Amino acid replacement: Q55term.
Nucleotide substitution: C?T.
Amino acid replacement: ?60term.
Amino acid replacement: ??term.
C18307422T
C?T
Q60term | upd1-PA; Q60term | upd1-PB; Q60term | upd1-PC
Q60term
gonad | ectopic & embryo
25% of upd1YM55 homozygous mutant embryos show defects in germ-band extension. Germ-band epithelial cells are normal in the head and dorsal-most regions of the embryo, however intercalating (ventrolateral) cells show a smaller apical cell surface. Germ-band cell intercalation is disrupted or, in extreme cases, blocked.
upd1YM55 embryos show a segmentation defect in which the A4 and A5 segments are fused.
The enlarged eye phenotype seen in flies carrying one copy of upd1GMR.PB is not modified if the flies are also carrying upd1YM55.
The pole cells of upd1YM55 mutant embryos are able to migrate normally and coalesce to form a pair of gonads in late embryos. However, one gonad often becomes located one segment offset from its proper location.
Migration of prospective border follicle cells in upd1sisC-5/upd1YM55 animals is delayed or defective. Marker analysis suggests that these cells are at least partially transformed to a nurse follicle cell fate.
Mosaic stage 9-10A follicles that have upd1[-] anterior polar cells contain fewer than normal border cells and the border cells fail to migrate. Morphologically normal stretched and centripetal cells are present in these follicles.
Mosaic stage 9-10 follicles that have upd1[-] posterior polar cells have a normally localised oocyte at the posterior part of the follicle and the oocyte nucleus is correctly positioned.
When homozygous somatic clones are made in the egg chamber, defects in border cell migration are seen. Whenever the polar cells are mutant, a complete failure in border cell migration is seen. However, in egg chambers in which the germ-line is mutant, no migration defect is seen. In mutant egg chambers the outer border cell clusters consist of an average of 2.2 cells, as compared to 6 in wild-type.
Homozygous clones within the eye field show no phenotype either in imaginal discs or in the adult eye. Clones adjacent to the optic stalk produce almost complete dorsalisation of the eye field as assayed by ommatidial polarity.
Defect in the fourth and fifth abdominal denticle belt. This does not produce embryonic lethality as mutant larvae, pupae and sometimes adult can develop lacking the abdominal region. T2, T3 and A8 are sometimes deleted, the head is usually involuted but most head structures are present. Germline clone analysis of os alleles of the upd complementation group indicate they are not required for germline viabilty and do not have a maternal effect. Zygotic lethality acts in the embryo, larval and pupal stages.
Interacts with RpII140wimp maternal effect.
embryonic lethal. Mutants show variable larval cuticular phenotype with defects predominantly in the mesothorax and the fifth abdominal segment (Nusslein-Volhard et al., 1984; Gergen and Wieschaus, 1986); also some head defects and fourth, sixth, seventh and eighth abdominal segment defects. Heterozygotes show 88-93% viability (Wieschaus and Noell, 1986). T2 defect; rudimentary filzkorper and posterior spiracles; A6 and A7 denticle belts fused; A8 denticle belt reduced
upd1YM55 has abnormal cell shape | extended germ band stage phenotype, suppressible by WASp[+]/WASp3
upd1YM55 has abnormal cell shape | extended germ band stage phenotype, suppressible by sqhAX3
upd1YM55 is an enhancer of partially lethal phenotype of hop32/hop25
upd1YM55 is an enhancer of partially lethal phenotype of hop33/hop25
upd1YM55 is an enhancer of partially lethal phenotype of hop3/hop25
upd1[+]/upd1YM55 is a non-enhancer of visible | adult stage phenotype of CtBP334Δ4, Scer\GAL4rn-GAL4-5, egrUAS.cUa
upd1[+]/upd1YM55 is a non-suppressor of visible | adult stage phenotype of CtBP334Δ4, Scer\GAL4rn-GAL4-5, egrUAS.cUa
os[+]/upd1YM55 is a non-suppressor of abnormal neuroanatomy phenotype of spin10403
hop12, upd1YM55 has partially lethal | recessive phenotype
hop14, upd1YM55 has partially lethal | recessive phenotype
hop27, upd1YM55 has partially lethal | recessive phenotype
upd1YM55 has ectoderm | extended germ band stage phenotype, suppressible by sqhAX3
upd1YM55 has ectoderm | extended germ band stage phenotype, suppressible by Rho1k02107b
upd1YM55 has ectoderm | extended germ band stage phenotype, suppressible by WASp[+]/WASp3
os[+]/upd1YM55 is an enhancer of egg chamber phenotype of hop27/hop25
os[+]/upd1YM55 is an enhancer of polar follicle cell | increased number phenotype of hop27/hop25
upd1[+]/upd1YM55 is a non-enhancer of wing | ectopic phenotype of CtBP334Δ4, Scer\GAL4rn-GAL4-5, egrUAS.cUa
upd1[+]/upd1YM55 is a non-suppressor of wing | ectopic phenotype of CtBP334Δ4, Scer\GAL4rn-GAL4-5, egrUAS.cUa
os[+]/upd1YM55 is a non-suppressor of glial cell phenotype of spin10403
Expression of egrUAS.cUa under the control of Scer\GAL4rn-GAL4-5 (with tub-Gal80[ts] restricting expression to third instar larvae) in upd1YM55/+ background does not lead to ectopic wings compared to controls.
An average of 4.5% upd1YM55, sqhAX3 homozygous mutant embryos show germ-band extension defects, much reduced compared to upd1YM55 homozygous mutant embryos. Ectopic apical cell constriction defects are rescued in upd1YM55, sqhAX3 homozygous mutant embryos.
An average of 6% upd1YM55, Rho1k02107b homozygous mutant embryos show germ-band extension defects, much reduced compared to upd1YM55 homozygous mutant embryos.
The reduced ectodermal apical cell surface size observed in upd1YM55 mutant embryos at mid germ-band extension is rescued in upd1YM55; WASp3/+ embryos.
upd1YM55 is rescued by Scer\GAL4VP16.mat.αTub67C/upd1UAS.cZa
Expression of upd1Scer\UAS.cZa under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16 rescues the germ-band extension and apical cell shape defects observed in upd1YM55 mutant embryos.
Maternal germline clonal analysis demonstrates there is no maternal effect.