Amino acid replacement: G2D.
G5982422A
G2D | Src42A-PA; G2D | Src42A-PC
G2D
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
embryonic leading edge cell & actomyosin
In Src42Amyri mutant embryos the extension of the dorsal branches lags behind the normally concurrent process of dorsal closure. The dorsal branches also contain fewer stalk cells. The dorsal trunk is a zigzag shape.
Src42Amyri embryos exhibit defects in leading edge cells: the actomyosin cable is disrupted and dorsal closure is slightly defective. 8% of stage 16 embryos show a very small dorsal hole and the remainder show an irregular arrangement of dorsal hairs. Embryonic lethality is 63% with 60% of unhatched embryos showing malformed mouthparts and a small anterior hole.
50.0 +/- 3.3% of homozygotes die as embryos and most of the remainder die during the first larval instar stage. Homozygous embryos do not show a dorsal open phenotype but have malformed mouth parts.
Src42Amyri has lethal | embryonic stage phenotype, enhanceable by FERΔex1
Src42Amyri has lethal | embryonic stage | recessive phenotype, enhanceable by Btkk05610/Btkk00206
Src42Amyri is an enhancer of lethal | embryonic stage phenotype of Btkk05610/Btkk00206
Src42Amyri is a suppressor | partially of increased mortality during development phenotype of CycEUAS.Tag:HA.Medsh, MedRNAi.UAS.CycE-HA, Ras85DG12D.UAS.p53sh, Scer\GAL4Ser.PU, p53RNAi.UAS.RasG12D
Src42Amyri has embryonic/larval dorsal tracheal branch | embryonic stage phenotype, enhanceable by Src64BPI
Src42Amyri has embryonic leading edge cell & actomyosin phenotype, enhanceable by Df(3L)FER-Δ1
Src42Amyri has embryonic/first instar larval cuticle phenotype, enhanceable by Df(3L)FER-Δ1
Src42Amyri has embryonic leading edge cell & actomyosin phenotype, enhanceable by FERΔex1
Src42Amyri has embryo | dorsal closure stage phenotype, enhanceable by FERΔex1
Src42Amyri has embryonic/larval mouth phenotype, enhanceable by FERΔex1
Src42Amyri has larval dorsal hair phenotype, enhanceable by FERΔex1
Src42Amyri has embryonic/first instar larval cuticle phenotype, enhanceable by FERΔex1
Src42Amyri has embryo | dorsal closure stage phenotype, enhanceable by Df(3L)FER-Δ1
Btkk05610/Btkk00206, Src42Amyri has embryonic/first instar larval cuticle | dorsal phenotype, suppressible | partially by JraAsp.hs.sev
Src42Amyri, p130CAS1 has embryonic head phenotype
Src42Amyri, p130CAS1 has embryo | late embryonic stage phenotype
Src42Amyri, p130CAS1 has larva | first instar larval stage phenotype
Src42Amyri, Src64BPI has embryonic/first instar larval cuticle | dorsal phenotype
Btkk05610/Btkk00206, Src42Amyri has embryonic/first instar larval cuticle | dorsal phenotype
Btkk05610/Btkk00206, Src42Amyri has embryo | dorsal closure stage phenotype
Approximately 90% of Src42Amyri; p130CAS1 double mutants have holes in or completely absent head cuticles and 10% of these embryos exhibit germ band retraction cuticle defects.
Src64BPI enhances the tracheal defects seen in Src42Amyri mutant embryos. Many dorsal branches fail to extend correctly, remaining in a multicellular state despite the progression of dorsal closure.
Src42Amyri; Fps85DΔex1 double mutant embryos show an enhanced embryonic phenotype compared to Src42Amyri embryos. Src42Amyri; Fps85DΔex1 leading edge cells show a greater disruption of the actomyosin cable, resulting in a more irregular profile. The embryos show delayed dorsal closure, as 85% are still undergoing closure at late stage 16. Embryonic lethality is increased to 100% (vs 63% in Src42Amyri embryos). 95% of the double mutant embryos show breaks and irregularities in the dorsal hair pattern and a small anterior hole in the mouthparts. The remaining embryos fail to complete dorsal closure and have a large anterior hole.
Src42Amyri; Df(3L)Fps85D-Δ1 embryos show an enhancement of the embryonic phenotypes of both Src42Amyri and Df(3L)Fps85D-Δ1 single mutants. The leading edge cells of Src42Amyri; Df(3L)Fps85D-Δ1 embryos are highly irregular and show a complete loss of the F-actin cable. Cuticle preparations from these embryos show that 30% have a large anterior hole, 59% show a small anterior hole with small scabs along the dorsal midline and the remaining 11% fail to secrete a cuticle.
Btk29Ak00206 Src42Amyri/Btk29Ak05610 Src42Amyri double homozygotes show complete embryonic lethality and some embryos have a dorsal open phenotype. The leading edge cells are only partially elongated during dorsal closure. The dorsal open phenotype is partially rescued by JraAsp.hs.sev. Src42Amyri; Src64BPI double homozygous embryos have a mild but clear dorsal open phenotype.