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General Information
Symbol
Dmel\MtlΔ
Species
D. melanogaster
Name
FlyBase ID
FBal0135898
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
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Imprecise excision of the P{EP} element, resulting in a 2068bp deletion that removes the entire Mtl open reading frame (but does not affect any other predicted gene).

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

Heterozygous flies show normal resistance to infection with P.aeruginosa by septic injury.

The planar polarity phenotype seen in the eyes of flies expressing MtlScer\UAS.cMa under the control of Scer\GAL4hs.2sev is enhanced in a MtlΔ/+ background.

Rac1J11 Rac2Δ MtlΔ triple mutants show enlarged foci, as well as increased numbers of actin foci. Enlarged foci are seen in these mutants from the earliest stages of fusion and foci persist after fusion would be complete in wild-type.

Salivary gland invagination and migration are disrupted in MtlΔ homozygous embryos, with a cluster of cells remaining at the ventral surface of the embryo and the gland failing to complete its posterior migration.

MtlΔ mutants do not affect F-actin enrichment or accumulation in rhabdomeres.

Homozygous mutants show a largely normal peripheral glial coverage of PNS axon tracts, with glial cells wrapping the lateral regions of the main ISN branch at stage 16.

Embryos lacking both maternal and zygotic Mtl function complete dorsal closure. Myoblast fusion appears complete in these embryos. 33% of MtlΔ mutant embryos show midline guidance defects (Fas2-positive longitudinal axons cross the midline).

Homozygous adults show some defects in branching of the mushroom body axons.

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

MtlΔ, Rac1J11, Rac2Δ has lethal | embryonic stage phenotype, suppressible | partially by hepCA.UAS/Scer\GAL4[-]

Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference

Rac1J11, Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1[+] is a non-enhancer of visible phenotype of Scer\GAL4en-e16E, kermitGS2053

Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1J10, Rac1[+] is a non-enhancer of lethal | recessive | embryonic stage phenotype of arm8

Mtl[+]/MtlΔ is a non-enhancer of neuroanatomy defective phenotype of PsGEFΔ21

Suppressor of
Statement
Reference

Rac2Δ, Mtl[+], Rac1J10, MtlΔ, Rac2[+], Rac1[+] is a suppressor | partially of visible | adult stage phenotype of Scer\GAL4GMR.PFa, egrUAS.cMa

Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1J10, Rac1[+] is a suppressor of neuroanatomy defective | heat sensitive phenotype of Nl1N-ts1

Rac2Δ, Mtl[+], Rac1J10, MtlΔ, Rac2[+], Rac1[+] is a suppressor of visible | adult stage phenotype of Scer\GAL4GMR.PU, pblDH-PH.UAS.Tag:HA

Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1J10, Rac1[+] is a suppressor of chemical resistant phenotype of RhoGAP18B1

NOT Suppressor of
Statement
Reference

Rac1J11, Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1[+] is a non-suppressor of visible phenotype of Scer\GAL4en-e16E, kermitGS2053

Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1J10, Rac1[+] is a non-suppressor of lethal | recessive | embryonic stage phenotype of arm8

Rac2Δ, Mtl[+], Rac1J10, MtlΔ, Rac2[+], Rac1[+] is a non-suppressor of lethal | pharate adult stage | temperature conditional phenotype of Scer\GAL4GMR.PU, pblΔN-term.UAS.Tag:HA

Rac2Δ, Mtl[+], MtlΔ, Rac2[+] is a non-suppressor of neuroanatomy defective phenotype of LIMK1UAS.Tag:HA, Scer\GAL4ey-OK107

Other
Statement
Reference

Mtl[+]/MtlΔ, Rac1J11, Rac2Δ/Rac2[+], sickΔ, tsr[+]/tsrN96A has neuroanatomy defective phenotype

MtlΔ, Rac1J11/Rac1[+], Rac2Δ/Rac2[+] has neuroanatomy defective phenotype

Phenotype Manifest In
Enhanced by
Suppressed by
Statement
Reference
Enhancer of
Statement
Reference

Rac1J11, Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1[+] is an enhancer of pigment cell phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, cindrdsRNA.PC.PD.UAS

Rac1J11, Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1[+] is an enhancer of cone cell phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, cindrdsRNA.PC.PD.UAS

Rac1J11, Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1[+] is an enhancer of ommatidium phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, cindrdsRNA.PC.PD.UAS

Rac1J11, Rac2Δ, MtlΔ is an enhancer of neuropil phenotype of DAAMEx68

Rac1J11, Rac2Δ, MtlΔ is an enhancer of fascicle phenotype of DAAMEx68

Rac1J11, Rac2Δ, MtlΔ is an enhancer of connective phenotype of DAAMEx68

Rac1J11, Rac2Δ, MtlΔ is an enhancer of embryo phenotype of DAAMEx68

MtlΔ is an enhancer of neuropil phenotype of DAAMEx68, Rac1J11, Rac2Δ

MtlΔ is an enhancer of fascicle phenotype of DAAMEx68, Rac1J11, Rac2Δ

MtlΔ is an enhancer of connective phenotype of DAAMEx68, Rac1J11, Rac2Δ

MtlΔ is an enhancer of embryo phenotype of DAAMEx68, Rac1J11, Rac2Δ

NOT Enhancer of
Suppressor of
Statement
Reference

Rac2Δ, Mtl[+], Rac1J10, MtlΔ, Rac2[+], Rac1[+] is a suppressor | partially of eye phenotype of Scer\GAL4GMR.PFa, egrUAS.cMa

Rac2Δ, MtlΔ, Rac1J10, Rac1[+] is a suppressor of intersegmental nerve | heat sensitive phenotype of Nl1N-ts1

Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1J10, Rac1[+] is a suppressor of intersegmental nerve branch ISNb of A1-7 | heat sensitive phenotype of Nl1N-ts1

Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1J10, Rac1[+] is a suppressor of segmental nerve branch SNa of A1-7 | heat sensitive phenotype of Nl1N-ts1

Rac2Δ, Mtl[+], Rac1J10, MtlΔ, Rac2[+], Rac1[+] is a suppressor of eye | adult stage phenotype of Scer\GAL4GMR.PU, pblDH-PH.UAS.Tag:HA

Mtl[+]/MtlΔ is a suppressor | partially of ommatidium phenotype of Rac1V12.hs.sev

Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1J10, Rac1[+] is a suppressor of eye & ommatidium phenotype of tumdsRNA.UAS.cBa, Scer\GAL4ey.PB

NOT Suppressor of
Statement
Reference

Rac1J11, Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1[+] is a non-suppressor of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053

Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1J10, Rac1[+] is a non-suppressor of abdominal ventral denticle belt | embryonic stage phenotype of arm8

Rac2Δ, Mtl[+], MtlΔ, Rac2[+] is a non-suppressor of adult mushroom body phenotype of LIMK1UAS.Tag:HA, Scer\GAL4ey-OK107

MtlΔ/MtlΔ is a non-suppressor of eye phenotype of trioGEF1.GMR.Tag:MYC

MtlΔ/MtlΔ is a non-suppressor of photoreceptor cell & axon phenotype of trioGEF1.GMR.Tag:MYC

Rac1J11, Rac2Δ, MtlΔ is a non-suppressor of photoreceptor cell & axon phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, msnEP549

Other
Statement
Reference

Mtl[+]/MtlΔ, Rac1J11, Rac2Δ/Rac2[+], sickΔ, tsr[+]/tsrN96A has mushroom body beta-lobe phenotype

Mtl[+]/MtlΔ, Rac1J11/Rac1[+], Rac2Δ/Rac2[+], shi2 has presumptive embryonic salivary gland | heat sensitive phenotype

MtlΔ, Rac1J11, Rac2Δ has embryonic leading edge cell & actin filament phenotype

MtlΔ, Rac1J10, Rac2Δ has embryonic leading edge cell & actin filament | germ-line clone phenotype

MtlΔ, Rac1J10, Rac2Δ has embryonic leading edge cell & actin filament phenotype

MtlΔ, Rac2Δ has photoreceptor cell & axon phenotype

MtlΔ, Rac1J10 has photoreceptor cell & axon phenotype

MtlΔ, Rac1J11, Rac2Δ has photoreceptor cell & axon phenotype

MtlΔ, Rac1J10, Rac2Δ has photoreceptor cell & axon phenotype

MtlΔ, Rac1J11/Rac1[+], Rac2Δ/Rac2[+] has adult mushroom body phenotype

Mtl[+]/MtlΔ, Rac1J11/Rac1[+], Rac2Δ has adult mushroom body phenotype

Mtl[+]/MtlΔ, Rac1J11, Rac2Δ/Rac2[+] has adult mushroom body phenotype

Additional Comments
Genetic Interactions
Statement
Reference

The dot-like small eye phenotype characteristic for flies expressing egrScer\UAS.cMa under the control of Scer\GAL4GMR.PFa is partially suppressed by combination with Rac1J10, together with Rac2Δ and MtlΔ, all in heterozygous state.

Pupal retina constituting almost entirely of somatic clones (induced specifically in the eye) triple homozygous for Rac2Δ,Rac1J11,MtlΔ do not show any extra cone cells or primary pigment cells, only extra inter-ommatidial cells are observed.

Rac1J11/Rac1J10, Rac2Δ, MtlΔ triple mutant larvae exhibit strong ECM detachment and epithelial enclosure of dendrites in class IV dendritic arborizing neurons.

The mushroom bodies of Rac1J11 Rac2Δ MtlΔ triple heterozygotes display short α/β axonal lobes compared with those of controls. The peduncle and ellipsoid body form normally.

The mushroom body axons of flies that are heterozygous for Rac1J11, Rac2Δ tsrN96A sickΔ and MtlΔ fail to extend to form peduncles and lobe structures (the 'posterior arrest' phenotype).

After single cell wounding (by laser ablation), Rac triple mutant embryos (Rac1J10, Rac2Δ, MtlΔ) show severe disruption of actin cortical flow, affecting both actin ring and actin halo formation, resulting in wound overexpansion and an aberrant oval (rather than rounded) wound shape.

The presence of Rac2Δ/+, Rac1J11/+ and MtlΔ/+ mutations fails to suppress the reduction of differentiation seen in eye-antennal disc clones expressing both RhoGEF2RE.Scer\UAS and Ras85DG12V.Scer\UAS under the control of Scer\GAL4tub.PU, and also fails to suppress the developmental delay shown by larvae containing these clones.

A mild, though not significant enhancement of the ommatidium-phenotype resulting from the co-expression of Arf51FGD13822 with Dcr-2Scer\UAS.cDa under the control of Scer\GAL4GMR.PF is observed in a Rac1J11, Rac2Δ, MtlΔ heterozygous background.

No rhabdomeric defect is seen at the base of the rhabdomere at eclosion in flies in which the eyes are triply mutant for Rac1J11 Rac2Δ MtlΔ, although there is an axon guidance defect in the optic lobe.

Heterozygosity for Rac1J10 Rac2Δ MtlΔ suppresses the axonal defects found in Nl1N-ts1 mutants.

Heterozygosity for a Rac1J10 Rac2Δ MtlΔ triple mutant chromosome does not alter arm8 mutant patterning nor its rate of hatching.

The eye phenotype seen when vavΔ1-207.Scer\UAS.T:Ivir\HA1 is expressed under the control of Scer\GAL4GMR.PU is suppressed in a homozygous MtlΔ mutant background.

Heterozygosity for MtlΔ has no effect on the phenotype in the alpha lobes of the mushroom bodies that is seen in PsGEFΔ21 animals.

One copy of each of Rac1J10, Rac2Δ and MtlΔ fails to suppress the lethality seen when pblΔN-term.Scer\UAS.T:Ivir\HA1 is expressed under the control of Scer\GAL4GMR.PU.

One copy of each of Rac1J10, Rac2Δ and MtlΔ strongly supresses the rough eye phenotype seen when pblDH-PH.Scer\UAS.T:Ivir\HA1 is expressed under the control of Scer\GAL4GMR.PU.

Stage 8 embryos lacking zygotic and maternal expression of Rac1J10, Rac2Δ and MtlΔ display mesoderm migration defects.

A Rac1J11 Rac2Δ MtlΔ heterozygous background enhances the patterning defects found in Scer\GAL4GMR.PF>cindrdsRNA.PC.PD.Scer\UAS mutants. The mean interommatidial precursor cell number and the number of cone and/or 1[o] cell errors is increased in these double mutants.

The Scer\GAL4elav-C155/DAAMC.Scer\UAS.P\T gain-of-function phenotype (i.e the appearance of thicker commissures and nerve roots) is not affected by a Rac1J10, Rac2Δ, MtlΔ background.

A Rac1J11; Rac2Δ, Mtl[Δ] heterozygous background enhances the zygotic DAAMEx68, DAAMEx68; Rac1J11/+ and DAAMEx68; Rac1J11/+; Rac2Δ/+CNS phenotypes.

Rac1J11, Rac2Δ, MtlΔ triple mutant clones in the eye result in a low frequency (approximately 5%) of planar polarity defects (such as achiral or misrotated ommatidia). Cdc425, Rac1J11, Rac2Δ, MtlΔ quadruple mutant clones in the eye result in a higher frequency of (14.2%) of planar polarity defects.

shi2 Rac1J11 Rac2Δ MtlΔ heterozygous embryos form normal salivary glands at the permissive temperature of 25[o]C. However, at the restrictive temperature of 30[o]C, posterior migration of the salivary gland is disrupted.

Heterozygosity for Rac1J10 Rac2Δ MtlΔ suppresses the RhoGAP18B1 ethanol-resistance phenotype.

The MtlΔ mutation fails to modify the cv-cM62 phenotype in the Malpighian tubules.

Developmental dispersal of hemocytes is abnormal in embryos triply mutant for Rac1J11, Rac2Δ and MtlΔ.

One hour after laser-induced wounding, approximately half the number of hemocytes are recruited to the wound in embryos triply mutant for Rac1J11, Rac2Δ and MtlΔ compared to wild type embryos. Hemocytes that are recruited in the triple mutant embryos have significantly reduced lamellar protrusions.

Contacts between the invaginated mesoderm and the ectoderm fail to be established properly in embryos derived from females with reduced Mtl, Rac2 and Rac1 function.

Germ line clones of the Rac1J11 Rac2Δ MtlΔ triple mutant fail to produce embryos. Zygotic Rac1J11 Rac2Δ MtlΔ triple mutants, that have wild-type maternal contribution of Rac1, survive beyond early dorsal closure, but still show 100% embryonic lethality. These embryos achieve dorsal closure, but show puckering along the dorsal side. The dorsal hole becomes a long slit-like shape as it closes in the triple mutants, while the hole has an oval shape in wild-type embryos. Although amnioserosa cells are significantly larger in the mutant than in wild type, these cells are able to contract at a similar rate to wild type. The leading edge of zygotic Rac1J11 Rac2Δ MtlΔ triple mutants is disorganized and, unlike in wild-type embryos, is not taut. Many of the triple mutant leading edge cells are polygonal in shape, instead of being dorsally-ventrally elongated, like in wild type. Some of the cells in the mutant edge assemble the actin cable and actin projections, while other cells fail to do so. Leaky expression of hepCA.Scer\UAS, with no GAL4 driver, partially rescues the lethality and dorsal puckering phenotype of Rac1J11 Rac2Δ MtlΔ triple mutants. Rac1J10 Rac2Δ MtlΔ triple mutant germ line clone embryos exhibit failure in germband retraction, head involution and dorsal closure. Not all of these phenotypes are fully penetrant; embryos with the least severe phenotype show only failure in dorsal closure. The epithelial cells of these embryos lack both actin cables and actin protrusions at the leading edges. The leading edge of zygotic Rac1J10 Rac2Δ MtlΔ triple mutants is somewhat disordered. Some of the cells in the mutant edge assemble the actin cable and actin projections, while other cells fail to do so. Cells without protrusions halt the "zipper" that closes the dorsal hole. However, the mutant exhibits a compensatory mechanism in which new zippering fronts emerge after the actin deficient stretches to complete closure.

Rac1J10 Rac2Δ MtlΔ triple mutant embryos (lacking both maternal and zygotic function of the Rac1, Rac2 and Mtl genes) are able to almost completely dominantly suppress the stidsRNA.Sym.Scer\UAS (under the regulation of Scer\GAL4ey.PB) phenotype, reverting the eye to wild-type size and appearance. Rac1J10 Rac2Δ MtlΔ triple mutant embryos (lacking both maternal and zygotic function of the Rac1, Rac2 and Mtl genes) are able to dominantly suppress the RacGAP50CdsRNA.Scer\UAS (under the regulation of Scer\GAL4ey.PB) eye phenotype.

Mosaic border follicle cell clusters, which contain some wild-type cells and some cells with the genotype Rac1J10 Rac2Δ MtlΔ/Rac1J10 Rac2Δ Mtl+ show impaired migration.

Homozygous Rac1J10 Rac2Δ MtlΔ embryos derived from homozygous Rac1J10 Rac2Δ MtlΔ female germline clones show the same macrophage migration defects as homozygous Rac1J10 Rac2Δ embryos derived from homozygous Rac1J10 Rac2Δ female germline clones.

The combination of heterozygous sli2 and MtlΔ leads to longitudinal axon ectopic midline crossing defects. An average of 1.4 defects are seen per animal, and an average of 13% of segments have defects.

Rac1J10 Rac2Δ MtlΔ triple mutant embryos (lacking both maternal and zygotic function of the Rac1, Rac2 and Mtl genes) fail to complete dorsal closure. There is little or no actin accumulation at the leading epidermal edge and both lamellipodia and filopodia are lacking. The underlying amnioserosa cells appear normal. Little or no myoblast fusion occurs in these embryos. Severe axon growth defects are seen; in the CNS, Fas2-positive axons rarely extend from one segment into the next and very few sensory axons from the PNS reach the CNS. Specification of neuronal and glial cell fate and dendritic growth and morphology appears relatively normal. Rac1J10 MtlΔ double mutant embryos (lacking both maternal and zygotic function of the Rac1 and Mtl genes) show dorsal closure defects. Myoblast fusion appears complete in these embryos. Rac2Δ MtlΔ double mutant embryos (lacking both maternal and zygotic function of the Rac2 and Mtl genes) successfully complete dorsal closure. A few isolated myoblasts fail to fuse in these embryos. Rac1J11 Rac2Δ MtlΔ triple mutant clones in the wing and eye do not show planar cell polarity defects. Rac1J10 enhances the frequency of midline guidance defects in MtlΔ mutant embryos to 75%. Axon stalling is occasionally seen in the double mutant embryos. Rac2Δ enhances the frequency of midline guidance defects in MtlΔ mutant embryos to 42%. Mosaic flies in which the eye is doubly mutant for MtlΔ and Rac2Δ show mild defects in the projection pattern of photoreceptor cell axons. Mosaic flies in which the eye is doubly mutant for MtlΔ and Rac1J10 show defects in the projection pattern of photoreceptor cell axons, showing a medulla bypass phenotype. Mosaic flies in which the eye is triply mutant for MtlΔ, Rac1J10 and Rac2Δ show severe defects in the projection pattern of photoreceptor cell axons, showing a medulla bypass phenotype. The projection defects in the triple mutant eyes can be rescued by Rac1GMR.PNe or MtlGMR.PN. Mosaic flies in which the eye is triply mutant for MtlΔ, Rac1J11 and Rac2Δ show severe defects in the projection pattern of photoreceptor cell axons, showing a medulla bypass phenotype. Specification of photoreceptor cell fate appears to be normal.

55% of Rac1J11 Rac2Δ MtlΔ single-cell γ neuron clones in the mushroom body show axon-stalling defects, mostly at the peduncle. There is a significant reduction in total dendritic length and number of dendritic segments per neuron compared to wild type. Mushroom body axon growth defects in single-cell Rac1J11 Rac2Δ MtlΔ γ neuron clones are largely rescued by expression of Rac1Scer\UAS.T:Hsap\MYC or Rac1Y40C.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4OK107. Mushroom body axon growth defects in single-cell Rac1J11 Rac2Δ MtlΔ γ neuron clones are not rescued by expression of Rac1F37A.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4OK107.

The phenotype caused by expression of msnEP549 under the control of Scer\GAL4GMR.PF is not modified by the addition of the triple mutant combination Rac1J11 Rac2Δ MtlΔ.

Rac1J10 Rac2Δ MtlΔ triple mutant embryos exhibit no significant retardation of wound closure.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
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Mutant
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Stocks (3)
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Synonyms and Secondary IDs (6)
References (54)