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General Information
Symbol
Dmel\Mmp2W307stop
Species
D. melanogaster
Name
FlyBase ID
FBal0150747
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
mmp2W307*, Mmp2W307
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

G9613582A

Amino acid change:

W307term | Mmp2-PB; W155term | Mmp2-PC; W199term | Mmp2-PD

Reported amino acid change:

W307term

Comment:

G to A nucleotide change at the second or third position of the Trp codon leads to a nonsense mutation. (exact site of mutation unspecified). Site of nucleic acid difference in mutant inferred by FlyBase based on reported amino acid change.

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

Amino acid replacement: W307term.

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

Mmp2W307stop/Mmp2W307stop mutant embryos exhibit defects in heart formation, with disorganized arrangement of cardioblasts, and a decrease in migration velocity of cardioblasts to the midline, with a significant decrease in the number of filopodia and lamellipodia at the leading edge; cardioblasts fail to change shape to form a medial pocket, fail to contact and adhere to their contralateral partners, and a lumen fails to form, in contrast to wild type.

Mmp2W307stop/Mmp2218 transheterozygotes exhibit a decrease in lifespan compared to controls.

Homozygous mutant Mmp2W307stop embryos exhibit defasciculation defects in 81% of hemisegments.

No Mmp1W439stop/Df(2R)Uba1-Mmp2 mutant third instar larvae display broken tracheal dorsal trunks. 94% survive to pupariation. Over 50% of dissected pupae show defects in head eversion.

Mmp2W307stop mutants show ectopic basal lamina formation around tunneled tracheae and dorsal air sac primordia of the wing disc. The depth at which the disc-associated transverse connective and dorsal air sac position within the wing disc is altered in these animals. Tunneled trachea and dorsal air sac primordium also show ectopic extrusions from the plane of the imaginal disc. Extension and growth of the dorsal air sac primordia is stunted in these mutants, and the developing air sac tubes are filled with polarised epithelial cells.

Mmp2W307stop homozygous embryos display marked defects in ISNb fasciculation - 85% of hemisegments display either loosely fasciculated or excessive branching of ISNb. SNa fasciculation is also decreased.

Mmp2W307stop/Df(2R)Uba1-Mmp2 embryos display marked defects in ISNb fasciculation - 74% of hemisegments display either loosely fasciculated or excessive branching of ISNb. SNa fasciculation is also decreased.

Mosaic animals in which the eyes are homozygous for Mmp2W307stop show normal location of photoreceptor nuclei in the retina.

Mmp2W307stop mutants exhibit abundant C4da neuron larval dendrites after head eversion, with approximately 8% retained after head eversion. Whereas in wild-type pupae at 20hrs after pupal formation all larval dendrites from C4da neurons are cleared from the extracellular space, in Mmp2W307stop mutants, larval dendrites that are severed from the soma remain. These larval dendrites persist to much later stages at 35 hours after pupal formation, just before the lethal phase of Mmp2W307stop at midpupariation.

83% of Mmp2W307stop mutant animals survive to 3rd instar, and 72% pupariate, but only 15% undergo head eversion, 2% develop head bristles and none eclose. 96% of Mmp2W307stop/Mmp2Df animals survive to third instar, and 89% pupariate, but only 18% undergo head eversion, 7% develop head bristles and none eclose. Mmp2W307stop mutant pupae retain their gastric caeca and proventriculus, even 22 hr after puparium formation.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
NOT Enhanced by
Suppressed by
Statement
Reference

Mmp2Y53N/Mmp2W307stop has increased cell number | female | adult stage | heat sensitive phenotype, suppressible by arm2/arm[+]

Mmp2Y53N/Mmp2W307stop has increased cell number | female | adult stage | heat sensitive phenotype, suppressible by dlp1/dlp[+]

Mmp2Y53N/Mmp2W307stop has increased cell number | female | adult stage | heat sensitive phenotype, suppressible by dlp[+]/dlp2

NOT suppressed by
Enhancer of
Other
Phenotype Manifest In
Enhanced by
NOT Enhanced by
Suppressed by
Statement
Reference
NOT suppressed by
Enhancer of
Other
Additional Comments
Genetic Interactions
Statement
Reference

The heart developmental defects observed in Mmp1Q112stop/Mmp1Q112stop, Mmp2W307stop/Mmp2W307stop double mutants are similar to those seen in Mmp2W307stop/Mmp2W307stop single mutants.

The increase in average cell number in the stalks between egg chambers which is seen in Mmp2Y53N/Mmp2W307stop females after being shifted to the restrictive temperature is dominantly suppressed if the females also carry a single copy of arm2, dlp1 or dlp2.

The increase in average cell number in the stalks between egg chambers which is seen in Mmp2Y53N/Mmp2W307stop females after being shifted to the restrictive temperature is enhanced if they are also expressing dlpScer\UAS.cBa under the control of Scer\GAL4C587.

Mmp2W307stop/+ ; fracΔ1/+ double heterozygotes exhibit elevated levels of ISNb and SNa guidance defects. The incidence of ISNb mis-projection rises from 1% and 2% in fracΔ1 and Mmp2W307stop single heterozygotes, respectively, to 18% in the double heterozygote.

Mmp1Q112stop,Mmp2W307stop double mutant embryos show normal haemocyte migration into the tail region of the embryo.

ISNb axon guidance defects in Mmp2W307stop Mmp1Q112stop or Mmp2W307stop/Df(2R)Uba1-Mmp2 Mmp1Q112stop/Mmp12 double mutants qualitatively and quantitatively mirror the phenotypes observed in the Mmp2 single mutants.

SNa axon defasciculation in Mmp2W307stop Mmp1Q112stop or Mmp2W307stop/Df(2R)Uba1-Mmp2 Mmp1Q112stop/Mmp12 double mutants is significantly increased relative to that of either single mutant.

Mmp1Q273stop Mmp2W307stop double mutant C4da clones not only exhibit dendritic branching patterns similar to wild-type clones during early pupariation, but also exhibit complete larval dendrite removal after head eversion at 20 hours after pupal formation as in wild-type controls.

The larval lethality due to Mmp1Q112stop/Mmp12 is enhanced by Mmp2218/Mmp2W307stop from 84% survival to 3rd instar and 7% pupariating to 54% survival to 3rd instar and 4% pupariating. The larval lethality of Mmp1Q112stop; Mmp2W307stop double homozygotes (73% survive to 2nd instar, 35% to 3rd instar, and none pupariate) is much greater than for either single homozygote.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Expression of Mmp2Scer\UAS.cPa under the control of Scer\GAL4Mef2.PU largely rescues the heart development defects (including cardioblast migration velocity, filopodial and lamellipodial activity, and lumen formation) seen in Mmp2W307stop/Mmp2W307stop mutant embryos.

Mmp2GPI.T:Avic\GFP-EGFP completely rescues the pupal lethality of Mmp2 mutants. It does not rescue the lifespan, fertility and follicle cell defects of Mmp2W307stop/Mmp2218 flies.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
Comments
Comments

frac is genetically downstream of Mmp2 in axon guidance.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (8)
References (14)