Homozygotes show a pleiotropic lethal phase ranging from embryonic lethality to weakly surviving adults.
Among embryos derived from females carrying homozygous germ-line clones, approximately 10% show abdominal deletions as well as deformed anterior structures. The remaining 90% of embryos die before cuticle formation.
Dcp1b53/Dcp1b53 ; Dcp1tT3 individuals show a partial female sterile phenotype, with 60% of the embryos failing to hatch. Among the unhatched embryos, more than 90% show a typical posterior group phenotype, and the remaining 10% have a minor posterior group phenotype. In addition, the pole cells are reduced in number or totally missing.
Dcp1[+]/DCP1b53 is an enhancer of ventral denticle belt | germline clone phenotype of Ge-1Δ5
P{Dcp1.T1} and P{Dcp1.T2} fully rescue the P{lArB}Dcp1b53 mutant phenotype.
P{Dcp1.T3} rescues the lethality of P{lArB}Dcp1b53 animals, however, the rescued flies show partial female sterility with a typical posterior group embryonic phenotype.
P{Dcp1.T4} cannot rescue the lethality of P{lArB}Dcp1b53 animals, although a few barely viable but sterile adult homozygous flies can survive.
P{Dcp1.T5} rescues the lethality of P{lArB}Dcp1b53 animals, but the rescued females show a partial female sterility.
The position of the P{lArB}Dcp1b53 insertion suggests that the mutant phenotypes may result from the disruption of Dcp1 and/or CG5602. Experiments using different rescue constructs show that a 22kDa N-terminal polypeptide of Dcp1 can rescue both the lethality and anterior phenotypes of the insertion, however a possible effect of the insertion on CG5602 cannot be ruled out. Experiments using rescue constructs confirm that the disruption of Dcp1, but not CG5602, is responsible for the posterior group phenotype of the P{lArB}Dcp1b53 insertion.
Excision of the P{lArB}Dcp1b53 insertion can revert the mutant phenotype.