Embryos at stages 4-5 from lok^p6/+, jnj^Δ35/jnj^Δ35 double mutant mothers exhibit reduced nuclear fallout as compared to those from jnj^Δ35/jnj^Δ35 single mutant mothers.

The developmental delay and arrest at cycle 3 characteristic for embryos from ddbt^Z4344 fathers is partially rescued in embryos from ddbt^Z4344 fathers and lok^p6 mothers - these embryos are allowed to progress past cycle 3 despite the number of chromosomal abnormalities they display (lagging chromosomes, anaphase bridges and nuclei with variable chromosome content).

lok^p6/+ fails to suppress the abnormal karyosome morphology observed in females expressing lid^GLV21071 under the control of Scer\GAL4^{nos.UTR.T:Hsim\VP16}.

lok^p6/+ suppresses the abnormal karyosome morphology observed in spn-A¹ mutants.

Most egg chambers develop into eggs in Rpp30^18.2 ; lok^p6 double mutant females, and these eggs can be laid and fertilised.

lok^p6 partially suppresses the dorsal appendage defects seen in eggs produced by armi^72.1/Df(3L)armi-J mutant mothers. The number of eggs produced is also significantly increased.

lok^p6 partially suppresses the dorsal appendage defects seen in eggs produced by armi^null mutant mothers (expressing CycJ^+t4 to restore CycJ[+] function). The number of eggs produced is also significantly increased.

lok^p6 does not suppress the developmental abnormalities seen in Df(3L)armi-J mutant flies. As in Df(3L)armi-J alone, the resulting females produce no eggs and have disorganised ovarioles.

lok^p6, Df(2L)His^C double mutants exhibit a Df(2L)His^C-like phenotype.

The mild abnormal spindle phenotype seen in syncytial embryos derived from homozygous DNApol-η^Exc2.15 females in the absence of UV irradiation is suppressed if the females are also homozygous for lok^p6. In addition, the spindle abnormalities seen after irradiation in embryos derived from homozygous DNApol-η^Exc2.15 females are also suppressed in embryos derived from double mutant females.

lok^p6 does not rescue the karyosome defects seen in SRPK^129-09/Df(2R)ED2436 mutant oocytes.

The ventralised eggshell phenotype seen in eggs derived from homozygous CycG^HR7 females is suppressed in more than 90% of eggs if the females are also carrying lok^p6/Df(2L)BSC258.

The inactivation of centrosome associated with asynchronous nuclei in RecQ5^D1 embryos is suppressed when maternal lok^p6 is also absent from the embryo. In addition, the nuclear descent from the cortex is also suppressed.

The dorsal appendage defects seen in eggs laid by aub^HN2/aub^QC42 females are suppressed if the females are also homozygous for lok^p6; 99.2% of the eggs have wild-type dorsal appendages.

The dorsal appendage defects seen in eggs laid by armi¹/armi^72.1 females are partly suppressed if the females are also homozygous for lok^p6; 16.1% of the eggs have fused dorsal appendages, 7.3% lack dorsal appendages and 76.6% have wild-type dorsal appendages.

80% of eggs derived from lok^p6 ; rhi^KG00910/rhi⁰²⁰⁸⁶ double mutant females have two normal dorsal appendages.

lok^p6 partially suppresses the phenotype of embryos derived from nopo^Z1447 females; the acentrosomal, barrel-shaped mitotic spindles are restored to normal spindles with attached centrosomes. However, DNA defects are common in embryos derived from the double mutant females, particularly during cortical divisions, with abnormal DNA aggregates that are shared by more than one spindle often being seen. The embryos derived from the double mutant females complete syncytial divisions, and arrest with aberrant morphology upon the initiation of gastrulation.

Embryos derived from lok^p6 nopo^Z1447 double mutant females have significantly shorter interphases during cycle 11 compared to wild-type or lok^p6 single mutant embryos.

Embryos derived from lok^p6 nopo^Z1447/lok^p6 Df(2R)Exel7153 females have significantly shorter interphases during cycle 11 compared to wild-type or lok^p6 single mutant embryos.

Embryos derived from lok^p6 nopo^Z1447/lok^p6 nopo^Exc142 females have significantly shorter interphases during cycle 11 compared to wild-type or lok^p6 single mutant embryos.

The eggshell patterning and karyosome formation defects of Brca2^KO/Brca2^56E females are rescued by lok^p6/lok^p6.

lok^p6 partially suppresses the increased levels of apoptosis seen in mitotically cycling ovarian follicle cells following expression of dup^{hsp70.T:Hsap\MYC}.

mei-41^29D abolishes the residual apoptotic response seen in the eye discs of lok^p6 mutants containing dicentric chromosomes (generated using Scer\FLP1^hs.PP-induced recombination in chromosomes containing inverted Scer\FRT sites). This effect is seen at 12-14 hours after heat shock, using either the DcYy⁺ or the P{inv.FRT}Dc3-FrTr1D chromosome. Wing disc apoptosis is suppressed in mei-41^29D lok^p6 double mutants 12-14 hours after heat shock of DcYy⁺ or P{inv.FRT}Dc3-FrTr1D. At 24 hours after heat shock wing disc apoptosis is suppressed in double mutant cells containing Y chromosome dicentrics, but apoptosis is still seen when dicentric chromosomes are generated on chromosome three. 25% of lok^p6 mei-41^29D double mutant larval neuroblast cells have normal karyotypes 48 hours after dicentric chromosomes production (generated using Scer\FLP1^hs.PP-induced recombination in P{inv.FRT}Dc3-FrTr1D, which contains inverted Scer\FRT sites), whereas 44% appear normal in the dicentric controls. Phenotypes observed in cells with abnormal karyotypes include the presence of multiple acentric chromatids, chromosome fusions and tetraploidy.

grp^fs1 partially suppresses the residual apoptotic response seen in lok^p6 mutants containing dicentric chromosomes (generated using Scer\FLP1^hs.PP-induced recombination in chromosomes containing inverted Scer\FRT sites). Eye disc apoptosis is abolished 12-14 hours after heat shock of DcYy⁺, P{FRT(w^hs)}(8F)105 or P{inv.FRT}Dc3-FrTr1D. Wing disc apoptosis is also suppressed in grp^fs1 lok^p6 mutants at 12-24 hours after heat shock of DcYy⁺, P{FRT(w^hs)}(8F)105 or P{inv.FRT}Dc3-FrTr1D. At 24 hours after heat shock wing disc apoptosis is suppressed in double mutant cells containing Y chromosome dicentrics, but apoptosis is still seen when dicentric chromosomes are generated on the X or autosome.

Expression of grp^GUS.cBa partially suppresses the apoptosis seen in lok^p6 grp^fs1 double mutant cells containing dicentric chromosomes (generated using Scer\FLP1^hs.PP-induced recombination in chromosomes containing inverted Scer\FRT sites). This effect is seen at 12-14 hours after heat shock of DcYy⁺.

The fused dorsal appendage phenotype of armi^72.1/armi¹ eggs is suppressed in lok^p6; armi^72.1/armi¹ eggs with 92% of double mutants showing wild-type appendage morphology.

The fused dorsal appendage phenotype of aub^HN/aub^QC42 eggs is suppressed in lok^p6; aub^HN/aub^QC42 eggs with 98% of double mutants showing wild-type appendage morphology.

The microtubule-organizing center phenotype of armi^72.1/armi¹ oocytes is suppressed by the lok^p6 mutation.

The microtubule-organizing center phenotype of spn-D² oocytes is suppressed by the lok^p6 mutation.

The fused dorsal appendage phenotype of spn-D² eggs is suppressed by lok^p6.

The dorsoventral patterning defects seen in eggs derived from squ^HE47/squ^PP32 females are nearly completely suppressed if the females are also homozygous for lok^p6; 9.3% have a single dorsal appendage or the appendages are fused at the base and 90.6% of the eggs are similar to wild type.

The mitotic defects seen in embryos derived from MCPH1^Z1861 females are suppressed if the females are also mutant for lok^p6; mitotic spindles are restored to near normality and the early developmental arrest is suppressed, such that most of the double mutant embryos complete syncytial divisions, cellularise and cease developing near gastrulation (most of the embryos initiate gastrulation but it is grossly aberrant). The double mutant embryos occasionally have abnormal DNA aggregates shared by more than one spindle and multipolar spindles.

A significant number of embryos derived from grp^fs1 lok^p6 double mutant females have a uniform monolayer of cortical nuclei surrounded by a hexagonal actin network, indicating that they have initiated or completed cellularisation. The nuclei in the double mutant embryos are larger than in wild-type controls. The double mutant embryos consistently proceed through a fifth cortical mitotic cycle (14th cycle) before cellularisation (in wild-type embryos, cellularisation occurs after the 13th cycle). The double mutant embryos also undergo gastrulation. The cephalic furrow does not form in the double mutant embryos.

grp^fs1 lok^p6 double mutants exhibit normal telomere protection and chromosome break repair.

Apoptosis is substantially reduced in nbs¹ lok^p6 double mutant third instar larval wing discs compared to nbs¹ single mutants.

lok^p6 mutants that are also heterozygous for Df(3L)H99 display significantly lower levels of acridine orange staining (indicating cell death) at 18 and 24 hours after irradiation compared with lok^p6 mutants. By 30 hours after irradiation, however, there is a substantial increase in cell death in lok^p6, Df(3L)H99/+ double mutants.

Double mutants of p53^5A-1-4 and lok^p6 display similar levels of acridine orange staining (indicating cell death) after radiation (visualised in third instar imaginal discs irradiated with 4,000 R).

lok^p6; mei-41^29D mutants develop normally and males are fertile. lok^p6 fails to enhance the chromosome fusion phenotype seen in the nuclei of third instar larval neuroblasts of mre11^unspecified.

Mutation of lok^p6 in wee^ES1 mutants rescues the anastral spindle and γTURC phenotypes, but fails to rescue the promiscuous spindle interaction and multipolar spindle phenotypes. The displacement of centrosomes from the cortex in interphase of cycle 12 is only partially rescued in wee^ES1, lok^p6 double mutants.

lok^p6 enhances the partial loss of cell cycle arrest seen in grp^fs1 mutant third instar larval wing discs in response to X-ray induced irradiation. No arrest is seen in the double mutant larvae.

Cellularisation and cortical retention of DNA is partially restored in wee^ES1 lok^p6 double mutant embryos and about 60% of the double mutant embryos show evidence of migration changes that normally occur in cellularised embryos (such as the migration of pole cells toward the embryo anterior). The extent of this rescue is variable and none of the double mutant embryos survive to hatching. The distribution and appearance of DNA in these embryos is abnormal.

The loss of germline stem cells (GSCs) observed upon heat-shock induced expression of Crei\I-CreI^hs.PR (to introduce DNA damage) is rescued by combination with lok^p6 or lok^KD in hetero-, homo- or transheterozygosity as these double mutant flies contain significantly higher number of GSCs both at 3 days and 1 week post heat-shock compared to Crei\I-CreI^hs.PR single mutants.

lok^KD/lok^p6;Crei\I-CreI^hs.PR mutants have more GSCs than wild-type controls even without the induction of DNA damage by heat-shock.

Crei\I-CreI^hs.PR germaria in which DNA damage has been evoked by heat-shock accumulate cystoblast-like single cells and this accumulation is accelerated by lok^p6 or lok^KD heterozygosity (significantly increased number of CB-like cells observed already at 3 days post heat-shock). By contrast, both lok^p6 or lok^KD homo- or transheterozygosity completely abolishes the CB-like cell accumulation phenotype.

A lok^p6 mutant background cannot alleviate the overgrowth or anterior cell cycle arrest of wing discs with posterior 'undead' Scer\GAL4^hh-Gal4>W^Scer\UAS.cYa, BacA\p35^Scer\UAS.cHa cells.