Amino acid replacement: A205V.
C30055263T
A205V | spn-A-PA; A148V | spn-A-PB
A205V
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
Mutants show sensitivity to ionising radiation compared to controls, with almost no survival of the mutants after exposure to 750rads ionising radiation.
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%).
In contrast to wild-type ovaries, where the synaptonemal complex (SC) is always restricted to the oocyte by region 2b, spn-A3 mutant females show a significant delay in the process, with cysts with more than 1 cell in synapsis in region 3 of the germarium and in stage 1 and stage 2 of the vitellarium.
Transheterozygous eggs with spn-A2 exhibit either a strong or weak ventralised phenotype: eggs are longer than wild type and are completely symmetric along the DV axis or the eggs display fused dorsal appendages. Germline clones in egg chambers are composed of wild type follicle cells, mutant nurse cells, misplaced oocyte, oocytes that give rise to ventralised eggs and oocytes that lack a karyosome.
spn-A3 has radiation sensitive phenotype, enhanceable by PolQD5
spn-A093A/spn-A3 has radiation sensitive phenotype, enhanceable by DNAlig4169
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/spn-A3 is an enhancer of chemical sensitive phenotype of mus302D1/mus302Z1882
spn-A3/spn-A3 is an enhancer of short lived | chemical conditional phenotype of WRNexoΔ
spn-A3 is a non-enhancer of lethal - all die before end of larval stage phenotype of Brca2KO, PolD3L2
spn-A3/PolD3L2 is a non-enhancer of lethal - all die before end of larval stage phenotype of Brca2KO, Pif1167
spn-A3 is a non-enhancer of lethal - all die before end of larval stage phenotype of Brca2KO, Pif1167
spn-A3 is a non-suppressor of lethal - all die before end of larval stage phenotype of Brca2KO, Pif1167
spn-A3 is a non-suppressor of lethal - all die before end of larval stage phenotype of Brca2KO, PolD3L2
spn-A3/PolD3L2 is a non-suppressor of lethal - all die before end of larval stage phenotype of Brca2KO, Pif1167
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-A3 has synaptonemal complex phenotype, enhanceable by spn-D2
spn-A093A/spn-A3 has egg chorion phenotype, suppressible by eIF1ABH167/eIF-1A[+]
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.
spn-A3 mus308D5 double mutant animals are extremely sensitive to ionising radiation, with almost no survival of the mutants after exposure to 125rads ionising radiation.
There is a decrease in the percentage of end-joining repair products in studies of excision and repair events of P{hswa} in spn-A3 mus308D2/spn-A3 mus308ZIII-2003, spn-A3 mus308D2/spn-A3 mus308D2 and 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.
spn-A3 mus308D2/spn-A3 mus308ZIII-2003 double mutant males in which excision of P{hswa} is occurring show morphological defects such as abdominal cuticle mispatterning.
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.
Double mutant stage 5-6 egg chambers with mus301094, spn-D2 or spn-E1 exhibit a two-oocyte phenotype: the second pro-oocyte develops as an oocyte rather than a nurse cell. The double mutants delay but do not block the decision between the two pro-oocytes as one of the two cells always becomes a nurse cell eventually.
Strong mutation.