DNApol-ε^pl10R homozygous embryos hatch normally and initially develop like their heterozygous siblings. However, at the beginning of the third instar larval stage they begin to show developmental and other defects. Early to mid third instar DNApol-ε^pl10R larvae gradually become akinetic and persist as thin larvae for several days. They show small melanotic patches. The puparia formed are abnormal, being markedly narrower and elongated. All homozygous DNApol-ε^pl10R progeny die as late larvae/early pupae. No phenotypes are seen in DNApol-ε^pl10R heterozygotes.

All imaginal discs and brain ganglia in 6 or 9 day old DNApol-ε^pl10R larvae are very small, similar to those in second instar wild type larvae. The discs are misshapen and difficult to identify. The salivary glands are also small in size. No reduction is seen in the number of endoreplicating cells but the size of the cells is reduced compared to wild type. The number of diploid imaginal cells in salivary gland ducts is significantly reduced. The overall dimensions of the gut are generally comparable to wild type. However the number of gut imaginal cells is reduced in DNApol-ε^pl10R mutants, with 7-10 cells in each cluster compared to 18-20 in wild type.

The cells of DNApol-ε^pl10R mutant wing discs are similar in size to wild type, but the discs contain fewer cells.

Ommatidial units are completely absent in the eye discs of 6-9 day old DNApol-ε^pl10R mutant larvae.

DNApol-ε^pl10R mutant clones can rarely be recovered in imaginal discs. Those that are seen contain fewer cells compared with controls.

DNApol-ε^pl10R mutant larvae show increased sensitivity to DNA damage in response to bleomycin compared to wild type flies. Most of the larvae die at the first instar larval stage and none reach the pupal stage. Wild type controls reach adulthood and appear healthy and fertile. Comet tail analysis shows that a higher proportion of DNA in DNApol-ε^pl10R mutants is damaged than in WT, even under conditions of normal feeding. The proportion of damaged DNA due to bleomycin increases even in wild type, but the increase is more dramatic in DNApol-ε^pl10R larvae.

l(3)pl10R^R mutants exhibit abnormal distribution of Hsrω speckles and causes prolonged larval life and pupal lethality when homozygous. In all l(3)pl10R^R homozygous late larval cells, the Hsrω transcripts localise to one or a few large clusters, this appears to be associated with prolonged larval life and pupal lethality.

l(3)pl10^R mutants exhibit abnormal distribution of omega speckles and causes prolonged larval life and pupal lethality when homozygous. In all l(3)pl10^R homozygous late larval cells, the omega transcripts localise to one or a few large clusters.

PolE1^pl10R has lethal | recessive | third instar larval stage phenotype, non-suppressible by pnt^KG04968/pnt[+]

PolE1^pl10R has lethal | recessive | third instar larval stage phenotype, non-suppressible by pnt[+]/pnt⁰⁷⁸²⁵

PolE1^pl10R has lethal | recessive | third instar larval stage phenotype, non-suppressible by Sec13⁰¹⁰³¹/sec13[+]

PolE1^pl10R has lethal | recessive | third instar larval stage phenotype, non-suppressible by RpS3[+]/RpS3^Plac92

PolE1^pl10R has lethal | recessive | third instar larval stage phenotype, non-suppressible by ATPsyn-Cf6[+]/ATPsynCF6^EY22484

PolE1^pl10R has lethal | recessive | third instar larval stage phenotype, non-suppressible by CG42828[+]/CG42828^f01032

l(3)pl10[+]/PolE1^pl10R is an enhancer of partially lethal - majority die | third instar larval stage phenotype of PolE1^NIG.6768R

l(3)pl10[+]/PolE1^pl10R is an enhancer of partially lethal - majority die | pupal stage phenotype of PolE1^NIG.6768R

l(3)pl10[+]/PolE1^pl10R is an enhancer of abnormal neuroanatomy phenotype of Scer\GAL4^GMR.PF, Zzzz\CAG^{127Q.UAS.Tag:HA}