Amino acid replacement: Q70term.
C30055669T
Q70term | spn-A-PA; Q13term | spn-A-PB
Q70term
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
The complete copia element in wa.hs has an LTR at each end. Following excision of P{hswa}, repair by SDSA (synthesis-dependent strand annealing) can lead to excision of this copia element due to annealing at these LTRs, resulting in red eyed progeny. Incomplete SDSA, where joining has occurred independently of annealing of homologous ends, can delete parts of the w ORF in wa.hs resulting in yellow eyed progeny. The frequency of red eyed progeny (and therefore of complete SDSA) following excision of P{hswa}sdwa using H{PΔ2-3}HoP2.1 is decreased from 6% to zero in a spn-A3/spn-A093A background, but the frequency of yellow eyed progeny (and therefore of incomplete SDSA) is increased from 10% to 17%. This background does not significantly affect the proportion of hemizygous lethal sd deletions resulting from this excision, but does decrease the proportion of excisions resulting non-lethal deletions (from 7% to 1.7%).
spn-A093A/Df(3R)X3F germ-line clones produce oocytes who DNA is less organised than the wild-type karyosome. The DNA clusters along the periphery of the nucleus adjacent to the nuclear membrane. Homozygous mutant animals and spn-A048B/spn-A093A mutants are sensitive to X ray irradiation when irradiated at either 24-48 or 48-72 hours after egg laying (AEL). Little difference in viability is seen in irradiated at 0-24 hours AEL. The synaptonemal complex in spn-A093A/Df(3R)X3F ovaries persists longer than in wild-type, suggesting a delay in the resolution of synapsis. Double strand breaks form at the normal time, but their resolution is delayed. When spn-A093A/Df(3R)X3F eggs are produced ,about 31% of eggs are wild-type in appearance, 69% have a mild ventralisation phenotype, the dorsal appendages are fused. spn-A048B/spn-A093A animals are sensitive to X ray irradiation when irradiated at either 24-48 or 48-72 hours after egg laying (AEL). Little difference in viability is seen in irradiated at 0-24 hours AEL.
spn-A093A/spn-A3 has radiation sensitive phenotype, enhanceable by DNAlig4169
spn-A093A has radiation sensitive phenotype, non-enhanceable by spn-B1
Df(3R)PolQΔ, spn-A093A/spn-A3 has radiation sensitive | third instar larval stage phenotype, suppressible by PolQ+tBa
Df(3R)PolQΔ, spn-A093A/spn-A3 has radiation sensitive | third instar larval stage phenotype, suppressible by PolQATPase-dead
spn-A093A/spn-A3 has visible phenotype, suppressible by eIF1ABH167/eIF-1A[+]
Df(3R)PolQΔ, spn-A093A/spn-A3 has radiation sensitive | third instar larval stage phenotype, non-suppressible by PolQpol-dead
spn-A093A has radiation sensitive phenotype, non-suppressible by spn-B1
spn-A093A/spn-A3 is an enhancer of chemical sensitive phenotype of mus302D1/mus302Z1882
spn-A093A is a non-enhancer of radiation sensitive phenotype of spn-B1
spn-A093A is a non-suppressor of radiation sensitive phenotype of spn-B1
Df(3R)PolQΔ, spn-A093A/spn-A3 has radiation sensitive | third instar larval stage phenotype
Fancm0693/Df(3R)ED6058, GenZ5997, mus81Nhe, spn-A093A/spn-A3 has partially lethal - majority die phenotype
BlmN1/BlmD2, mus312D1/mus312Z1973, spn-A093A/spn-A3 has lethal - all die during pupal stage phenotype
PolQD5/PolQD2, spn-A093A/spn-A3 has partially lethal phenotype
BlmN1/BlmD2, mus312D1/mus312Z1973, spn-A093A/spn-A3 has lethal | pupal stage phenotype
DNAlig4169, spn-A093A/spn-A3 has viable phenotype
spn-A093A/spn-A1 has dorsal appendage phenotype, non-enhanceable by Xrcc2CC/Xrcc2CC
spn-A093A/spn-A3 has egg chorion phenotype, suppressible by eIF1ABH167/eIF-1A[+]
spn-A093A/spn-A1 has dorsal appendage | maternal effect phenotype, suppressible by Lnkd07478/LnkCR642
spn-A093A/spn-A1 has egg chorion phenotype, suppressible by mei-W681/mei-W681
spn-A093A/Df(3R)X3F has egg chorion | dorsal phenotype, suppressible by barr+tMa/vls+tMa/Df(2L)pr2b/Df(2L)be408
spn-A093A/Df(3R)X3F has egg chorion | dorsal phenotype, suppressible by mei-W681
spn-A093A/Df(3R)X3F has dorsal appendage phenotype, suppressible by barr+tMa/vls+tMa/Df(2L)pr2b/Df(2L)be408
spn-A093A/Df(3R)X3F has dorsal appendage phenotype, suppressible by mei-W681
spn-A093A/Df(3R)X3F has karyosome phenotype, suppressible by barr+tMa/vls+tMa/Df(2L)pr2b/Df(2L)be408
spn-A093A/spn-A1 has dorsal appendage phenotype, non-suppressible by Xrcc2CC/Xrcc2CC
Xrcc2CC, spn-A093A has dorsal appendage phenotype
The hypersensitivity of Df(3R)mus308Δ/Df(3R)mus308Δ;spn-A3/spn-A093A double mutant third instar larvae to ionizing radiation is rescued by combination with either the mus308+tBa or the mus308ATPase-dead transgene but not by mus308pol-dead.
Df(3R)mus308Δ/Df(3R)mus308Δ;spn-A3/spn-A093A mutants show a significant reduction in the frequency of end joining repair events in a P{hsw[a]}-excision repair assay, which can be rescued with mus308+tBa and mus308ATPase-dead but not mus308pol-dead.
eIF-1ABH167 dominantly suppresses the eggshell patterning defects in spn-A3/spn-A093A mutants.
There is a decrease in the percentage of end-joining repair products in studies of excision and repair events of P{hswa} in spn-A093A mus308D5/spn-A3 mus308ZIII-2003 double mutant males compared to the percentage seen in spn-A single mutants. The double mutants show a substantial increase in the percentage of deletion-associated repair events isolated compared to controls, as occurs in mus308 single mutants. These males show increased sterility.
There is a decrease in the percentage of end-joining repair products in studies of excision and repair events of P{hswa} in spn-A093A mus308D5/spn-A093A mus308ZIII-3294 double mutant males compared to the percentage seen in spn-A single mutants. The double mutants show an increase in the percentage of deletion-associated repair events isolated compared to controls, as occurs in mus308 single mutants. These males show increased sterility.
spn-A3/spn-A093A suppresses the increase deletions resulting from the H{PΔ2-3}HoP2.1 driven of excision of P{hswa}sdwa due to a mus309D2/mus309D3 background.
The addition of homozygous mei-W681 completely suppresses the ventralisation phenotype seen in spn-A093A/Df(3R)X3F mutants. The addition of homozygous lok (Using a combination of Df(2L)pr2b, Df(2L)be408, vls+tMa and barr+tMa) completely suppresses the ventralisation phenotype seen in spn-A093A/Df(3R)X3F mutants. The karyosome also appears normal in these mutants.