Amino acid replacement: G19R.
G21128748A
G19R | mago-PA
microtubule & egg chamber
microtubule & oocyte
The nucleus fails to migrate to the anterior of the oocyte in approximately 30% of the egg chambers of mago1/Df(2R)F36 females at 18oC. The penetrance of this phenotype is less than 3% at 25oC. The nucleus also fails to migrate to the anterior of the oocyte in some of the egg chambers of mago1/mago1 and mago1/mago2 females. Stage 9 mago1/Df(2R)F36 egg chambers have an abnormal distribution of microtubules at 18oC, with high levels of microtubules at both poles of the oocyte and lower levels in the centre. Microtubule organisation appears more normal in later stage egg chambers at 18oC, although a small posterior focus of microtubules often persists until stage 10-11. Microtubule organisation appears more normal in mago1/Df(2R)F36 egg chambers at 25oC, although a small focus of microtubules is seen at the posterior pole during stages 8-9. Approximately 30% of eggs laid by mago1/Df(2R)F36 females are symmetrical along the dorsal-ventral axis. These eggs are completely ventralised at the anterior end; they lack dorsal appendages, the operculum develops as a symmetric ring around the micropyle and the micropyle points anteriorly rather than dorsally. The egg shell is more pointed at the posterior pole than normal, and the posterior aeropyle is larger and more symmetric than wild-type.
Approximately 1% of eggs derived from hemizygous females raised at 25oC are ventralised. Approximately 38% of eggs derived from hemizygous females shifted from 25oC to 17oC are ventralised. The dorsal appendages are missing in these ventralised eggs and the micropyle canal is defective, although the aeropyle appears normal. Approximately 1% of eggs derived from hemizygous females raised at 25oC contain a mislocalised oocyte nucleus. Approximately 36% of eggs derived from hemizygous females shifted from 25oC to 17oC contain a mislocalised oocyte nucleus. Homozygous female germline clones also give rise to egg chambers containing mislocalised oocyte nuclei and ventralised eggs. The polarisation of the microtubule cytoskeleton is abnormal in hemizygous egg chambers shifted from 25oC to 17oC.
Prevents the posterior accumulation of G-iα65A protein.
Offspring fail to make pole cells. Shows temperature sensitive defects in abdominal segmentation and embryonic body plan.
When mutant females are raised at 25oC some of the resulting embryos have double abdomens. At 17oC the females produce embryos displaying abdominal defects typical of the posterior group, with no incidence of head defects or double abdomens.
Grandchildless-like phenotype. Eggs from homozygous females have no apparent posterior determinants in the posterior pole. At 17oC the inviable embryos lack abdominal segments, at 25oC a novel gene product is produced that is capable of inducing the formation of symmetrical double abdomen embryos (behave as recessive antimorphs). The temperature sensitive period is during oogenetic stages 7--14.
mago1 has sterile phenotype, suppressible by Cele\mag-1mago.PN
mago1/mago[+] is a suppressor of visible phenotype of Ras85DV12.sev
Df(2R)F36/mago1, miraΔ103.αTub67C.mGFP6 has abnormal planar polarity phenotype
Df(3R)p-XT103, mago1 has embryonic head phenotype, suppressible | partially by osk+tMa
Df(3R)p-XT103, mago1 has embryonic abdominal segment phenotype, suppressible | partially by osk+tMa
Df(3R)p-XT103, mago1 has embryo phenotype, suppressible | partially by osk+tMa
mago1/mago[+] is a suppressor of eye phenotype of Ras85DV12.sev
Df(3R)p-XT103, mago1 has embryo phenotype
Df(3R)p-XT103, mago1 has embryonic abdominal segment phenotype
Df(3R)p-XT103, mago1 has embryonic head phenotype
Df(2R)F36/mago1, miraΔ103.αTub67C.mGFP6 has embryonic abdomen phenotype
Embryos derived from mago1/Df(3R)p-XT103 mutants exhibit abdominal and head defects (in up to 35% of embryos). The presence of one copy of oskt.WT partially suppresses these defects while the presence of one copy of oskS244A.S248A exacerbates these defects and increases the number of bicaudal embryos.
mago1 dominantly suppresses the rough eye phenotype caused by Ras85DV12.sev.
mago1 dominantly enhances the loss of wing vein phenotype seen in cswlf/Y flies.
The extra wing vein phenotype seen in EgfrE1/+ flies is dominantly suppressed by mago1.
The loss of wing veins and rough eye phenotype seen in rl1 homozygotes is dominantly enhanced by mago1.
A mago1 heterozygous background enhances eye degeneration found in Scer\GAL4GMR.PF>cln3Scer\UAS.T:Avic\GFP-YFP.Venus flies.
Wing phenotypes found with overexpression of cln3Scer\UAS.cTa with Scer\GAL4en-e16E are enhanced in a mago1 heterozygous background.
Embryos that express miraΔ103.αTub67C.T:Avic\GFP-m6 in a mago1/Df(2R)F36 background have no posterior abdomen and have an anterior abdomen of reversed polarity.
A single copy of Cele\mag-1mago.PN is sufficient to rescue the axis defects and sterility caused by mago1.
Defects in axis formation and germ-plasm assembly caused by mago1 are rescued by mago+t2.2.T:Hsap\MYC and also by mago+t2.2.T:Avic\GFP.
Although tud protein is present in mutant embryo extracts, its localization in the embryo is altered.
Shows interallelic complementation for zygotic lethality with magoE19A and magoWE7.
Germ line clonal analysis indicates that mago function is required in the germ line.