UASt regulatory sequences drive expression of an inverted repeat.
Males expressing HP1eGD13814 under the control of Scer\GAL4Act5C.PI produce abundant motile sperm that transfer to females, fertilize eggs and initiate embryogenesis.
The embryos produced by crossing males expressing HP1eGD13814 under the control of Scer\GAL4Act5C.PI with wild type mothers (referred to as Paternal Effect Lethal (PEL) embryos) arrest after only a few rounds of zygotic mitosis. Aged embryos exhibit increasingly asynchronous nuclear cycling and acute mitotic catastrophe. Condensation of the male and female chromosomes is asynchronous: the paternal chromosome is less condensed than the maternal genome. The embryos do not exhibit any gross defects in maternal chromatin dynamics, and exhibit stereotypical centrosome and spindle morphology. As in wild type, sperm DNA undergoes the protamine-to-histone transition, decondenses, migrates towards the maternal pronucleus and enters into the first mitosis. However, at metaphase the paternal DNA fails to condense synchronously with the maternal chromosomes and fails to separate on the mitotic spindle. A prominent chromatin bridge appears at the first anaphase following this asynchronous metaphase.
The telophase chromatin bridge seen in embryos fathered by flies expressing HP1eGD13814 under the control of Scer\GAL4Act5C.PI is contains the Y chromosome in 94% of male embryos. The maternal X is never found in the bridge. In female embryos only the paternal X chromosome is trapped as a bridge. Chromosomes 2 and 3 are trapped at low levels in both male and female embryos.
Adults expressing HP1eGD13814 under the control of Scer\GAL4elav.PLu (in the presence of Dcr-2Scer\UAS.cDa to increase the efficiency of RNAi) do not show a significant defect in avoidance of noxious temperature (46[o]C) compared to control flies.
Expression of HP1eGD13814 under the control of Scer\GAL4elav.PLu (in the presence of Dcr-2Scer\UAS.cDa to increase the efficiency of RNAi) results in viable flies or partial lethality, depending on the particular P{GD13814} insertion line used.
HP1eGD13814 has abnormal mitotic cell cycle | paternal effect | embryonic stage 1 phenotype, non-suppressible by Hira185b
HP1eGD13814/Scer\GAL4Act5C.PI is a non-suppressor of abnormal mitotic cell cycle | embryonic stage 1 phenotype of Hira185b
HP1eGD13814 has embryo | embryonic stage 1 phenotype, non-suppressible by Hira185b
Crossing to homozygous Hira185b mutant females suppresses the early mitotic arrest phenotype observed in embryos produced when males expressing HP1eGD13814 under the control of Scer\GAL4Act5C.PI are crossed to wild type females. As in homozygous Hira185b mutants alone, the maternal DNA continues to cycle until late embryogenesis.
HP1eGD13814 is rescued by HP1erescue/Scer\GAL4Act5C.PI
Expression of HP1erescue rescues the male sterility seen when HP1eGD13814 is expressed under the control of Scer\GAL4Act5C.PI.