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