Mobilization of P{EP}cupEP2349 caused a 1175bp deletion downstream of the insertion site. This deletion includes the first 275bp of Spn27A.
Mutant animals show spontaneous melanisation.
Approximately 6% of homozygotes are viable as adults, and approximately 80% of these escapers show constitutive melanization.
Embryos from Spn27A1 homozygous mothers do not develop beyond the syncytial blastoderm stage. Embryos from Spn27A1/Df(2L)BSC7 mothers show a ventralized phenotype and therefore fail to differentiate a cuticle at the end of embryogenesis. This phenotype can be rescued by injection of Spn27A mRNA.
70% of Spn27A1 mutants die as pupae. Those that survive to adulthood often have wing defects and are female sterile. Ectopic melanisation is seen in mutant adults and larvae in the absence of any injury. Melanization in larvae or adults in response to clean injury, septic injury (with Erwina cartovora) or wasp infection (with L.boulardi), is much more extensive than in similarly treated wild-type animals. In the case of wasp infection or clean injury of larvae, the melanization is usually systemic rather than discrete as in wild-type. 50-70% of mutant larvae pricked with a needle die within 5 hr of injury, compared to 10% of wild-type controls. In most cases, the melanization reaction diffuses throughout the larval body cavity and dead larvae turn completely black. Spn27A1 homozygotes adults have reduced resistance to natural infection with B.bassiana compared to wild-type (survival after 6 days is around 20% compared to around 90% for controls). However, survival 6 days after infection by pricking with cultures of E.coli, M.luteus, or A.fumigata is similar to that after clean injury of mutants.
Spn27A1 has melanotic mass phenotype phenotype, enhanceable by PPO2Δ
Spn27A1 has partially lethal phenotype, enhanceable by PPO2Δ
Spn27A1 has melanotic mass phenotype phenotype, suppressible by PPO1Δ/PPO2Δ
Spn27A1 has partially lethal phenotype, suppressible by PPO1Δ/PPO2Δ
Spn27A1 has melanotic mass phenotype | adult stage phenotype, suppressible by Df(3R)ME15/+
Spn27A1 has melanotic mass phenotype | adult stage phenotype, suppressible by Df(3R)dsx11/+
Spn27A1 has partially lethal - majority die | recessive | pupal stage phenotype, suppressible by PPO1Bc
Spn27A1 has female sterile phenotype, non-suppressible by PPO1Bc
Spn27A1 is a non-suppressor of abnormal immune response | adult stage phenotype of PPO1Bc
PPO1Δ, Spn27A1 has melanotic mass phenotype phenotype
Spn27A1 has melanotic mass | adult stage phenotype, suppressible by Df(3R)ME15/+
Spn27A1 has melanotic mass | adult stage phenotype, suppressible by Df(3R)dsx11/+
Spn27A1/Df(2L)BSC7 has embryonic/first instar larval cuticle | maternal effect phenotype, suppressible by spzD1-RPQ/Df(3R)Tl-D
Spn27A1/Df(2L)BSC7 has embryonic/first instar larval cuticle | maternal effect phenotype, suppressible by ea4/Df(3R)ea-5022rx1
The spontaneous melanisation seen in Spn27A1 mutant animals is suppressed if they are also mutant for both PPO1Δ and PPO2Δ.
50% of Spn27A1 PPO1Δ double mutant larvae and pupae show a characteristic pattern of melanisation spots under the epidermis.
The spontaneous melanisation seen in Spn27A1 mutant animals is stronger if they are also mutant for PPO2Δ; the double mutant pupae turn black and adults have large spots and wing defects.
The constitutive melanization phenotype of Spn27A1 homozygous escapers is suppressed more than 5-fold if they are also heterozygous for Df(3R)ME15 or Df(3R)dsx11.
The ventralized phenotype that causes the failure of cuticle differentiation in embryos from Spn27A1/Df(2L)BSC7 mothers is abolished when mothers also have the mutant genotype ea4/Df(3R)ea-5022rx1 or spzD1-RPQ/Df(3R)Tl-D. Such embryos have a dorsalized phenotype that is indistinguishable from those produced by single mutant ea4/Df(3R)ea-5022rx1 or spzD1-RPQ/Df(3R)Tl-D mothers.
Pupal lethality, wing phenotypes and ectopic melanisation in larvae after clean injury in Spn27A1 mutants are all suppressed by homozygosity for Bc1. The female sterility phenotype of Spn27A1 mutants is not suppressed.
The melanization response in Bc1 homozygotes is unaffected by Spn27A1, as is the reduced resistance to natural infection with B.bassiana.
Pupal lethality, wing phenotypes and ectopic melanisation in larvae after clean injury in Spn27A1 mutants are all suppressed by homozygosity for Bcunspecified. The female sterility phenotype of Spn27A1 mutants is not suppressed.
Recombinant Spn27A protein purified from S2 cells transfected with Spn27AMtnA.T:SV5\V5,T:Zzzz\His6, rescues ectopic melanisation due to clean injury of Spn27A1 homozygous adults, when injected into the injury site.
Spn27A1 complements cupunspecified : Unlike Spn27A1 or cupunspecified homozygotes, Spn27A1/cupunspecified females are not sterile.