

Expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4prd.RG1 results in deep segmental grooves in the embryo.

Stage 16 embryos overexpressing Ggal\MLCKct.Scer\UAS driven by Scer\GAL4ftz.ng display axon bundles that cross the midline inappropriately.

When Ggal\MLCKct.Scer\UAS is driven by Scer\GAL4ftz.ng, midline crossovers are seen in the pCC/MP2 pathway axons in 8.2% of embryos. An average of 1.4 crossovers are seen per embryo.

Expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4elav.PLu causes specific defects in the formation of the pCC/MP2 pathway. Initial extension of the pCC axons at stage 12 appears normal. By stage 14, the common MP2 pathway and the separate MP1 pathway are formed normally, but some of the axons of the vMP2 pathway cross the midline. By stage 16, pCC/MP2 pathway axons are seen to cross the midline in several segments, while the remaining longitudinal connectives appear unaffected. Expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng causes axons of the pCC/MP2 pathway to cross the midline incorrectly in 9-19% of embryos.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Suppressed by
Enhancer of
Suppressor of
Phenotype Manifest In
Enhanced by
Statement
Reference
Suppressed by
Statement
Reference
Enhancer of
Suppressor of
Additional Comments
Genetic Interactions
Statement
Reference
Xenogenetic Interactions
Statement
Reference

The abnormal cell protrusions that are seen extending from amnioserosa cells in the progeny of dia2 Rho172O double heterozygous females during dorsal closure are suppressed by expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4e22c.

Co-expression of Ggal\MLCKct.Scer\UAS with Rac1V12.Scer\UAS under the control of Scer\GAL4ftz.ng results in a synergistic increase in the frequency of incorrect axon projections across the midline, compared with Rac1V12.Scer\UAS-overexpression alone.

When fraScer\UAS.cKa is co-expressed with both Rho1V14.Scer\UAS and Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng, all embryos exhibit severe defects in scaffold formation. Many ventral nerve cord axons either cross the midline or collapse into the midline region.

Co-expression of sqhT20A.S21A.Scer\UAS under the control of Scer\GAL4ftz.ng suppresses the midline crossing phenotype in embryos expressing both Rho1V14.Scer\UAS and Ggal\MLCKct.Scer\UAS.

No embryos heterozygous for Abl4 and expressing Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng exhibit axonal midline crossing defects.

Co-expression of fraScer\UAS.cKa with Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng increases the frequency of axonal midline crossing abnormalities.

Heterozygous Abl4 almost completely suppresses the axonal midline crossing phenotype of embryos co-expressing Ggal\MLCKct.Scer\UAS with fraScer\UAS.cKa under the control of Scer\GAL4ftz.ng.

Homozygous Abl4 enhances the axonal midline crossing phenotype of embryos co-expressing Ggal\MLCKct.Scer\UAS with fraScer\UAS.cKa under the control of Scer\GAL4ftz.ng.

The heterozygous Abl4-dependent suppression of the axonal midline crossing phenotype in embryos expressing Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng is lost if Rho1V14.Scer\UAS is also expressed.

The addition of Rho1N19.Scer\UAS to Ggal\MLCKct.Scer\UAS, Scer\GAL4ftz.ng embryos enhances the midline crossover phenotype seen in the pCC/MP2 pathway axons. 28% of embryos exhibit the phenotype. An average of 1.3 crossovers are seen per embryo. The addition of Rho1V14.Scer\UAS to Ggal\MLCKct.Scer\UAS, Scer\GAL4ftz.ng embryos enhances the midline crossover phenotype seen in the pCC/MP2 pathway axons. 45% of embryos exhibit the phenotype. An average of 2.1 crossovers are seen per embryo. The addition of Rac1N17.Scer\UAS to Ggal\MLCKct.Scer\UAS, Scer\GAL4ftz.ng embryos partially suppresses the midline crossover phenotype seen in the pCC/MP2 pathway axons. 4.0% of embryos exhibit the phenotype. An average of 1.o crossovers are seen per embryo. The addition of Rac1V12.Scer\UAS to Ggal\MLCKct.Scer\UAS, Scer\GAL4ftz.ng embryos enhances the midline crossover phenotype seen in the pCC/MP2 pathway axons. 95% of embryos exhibit the phenotype. An average of 4.2 crossovers are seen per embryo. The addition of Cdc42N17.Scer\UAS to Ggal\MLCKct.Scer\UAS, Scer\GAL4ftz.ng embryos partially suppresses the midline crossover phenotype seen in the pCC/MP2 pathway axons. 4.4% of embryos exhibit the phenotype. An average of 1.3 crossovers are seen per embryo. The addition of Cdc42V12.Scer\UAS to Ggal\MLCKct.Scer\UAS, Scer\GAL4ftz.ng embryos enhances the midline crossover phenotype seen in the pCC/MP2 pathway axons. 97% of embryos exhibit the phenotype. An average of 7.8 crossovers are seen per embryo.

The midline crossover phenotype caused expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng is partially suppressed by sqh1 or sqhA20.A21.T:Zzzz\FLAG and is enhanced by sqhE20.E21. Fas2-positive axon bundles cross the midline in about 83% or 88% of robo1/+ embryos which are also expressing Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng. Fas2-positive axon bundles cross the midline in 100% of sli2/+ embryos which are also expressing Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng. The midline crossover phenotype caused expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng is partially suppressed by fra4/+ and completely suppressed by fra3/+. The midline crossover phenotype caused expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng is enhanced by coexpression of fraScer\UAS.cKa. Expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng in comm1 embryos results in 49% of embryos showing some axons crossing the midline and in many cases thin commissures are present. Expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4elav.PLu in comm1 embryos results in partial commissure formation in 71% of embryos.

Complementation and Rescue Data
Comments
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Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Symbol Synonym
Ggal\MLCKct.Scer\UAS
Ggal\MLCKct.UAS
Name Synonyms
Secondary FlyBase IDs
    References (9)