FlyBase Allele Report: Dmel\polo[1]

Neuroblasts in polo¹/polo^S025604 and polo¹/polo^S132408 transheterozygous third instar larval brains are increased in number and show increased time in mitosis, with a delay between spindle assembly checkpoint silencing and anaphase onset. Brain material transplanted into wild-type host abdomens develops into tumors.

polo¹/polo^S132408 transheterozygous third instar larval brains show low but significant levels of aneuploidy/polyploidy.

(Gallaud et al., 2022)

In polo¹ homozygous embryos, VL1, DT1 and LO1 muscles are missing, or show attachment or elongation defects.

(Yang et al., 2022)

Unlike controls, polo¹/polo¹¹ S1-3 egg chambers show centrosomes retained at nurse cells; mid-to-late stage egg chambers show disrupted membranes between nurse cells.

(Braun et al., 2021)

polo¹/+ does not significantly affect number of boutons or branches at the larval neuromuscular junction, locomotion (larval or adult), or lifespan.

(Peng et al., 2015)

Approximately 90% of polo¹/polo^S025604 germaria have a 'two-oocyte phenotype' in region 3 (a single oocyte is already determined in approximately 70% of wild-type germaria by this stage).

(Pek et al., 2012)

In polo¹ neuroblasts, the aster is lost soon after mitosis and none of the two centrosomes remain cortex bound in interphase.

(Januschke and Gonzalez, 2010)

polo¹ homozygotes are viable, though females are completely sterile.

(Archambault et al., 2007)

Meiosis does not initiate properly in region 2a of the polo¹/polo^S025604 germarium. Cysts often contain abnormal synaptonemal complexes and meiosis restriction to one cell is delayed.

(Mirouse et al., 2006)

The non-disjunction phenotype seen in mei-S332⁸/+ sperm is partially suppressed by polo¹.

(Clarke et al., 2005)

polo¹/polo^16-1 females do not show gross defects in meiotic spindle formation.

(Jang et al., 2005)

Mutant larval brains have a mitotic index that is elevated about 4-fold above that of wild-type cells. The metaphase/anaphase ratio is 11.6 compared to 5.8 in wild-type cells. 2.3% of mitotic cells are aneuploid or polyploid. A small fraction (0.7%) of circular mitotic figures is seen.

(Donaldson et al., 2001)

No appreciable differences are seen between the organisation of the first meiotic spindle in oocytes produced by homozygous females and wild-type oocytes.In contrast, eggs derived from homozygous females show a number of abnormal features that appear to be linked to a delay in progression through the second meiosis. The metaphase II spindles appear abnormal; firstly, the meiotic figures are not aligned particularly well perpendicular to the egg surface, and secondly, although the microtubule array of the central spindle pole body is well developed, the microtubules do not appear to have a well organised focus. It appears that as metaphase progresses in these eggs, the twin spindles move away from each other and the central aster expands as a disorganised array of microtubules. This pattern of spindle organisation appears to persist through early anaphase.

The central aster is reduced in size to become barely detectable from late anaphase onwards. At this time, the meiotic spindles appear elongated and narrowed in their midzone. During telophase the spindle is no longer visible and the two minispindles appear connected by a thin bridge of microtubules. These spindle microtubules appear to have regressed by the end of telophase such that the haploid complements of chromosomes are misaligned. Midbody microtubules have been detected in only 2 out of 38 telophase figures examined. The sperm aster in eggs derived from homozygous females is comparable in size and organisation to that seen in wild type towards the end of meiosis I and the onset of meiosis II. Astral microtubules are short and focused toward several points. By the end of metaphase II the sperm aster is often seen to have divided to give two smaller astral arrays of microtubules which are more widely separated from the male pronucleus than in wild-type. The sperm aster increases in dimensions from telophase onwards, but the microtubules never extend to the egg cortex (as in wild type) and do not interact with the putative female pronucleus. The sperm aster defects cannot be rescued by a paternal copy of polo[+]. 88% of eggs derived from wild-type females can be fertilised by homozygous males, and all show a wild-type meiotic phenotype.

Female meiosis and the sperm centrosome cycle are uncoupled in eggs derived from homozygous females. Close juxtaposition or contact of the male and female pronuclei after the completion of meiosis is only seen in 2.1% of eggs derived from homozygous females. The gonomeric spindle is never formed, and instead a bipolar spindle is established around the haploid paternal complement. In 87% of cases only one centrosome is found in association with a single pole at this spindle, whereas the other centrosome remains free at a slight distance. Pronuclear fusion does not occur in eggs derived from homozygous females, and all four haploid complements derived from the female meiosis retreat to a position immediately below the embryo surface. All four haploid components continue to undergo division cycles (in contrast to wild type where they stop cycling during the first metaphase). The chromosomes become associated with anastral bipolar spindles strongly resembling meiotic spindles. The nuclei associated with these anastral spindles undergo several divisions and populate the embryo surface, while the spindle organised around the male complement is generally unable to divide, although its centrosomes replicate. Only those male derived nuclei associated with spindles retaining both centrosomes are able to divide several times, in which case embryos are seen in which anastral and biastral spindles populate the same cytoplasm. The biastral spindles behave abnormally and give rise to occasional syncytial blastoderm embryos with scattered centrosomes and irregularly sized nuclei. Although sister chromatids successfully segregate during anaphase of these haploid divisions, spindles with abnormal chromosome content are frequently seen.

Eggs derived from virgin homozygous females under meiosis (as in wild type) but do not form polar bodies. About 60% of eggs observed 30 minutes after oviposition contain many anastral bipolar spindles, that are similar to spindles observed in fertilised eggs derived from homozygous females.

Eggs derived from polo¹/polo^DD1 females complete meiosis and show a phenotype similar to that of eggs derived from polo¹ females; they contain many bipolar anastral spindles but lack structures containing polar bodies.

56.7% of fertilised eggs derived from polo¹/polo^DD6 females have two major bipolar anastral spindles 30 minutes after oviposition, indicating arrest in meiosis. 15.3% have 3 spindles and 11.3% have 4 spindles, suggesting some progression through anaphase/telophase of the second meiosis. In these cases, chromosomes are found at the equator of spindles or scattered within them. No more than 5 anastral spindles are seen in these embryos. The sperm aster splits in two during late metaphase II, but its centrosome is unable to drive the formation of a biastral spindle, so that the male haploid complement is associated with a bipolar anastral spindle.

(Riparbelli et al., 2000)

Giant gonial cells containing multiple microtubule-organising centres (MTOCs) are seen in the testes of homozygous males. Primary spermatocyte cysts may contain enlarged cells and the number of ring canals is reduced. Many late anaphase-telophase spermatocytes show defects in the appearance of the central region of the spindle. Many bipolar spindles fail to constrict at telophase, failing to form the mid-body seen in wild-type cysts. Cells which have not formed the mid-body lack the actin ring. Tetrapolar cells containing 4 MTOCs in which cytokinesis has failed in both meiotic divisions are seen. 69% of meiotic cells in homozygous testes show normal meiosis. Meiotic abnormalities are very rare at metaphase of the first division, but defects from anaphase I onwards are found in 31% of cells. There is a loss of synchrony of meiotic divisions compared to wild-type. 82.8% of onion stage spermatids appear normal. Others have varying numbers of nuclei, with binucleate (13.1%) and tetranucleate cells (2.7%) being the most frequent. These abnormal cells have a single enlarged Nebenkern, and indicate a failure of cytokinesis in either one or both meiotic divisions. Spermatids with two or four axonemes are frequently seen. polo¹/polo^DD6 and polo¹/polo^DD1 males show defects in spermatogenesis.

(Carmena et al., 1998)

The frequency of mitotic figures in the polo¹ larval brain is higher than in wild-type. 20.1% of mitotic figures are polyploid and 15.5% are circular.

(Gonzalez et al., 1998)

Approximately 20% of homozygotes survive to adulthood. The testes of homozygous, hemizygous and polo¹/polo² males show cytological abnormalities during all stages of spermatogenesis. Primary spermatocytes containing less than the wild-type number of 16 cells (usually containing 14 cells of normal size and 1 large cell) are seen. The overall organisation of the spindles of metaphase I cysts is defective. Metaphase II cysts have severe abnormalities. Cysts in the second meiotic division are mostly incomplete and highly disorganised. Onion stage cysts contain a variable number of cells, with variable nuclear and Nebenkern volume. The overall organisation of the spindles of metaphase I cysts in the testes of polo¹/polo² males is defective; the spindles appear shorter and thicker than wild-type, showing large asters of microtubule bundles.

(Herrmann et al., 1998)

rl^Su14 and Dsor1^Su1 have no effect on the mutant phenotype.

(Inoue and Glover, 1998)

Homozygous larval neuroblasts have smaller centrosomes than normal. The cells often contain one broad/disorganised centrosome while the other is smaller. Abnormal anaphases are seen where the chromatids have migrated normally to the organised pole but are completely misaligned on the other half spindle.

(Logarinho and Sunkel, 1998)

Semilethal, 7% homozygotes survive as adults. Homozygous females produce embryos with severe mitotic abnormalities; multiple rounds of DNA replication with limited nuclear division, embryos do not cellularise and never hatch.

(Tavares et al., 1996)

Third instar larvae often show aberrant mitosis in neuroblasts in the brain.

(Llamazares et al., 1991)

recessive semi-lethal; a few survivors

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

polo^S025604/polo¹ has decreased occurrence of cell division | third instar larval stage phenotype, enhanceable by mad2^G6595

(Gallaud et al., 2022)

polo^S025604/polo¹ has abnormal neuroanatomy | third instar larval stage phenotype, enhanceable by mad2^G6595

(Gallaud et al., 2022)

polo^S025604/polo¹ has increased cell number | third instar larval stage phenotype, enhanceable by mad2^G6595

(Gallaud et al., 2022)

polo^S025604/polo¹ has neoplasia | third instar larval stage phenotype, enhanceable by mad2^G6595

(Gallaud et al., 2022)

polo^S132408/polo¹ has abnormal neuroanatomy | third instar larval stage phenotype, enhanceable by mad2^G6595

(Gallaud et al., 2022)

polo^S132408/polo¹ has increased cell number | third instar larval stage phenotype, enhanceable by mad2^G6595

(Gallaud et al., 2022)

polo^S132408/polo¹ has abnormal mitotic cell cycle | third instar larval stage phenotype, enhanceable by mad2^G6595

(Gallaud et al., 2022)

polo^S132408/polo¹ has neoplasia | third instar larval stage phenotype, enhanceable by mad2^G6595

(Gallaud et al., 2022)

gwl^scant, polo[+]/polo¹ has female semi-sterile | dominant phenotype, enhanceable | maternal effect by mts[+]/mts^XE-2202

(Rangone et al., 2011)

gwl^scant, polo[+]/polo¹ has female semi-sterile | dominant phenotype, enhanceable | maternal effect by endos^+tRa/endos[+]

(Rangone et al., 2011)

gwl^scant, polo[+]/polo¹ has female semi-sterile | dominant phenotype, enhanceable | maternal effect by tws^aar-1/tws[+]

(Rangone et al., 2011)

gwl^scant, polo[+]/polo¹ has female semi-sterile | dominant phenotype, enhanceable | maternal effect by tws[+]/tws^j11C8

(Rangone et al., 2011)

polo¹ has lethal phenotype, enhanceable by Cdc27^S092309

(Deak et al., 2003)

polo¹ has abnormal mitotic cell cycle phenotype, enhanceable by Cdc27^S092309

(Deak et al., 2003)

NOT Enhanced by

Statement

Reference

polo^S132408/polo¹ has decreased occurrence of cell division | third instar larval stage phenotype, non-enhanceable by mad2^G6595

(Gallaud et al., 2022)

Suppressed by

Statement

Reference

gwl^scant, polo[+]/polo¹ has female semi-sterile | dominant phenotype, suppressible | maternal effect | partially by endos[+]/endos^EY01105

(Rangone et al., 2011)

gwl^scant, polo[+]/polo¹ has female semi-sterile | dominant phenotype, suppressible | maternal effect | partially by endos[+]/endos^EY01103

(Rangone et al., 2011)

NOT suppressed by

Statement

Reference

polo^S132408/polo¹ has decreased occurrence of cell division | third instar larval stage phenotype, non-suppressible by mad2^G6595

(Gallaud et al., 2022)

polo^S025604/polo¹ has female sterile phenotype, non-suppressible by Mmus\Plk1^UASp.GFP/Scer\GAL4^{VP16.mat.αTub67C}

(Pearson et al., 2006)

Enhancer of

Statement

Reference

polo^S025604/polo¹ is an enhancer of abnormal mitotic cell cycle | third instar larval stage phenotype of mad2^G6595

(Gallaud et al., 2022)

polo^S132408/polo¹ is an enhancer of abnormal mitotic cell cycle | third instar larval stage phenotype of mad2^G6595

(Gallaud et al., 2022)

polo¹ is an enhancer of lethal phenotype of Cdc27^S092309

(Deak et al., 2003)

polo¹ is an enhancer of abnormal mitotic cell cycle phenotype of Cdc27^S092309

(Deak et al., 2003)

Suppressor of

Statement

Reference

polo[+]/polo¹ is a suppressor | partially of abnormal neuroanatomy | third instar larval stage phenotype of Hsap\APP^695.UAS, Scer\GAL4^Appl.G1a

(Peng et al., 2015)

polo[+]/polo¹ is a suppressor | partially of abnormal locomotor behavior | third instar larval stage phenotype of Hsap\APP^695.UAS, Scer\GAL4^Appl.G1a

(Peng et al., 2015)

polo[+]/polo¹ is a suppressor | partially of abnormal locomotor behavior | adult stage phenotype of Hsap\APP^695.UAS, Scer\GAL4^Appl.G1a

(Peng et al., 2015)

polo[+]/polo¹ is a suppressor | partially of short lived phenotype of Hsap\APP^695.UAS, Scer\GAL4^Appl.G1a

(Peng et al., 2015)

polo¹ is a suppressor | partially of abnormal meiotic cell cycle phenotype of mei-S332⁸

(Clarke et al., 2005)

Other

Statement

Reference

mts^XE-2202, polo[+]/polo¹ has female fertile phenotype

(Rangone et al., 2011)

gwl^scant, polo[+]/polo¹, tws[+]/tws^j11C8 has female sterile | dominant phenotype

(Rangone et al., 2011)

gwl^scant, mts[+]/mts^XE-2202, polo[+]/polo¹ has female sterile | dominant phenotype

(Rangone et al., 2011)

endos^+tRa/endos[+], gwl^scant, polo[+]/polo¹ has female sterile | dominant phenotype

(Rangone et al., 2011)

endos^EY01105, polo[+]/polo¹ has female fertile phenotype

(Rangone et al., 2011)

endos^EY01103, polo[+]/polo¹ has female fertile phenotype

(Rangone et al., 2011)

polo[+]/polo¹, tws^aar-1 has female fertile phenotype

(Rangone et al., 2011)

polo[+]/polo¹, tws^j11C8 has female fertile phenotype

(Rangone et al., 2011)

gwl^scant, polo[+]/polo¹ has female semi-sterile | dominant phenotype

(Rangone et al., 2011)

gwl^scant, polo[+]/polo¹, tws^aar-1/tws[+] has female sterile | dominant phenotype

(Rangone et al., 2011)

gwl^scant, polo¹ has abnormal mitotic cell cycle phenotype

(Archambault et al., 2007)

Phenotype Manifest In

Enhanced by

Statement

Reference

polo^S025604/polo¹ has larval neuroblast | third instar larval stage phenotype, enhanceable by mad2^G6595

(Gallaud et al., 2022)

polo^S025604/polo¹ has larval neuroblast | third instar larval stage | increased number phenotype, enhanceable by mad2^G6595

(Gallaud et al., 2022)

polo^S025604/polo¹ has larval brain | third instar larval stage phenotype, enhanceable by mad2^G6595

(Gallaud et al., 2022)

polo^S132408/polo¹ has larval neuroblast | third instar larval stage | increased number phenotype, enhanceable by mad2^G6595

(Gallaud et al., 2022)

polo^S132408/polo¹ has larval brain | third instar larval stage phenotype, enhanceable by mad2^G6595

(Gallaud et al., 2022)

polo¹ has aster & neuroblast phenotype, enhanceable by Cdc27^S092309

(Deak et al., 2003)

polo¹ has spindle & neuroblast phenotype, enhanceable by Cdc27^S092309

(Deak et al., 2003)

NOT Enhanced by

Statement

Reference

polo^S132408/polo¹ has larval neuroblast | third instar larval stage phenotype, non-enhanceable by mad2^G6595

(Gallaud et al., 2022)

Suppressed by

Statement

Reference

polo^S025604/polo¹ has germarium region 3 phenotype, suppressible | partially by Scer\GAL4^nanos.PG/mael^{S138D.UASp.Tag:FLAG}

(Pek et al., 2012)

polo^S025604/polo¹ has germarium region 3 phenotype, suppressible by Sirt1¹⁷/Sir2[+]

(Pek et al., 2012)

polo^S025604/polo¹ has germarium region 3 phenotype, suppressible by pch2^EY01788a/pch2^EY01788a

(Pek et al., 2012)

NOT suppressed by

Statement

Reference

polo^S132408/polo¹ has larval neuroblast | third instar larval stage phenotype, non-suppressible by mad2^G6595

(Gallaud et al., 2022)

polo^S025604/polo¹ has germarium region 3 phenotype, non-suppressible by Scer\GAL4^nanos.PG/mael^{S138A.UASp.Tag:FLAG}

(Pek et al., 2012)

Enhancer of

Statement

Reference

polo^S025604/polo¹ is an enhancer of larval brain | third instar larval stage phenotype of mad2^G6595

(Gallaud et al., 2022)

polo^S132408/polo¹ is an enhancer of larval brain | third instar larval stage phenotype of mad2^G6595

(Gallaud et al., 2022)

polo¹ is an enhancer of aster & neuroblast phenotype of Cdc27^S092309

(Deak et al., 2003)

polo¹ is an enhancer of spindle & neuroblast phenotype of Cdc27^S092309

(Deak et al., 2003)

NOT Enhancer of

Statement

Reference

polo¹/polo¹ is a non-enhancer of dorsal transverse muscle cell | embryonic stage phenotype of bsd¹

(Yang et al., 2022)

polo¹/polo¹ is a non-enhancer of muscle cell of lateral oblique muscle 1 | embryonic stage phenotype of bsd¹

(Yang et al., 2022)

polo¹/polo¹ is a non-enhancer of muscle cell of ventral longitudinal muscle 1 | embryonic stage phenotype of bsd¹

(Yang et al., 2022)

polo¹/polo¹ is a non-enhancer of dorsal transverse muscle cell | embryonic stage phenotype of tum^DH15

(Yang et al., 2022)

polo¹/polo¹ is a non-enhancer of muscle cell of lateral oblique muscle 1 | embryonic stage phenotype of tum^DH15

(Yang et al., 2022)

polo¹/polo¹ is a non-enhancer of muscle cell of ventral transverse muscle 1 | embryonic stage phenotype of tum^DH15

(Yang et al., 2022)

Suppressor of

Statement

Reference

polo[+]/polo¹ is a suppressor | partially of NMJ bouton | third instar larval stage phenotype of Hsap\APP^695.UAS, Scer\GAL4^Appl.G1a

(Peng et al., 2015)

polo[+]/polo¹ is a suppressor | partially of type Is terminal bouton | third instar larval stage phenotype of Hsap\APP^695.UAS, Scer\GAL4^Appl.G1a

(Peng et al., 2015)

polo[+]/polo¹ is a suppressor | partially of wing phenotype of Hsap\APP^695.UAS, Scer\GAL4^Appl.G1a

(Peng et al., 2015)

polo[+]/polo¹ is a suppressor of nucleus | embryonic stage phenotype of lok^E51

(Xu and Du, 2003)

Other

Statement

Reference

gwl^scant, polo¹ has spindle phenotype

(Archambault et al., 2007)

gwl^scant, polo¹ has centrosome | embryonic stage 4 phenotype

(Archambault et al., 2007)

asp^E3, polo¹ has mitotic cell cycle phenotype

(Gonzalez et al., 1998)

Additional Comments

Genetic Interactions

Statement

Reference

Expression of mael^{S138D.Scer\UAS.P\T.T:Zzzz\FLAG} under the control of Scer\GAL4^nos.PG partially suppresses the defect in oocyte commitment (high frequency of 'two-oocyte phenotype' in region 3 of the germarium) that is seen in polo¹/polo^S025604 germaria.

Expression of mael^{S138A.Scer\UAS.P\T.T:Zzzz\FLAG} under the control of Scer\GAL4^nos.PG does not suppress the defect in oocyte commitment (high frequency of 'two-oocyte phenotype' in region 3 of the germarium) that is seen in polo¹/polo^S025604 germaria.

Sir2¹⁷/+ suppresses the defect in oocyte commitment (high frequency of 'two-oocyte phenotype' in region 3 of the germarium) that is seen in polo¹/polo^S025604 germaria.

pch2^EY01788a/pch2^EY01788a suppresses the defect in oocyte commitment (high frequency of 'two-oocyte phenotype' in region 3 of the germarium) that is seen in polo¹/polo^S025604 germaria.

(Pek et al., 2012)

polo¹/+ gwl^scant/+ double heterozygous females are nearly sterile. This phenotype is partially suppressed if the females are also heterozygous for either endos^EY01105 or endos^EY01103.

Heterozygosity for either tws^aar-1, tws^j11C8 or mts^XE-2202 enhances the reduced fertility phenotype of polo¹/+ gwl^scant/+ double heterozygous females, such that in each case the triple heterozygotes are completely sterile.

endos^+tRa enhances the reduced fertility phenotype of polo¹/+ gwl^scant/+ double heterozygous females, such that in each case the triple heterozygotes are completely sterile.

(Rangone et al., 2011)

polo¹ gwl^scant double heterozygous females produce 4% as many progeny as controls.

polo¹ gwl^scant mitotic nuclei exhibit centrosomal loss in just under approximately 60% of syncytial embryos.

polo¹ gwl^scant double heterozygous females produce embryos that frequently display centrosome disassociation from one pole. There is a slight but significant increase in defective spindles in embryos derived from polo¹ gwl^scant mutants compared to controls, indicating that a single mutant copy of these genes in mothers leads to mitotic defects at a low frequency. However, these embryos always hatch and develop fully, indicating that such low frequencies of defects can be tolerated.

(Archambault et al., 2007)

The lethal phase of Cdc27^S092309 is advanced to an earlier developmental stage when in combination with polo¹. The stage of death is also earlier than with polo¹ alone. In terms of the mitotic index, the metaphase:anaphase ratio, the condensation state of the chromosomes and the levels of mitotic cyclins, the phenotype of Cdc27^S092309 polo¹ cells do not differ significantly from that of the Cdc27^S092309 single mutant. The polo¹ phenotype with respect to centrosomal defects is enhanced by the Cdc27^S092309 mutation. Mitotically arrested Cdc27^S092309 polo¹ cells, lack the MPM2 epitope at their spindle poles, consistent with diminished levels of polo kinase activity at the spindle poles. Cdc27^S092309 is epistatic to polo¹ in respect of mitotic progression and cyclin degradation. Cdc27^S092309 polo¹ double mutant cells display overcondensed chromosomes. In Cdc27^S092309 polo¹ double mutants the mitotic index, proportions of metaphase:anaphase cells and the proportion of polyploids are similar to that in the Cdc27^S092309 mutant alone.

(Deak et al., 2003)

The fraction of embryos derived from lok^E51 females which have abnormal nuclei is reduced (from 61.5 +/- 1.1%) if the females also carry one copy of polo¹ (to 27.0 +/- 3.2% of embryos).

(Xu and Du, 2003)

polo¹ mgr^unspecified double mutants show a phenotype more similar to mgr^unspecified than polo¹ single mutants, although the frequency of circular figures appears to be additive. asp^E3 polo¹ double mutants show mitotic abnormalities similar to those seen in asp^E3 single mutants, including polyploid and aneuploid cells with various degrees of chromosome condensation. There are a large number of cells in metaphase, and unlike the polo¹ single mutant, no normal metaphase or anaphase figures and no circular mitotic figures are seen. The mitotic frequency of the double mutant and the frequency of polyploid cells are dramatically increased compared to that of either single mutant, indicating a synergistic effect.

(Gonzalez et al., 1998)

Xenogenetic Interactions

Statement

Reference

polo¹/+ partially suppresses the wing expansion defects, shorter lifespan, locomotion defects (larval and adult), and increases of Is bouton numbers (but does not suppress branch number changes or the decrease of Ib boutons) at the larval neuromuscular junction seen in animals with Hsap\APP^695.Scer\UAS driven by Scer\GAL4^Appl.G1a.

(Peng et al., 2015)

Expression of Mmus\Plk1^{Scer\UAS.P\T.T:Avic\GFP} under the control of Scer\GAL4^{mat.αTub67C.T:Hsim\VP16} does not rescue the sterility of polo¹/polo^S025604 females.

(Pearson et al., 2006)

Complementation and Rescue Data

Rescued by

polo^S025604/polo¹ is rescued by polo^GFP

(Pearson et al., 2006)

polo¹ is rescued by polo^GFP

(Moutinho-Santos et al., 1999)

polo¹ is rescued by polo^t10

(Llamazares et al., 1991)

Partially rescued by

polo¹/Df(3L)rdgC-co2 is partially rescued by polo^wt.GFP

(Bonner et al., 2013)

Not rescued by

polo¹/Df(3L)rdgC-co2 is not rescued by polo^{H518A.K520M.GFP}

(Bonner et al., 2013)

Comments

polo^{wt.T:Avic\GFP} substantially rescues the sterility of polo¹/Df(3L)rdgC-co2 females: in the presence of one copy of polo^{wt.T:Avic\GFP} the rescued females produce an average of 23.9 progeny per female over 18 days when mated to wild-type males and in the presence of two copies, produce an average of 30.9 progeny per female.

polo^{H518A.K520M.T:Avic\GFP} fails to rescue the sterility of polo¹/Df(3L)rdgC-co2 females.

(Bonner et al., 2013)

polo^T:Avic\GFP rescues the sterility of polo¹/polo^S025604 females.

(Pearson et al., 2006)

Images (0)

Mutant

Wild-type

Stocks (2)

Bloomington

546

Dp(1;Y)Bar^S, Bar⁺; ru¹ st¹ polo¹ e^s ca¹/TM3, Sb¹

Kyoto

105973

Dp(1;Y)Bar^S; ru¹ st¹ polo¹ e^s ca¹/TM3, Sb¹

Notes on Origin

Discoverer

Nusslein-Volhard.

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (1)

Reported As

Symbol Synonym

polo¹

(Gallaud et al., 2022, Yang et al., 2022, Braun et al., 2021, Gallaud et al., 2020, Liaw and Chiang, 2019, Peng et al., 2015, Bonner et al., 2013, Pek et al., 2012, Rangone et al., 2011, Januschke and Gonzalez, 2010, Zhang et al., 2009, Archambault et al., 2007, Xiang et al., 2007, Mirouse et al., 2006, Pearson et al., 2006, Clarke et al., 2005, Jang et al., 2005)

Name Synonyms

Secondary FlyBase IDs

References (38)

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