FlyBase Allele Report: Dmel\Khc[27]

Khc²⁷ mutant oocytes display defects in the directed movement of osk messenger ribonucleoprotein particles as they fail to show the dominance of plus-end-directed runs over the minus-end-directed runs normally observed in wild-type oocytes.

(Gáspár et al., 2017)

In Khc²⁷ germline clones the microtubules grow more rapidly close to the posterior region of the oocyte and the lifespan of growing microtubule plus ends are reduced near the posterior cortex when compared to controls.

(Nieuwburg et al., 2017)

The ooplasmic streaming rate of Khc²⁷ heterozygous mutant oocytes is comparable to wild-type controls.

(Lu et al., 2016)

Khc²⁷ homozygotes are lethal (fail to pupariate) but the heterozygotes display no significant viability or larval locomotion defects.

(Winding et al., 2016)

Khc²⁷/Khc⁶³ mutant brains exhibit centrosome separation defects, that lead to a small angle between centrosomes at nuclear envelope breakdown but that have no effect on spindle assembly.

(Gallaud et al., 2014)

Khc²⁷ mutants exhibit polarity defects in the oocyte.

Approximately 70% of Khc²⁷ mutants oocytes exhibit incorrect nucleus positioning, with the nucleus found separated from the anterior membrane by more than half a nucleus radius.

Khc²⁷ mutant embryos do not develop dorsal appendages.

The presence of Khc^{1-975.αTub67C.T:Avic\GFP} rescues the polarity defects (such as osk mRNA transport) found in Khc²⁷ mutants.

The presence of Khc^{1-975.αTub67C.T:Avic\GFP} rescues the nucleus mis-positioning defects found in Khc²⁷ mutants.

The presence of Khc^{1-975.αTub67C.T:Avic\GFP} rescues the absence of dorsal appendages found in Khc²⁷ mutants.

The presence of Khc^{1-849.αTub67C.T:Avic\GFP} rescues the absence of dorsal appendages found in Khc²⁷ mutants in 48% of cases. Only 3.5% of these mutants have two fully formed dorsal appendages.

The presence of Khc^{1-700.αTub67C.T:Avic\GFP} rescues the absence of dorsal appendages found in Khc²⁷ mutants in 33% of cases.

Khc²⁷ mutants expressing Khc^{330-975.αTub67C.T:Avic\GFP} exhibit nucleus mis-positioining in the oocyte and abnormalities in dorsal appendage formation.

Khc²⁷ mutants expressing Khc^{231-975.αTub67C.T:Avic\GFP} exhibit nucleus mis-positioining in the oocyte and abnormalities in dorsal appendage formation.

Khc²⁷ mutant oocytes exhibit actin spheres close to mis-localized nuclei.

The presence of Khc^{1-975.αTub67C.T:Avic\GFP} rescues the actin spheres found close to mis-localized nuclei in Khc²⁷ mutants.

The presence of Khc^{1-975.ΔIAK.αTub67C.T:Avic\GFP} fails to rescue the actin spheres found close to mis-localized nuclei in Khc²⁷ mutants.

The presence of Khc^{1-849.αTub67C.T:Avic\GFP} fails to rescue the actin spheres found close to mis-localized nuclei in Khc²⁷ mutants.

Khc²⁷ mutants expressing Khc^{1-975.ΔIAK.αTub67C.T:Avic\GFP} exhibit a strong nucleus positioning phenotype. Accordingly, dorsal appendage formation is also affected in these flies.

Approximately 60% of Khc^{1-849.αTub67C.T:Avic\GFP} mutants oocytes exhibit incorrect nucleus positioning, with the nucleus found separated from the anterior membrane by more than half a nucleus radius.

The presence of Khc^{1-849.αTub67C.T:Avic\GFP} fails to rescue osk mRNA transport but does rescue the dynein transport defects found in Khc²⁷ mutants.

Approximately 70% of Khc^{1-700.αTub67C.T:Avic\GFP}, Khc²⁷ mutants oocytes exhibit incorrect nucleus positioning, with the nucleus found separated from the anterior membrane by more than half a nucleus radius.

Oocytes expressing Khc^{1-700.αTub67C.T:Avic\GFP} exhibit a Dynein localization phenotype indistinguishable from that of Khc²⁷ mutants.

Khc^{Δ521-641.αTub67C.T:Avic\GFP}, Khc²⁷ mutants eggs exhibit normal dorsal appendages and no aberrant actin spheres.

Approximately 33% of Khc^{1-938.αTub67C.T:Avic\GFP}, Khc²⁷ mutants eggs show aberrant nucleus positioning and dorsal appendage formation is strongly affected. These mutants also show the aberrant accumulation of actin-recruiting spheres.

(Williams et al., 2014)

Microtubule motility is dramatically decreased in neurons from maternal Khc²³/Khc²³ (Khc²³ germline clone) and zygotic Khc²³/Khc²⁷ embryos. Most of the neurons cultured from these embryos die after overnight culture.

(Lu et al., 2013)

The 50% lethal phase of Khc⁶/Khc²⁷, Khc²²/Khc²⁷ and Khc⁷⁴/Khc²⁷ animals on normal and rich food is the third larval instar stage. On poor food, the 50% lethal phase is shifted to the pupal stage.

Khc⁷⁴/Khc²⁷, Khc⁷⁵/Khc²⁷ and Khc⁷⁷/Khc²⁷ larvae show reduced flux of neurosecretory dense core vesicles compared to wild type and no flux of mitochondria along the axons.

Khc⁶⁸/Khc²⁷, Khc²³/Khc²⁷, Khc⁶¹/Khc²⁷, Khc⁶⁶/Khc²⁷, Khc⁶²/Khc²⁷, Khc⁶³/Khc²⁷, Khc⁴/Khc²⁷, Khc⁶⁴/Khc²⁷ and Khc⁵⁸/Khc²⁷ larvae show reduced flux of neurosecretory dense core vesicles along the axons compared to wild type.

Khc³²/Khc²⁷, Khc¹⁹/Khc²⁷, Khc¹⁷/Khc²⁷, Khc²/Khc²⁷, Khc¹⁰/Khc²⁷, Khc¹¹/Khc²⁷, Khc³⁴/Khc²⁷, Khc⁶/Khc²⁷, Khc⁷⁶/Khc²⁷, Khc¹⁵/Khc²⁷ and Khc²²/Khc²⁷ larvae show reduced flux of both neurosecretory dense core vesicles and mitochondria along the axons compared to wild type.

(Djagaeva et al., 2012)

Both anterograde and retrograde flux of axonal mitochondria is inhibited in Khc²²/Khc²⁷, Khc⁷⁷/Khc²⁷, Khc¹⁷/Khc²⁷, Khc⁷⁶/Khc²⁷ and Khc²³/Khc²⁷ larvae.

100% of eggs from females containing homozygous germline clones show defects in dorsal appendage morphology; 11% have fused dorsal appendages, 2% have reduced dorsal appendages and 87% have missing dorsal appendages.

The velocity of ooplasmic streaming in stage 10B oocytes is dramatically reduced in mutant females compared to wild type.

(Moua et al., 2011)

Homozygous Khc²⁷ mutant class IV dendritic arborization (da) neurons in the third instar larva display abnormal dendritic and axonal morphologies.

(Satoh et al., 2008)

Cytoplasmic streaming is completely arrested in mutant egg chambers.

(Mische et al., 2007)

In stage 9 oocytes from Khc²⁷ homozygous germline clones, the accumulation of microtubule plus ends in the posterior of the oocyte fails to occur.

(Zimyanin et al., 2007)

Khc²⁷ mutant clonal prefollicular cysts show premature mitochondrial accumulation at the middle of the fusome compared to wild-type cysts. The Balbiani body is abnormally large in the oocytes that develop from these clones. These defects persist in older follicles.

Mitochondria cluster at the apical side of Khc²⁷ young mutant follicle cells (from germline clones) but the mitochondrial distribution is normal in follicles older than stage 7. In Khc²⁷ mutant germline stem cells, all the mitochondria are clumped at the opposite side from the spectrosome, instead of being clustered around the spectrosome as in wild-type stem cells. While mitochondria in dividing cysts are normally spread evenly throughout the cytoplasm, in cysts from Khc²⁷ germline clones, the mitochondria clump away from the fusome.

(Cox and Spradling, 2006)

In Khc¹⁷/Khc²⁷ larval motor axons, the anterograde and retrograde flux of mitochondria is reduced by 70-90%. The number of mitochondria in these mutant nerves is reduced by 50.5% in segments A2-A3. The reduction in mitochondrial anterograde and retrograde flux is also seen in Khc⁶/Khc²⁷ larval motor axons.

Khc²⁷/+ larval nerves contain abundant mitochondria but show a small shift in the mitochondrial anterograde duty cycle from forward runs to pauses and a 16% decrease in anterograde run duration. However, mitochondria in these nerves show an increase in retrograde flux.

(Pilling et al., 2006)

Khc²⁷ mutants are embryonic lethal. In stage 8-9 Khc²⁷ oocytes, no slow streaming currents are observed, but endosomes do show short-range saltation. The mean velocity for anterior endosomes is approximately 2.8-fold less than in wild-type. In stage 10B-11 Khc²⁷ oocytes, no fast streaming currents are observed. Rather, endosomes undergo short-range saltation and little net displacement, moving approximately 32-fold slower than in wild-type. Yolk endosomes are concentrated towards the posterior, leaving a clear zone at the anterior.

(Serbus et al., 2005)

When homozygous germ-line clones are made the resulting eggs show defects in their dorsal appendages. Only 1% have normal appendages. Of the remainder 17% have fused appendages. 26% have a rudimentary dorsal bump, and 56% showed no dorsal material. Nuclear positioning is defective in about half of stage 9 and 10 null oocytes. Nuclei appear to accomplish the initial posterior to anterior shift during stage 7. Although some nuclei are mispositioned in stage -8 mutants, there is a marked shift away from the anterior margin in stages 9 and 10.

(Brendza et al., 2002)

Khc²⁷ germ-line clone oocytes have normal microtubule organization, but markers of the pole plasm are relocated from the posterior pole to other parts of the oocyte cortex. The stage 8 oocytes of Khc²⁷ heterozygotes show partial mislocalisation of pole plasm markers away from the posterior pole, but this defect is largely corrected by stage 9.

(Cha et al., 2002)

Females in which Khc²⁷ germ-line clones have been induced lay eggs with dorsal appendage defects, ranging from fusion (37%) to posterior displacement and reduction (43%), to complete loss (28%). All of these eggs form an aeropyle at the posterior. The oocyte nucleus is mis-placed in 62% of stage 9-10 Khc²⁷ germ-line clone oocytes.

(Duncan and Warrior, 2002)

Khc²⁷ germ line clone oocytes have mis-positioned nuclei: the nucleus migrates correctly to the anterior during stage 8, but in about 50% of stage 9 oocytes it does not maintain its anterior position. After anterior detachment, the nucleus maintains a tight association with the lateral cortex.

(Januschke et al., 2002)

The movement of stau^{αTub67C.T:Avic\GFP-m6}-expressing particles in the nurse cell cytoplasm is indistinguishable from that of wild type in egg chambers derived from homozygous female germline clones, but in the ooplasm most of the particles are static (in contrast to wild type) except for those in the vicinity of the ring canals. The ooplasmic streaming seen in stage 9 and 10b wild-type oocytes is completely abolished in oocytes derived from homozygous female germline clones. The yolk vesicles fail to move in mutant oocytes, although the uptake of the yolk from the follicle cells is unaffected and the oocyte grows at the normal rate.

(Palacios and St. Johnston, 2002)

Homozygous clones of substantial size can be produced in the eye when the clones are induced 1-2 days after egg laying. Homozygous clones in the wing disc appear to proliferate normally. The mechanosensory bristles in homozygous wing clones are sometimes kinked. Homozygous clones in the eye produce a slightly roughened eye surface. Approximately 20% of the ommatidia within these clones are missing one or two photoreceptors. Some photoreceptors show structural defects, including disordered packing of microvilli and split or buckled rhabdomeres. The number of photoreceptors with such abnormal rhabdomeres varies from clone to clone but never exceeds 5-10%. Defects appear equally severe in small or large clones. No dramatic differences in the organisation of the rough ER or Golgi membranes is seen in homozygous (those with or without contorted rhabdomeres) or neighbouring wild-type photoreceptors. Occasionally, homozygous photoreceptors show a slight increase in the abundance of ER near the Golgi and slightly increased levels of vesicles and multivesicular bodies. No defects in the positioning of mitochondria or nuclei are seen. The defects seen appear to be cell autonomous. Degenerating photoreceptors are seen at a low frequency in flies aged for more than two weeks after eclosion. Bristles in clones in the adult epidermis may lie flat or twisted along the epidermal sheet rather than projecting outward from its surface. The deflection of individual bristles with a tungsten needle usually causes a bend or kink rather than the pivoting needed to elicit the wild-type grooming reflex. The scutellar macrochaetae are usually approximately 20% shorter than normal. This length defect is less evident in shorter macrochaetae and is not seen in microchaetae. The tips of bristles are often contorted and the contortions are most severe at the tips of long macrochaetae, which always have flattened, flared or twisted tips. Microchaetae show bluntness or a slight tip swelling. No defects are seen in the remainder of the integument, including the bristle sockets, the nonsensory hairs of the epidermal cells or the epidermal cuticle sheet. The severity of the defects are not detectably affected by clone size. The cuticle layers of homozygous scutellar bristles are quite thin. This effect is more pronounced at the tips of the bristles than at their bases.

(Brendza et al., 2000)

Homozygous Khc²⁷ germ-line clones produces embryos that usually arrest before blastoderm formation, with the occasional embryo surviving until early gastrulation stages.

(Brendza et al., 2000)

Hemizygotes show at least 50% lethality during the second larval instar stage.

(Brendza et al., 1999)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

Khc²⁷/Khc⁶³ has abnormal mitotic cell cycle | larval stage phenotype, suppressible by ens^UAS.Venus/Scer\GAL4^69B

(Métivier et al., 2019)

Other

Statement

Reference

Aplip1^EK4, Khc²⁷/Khc[+] has paralytic | posterior | dominant | larval stage phenotype

(Horiuchi et al., 2005)

Aplip1^EK4, Khc²⁷ has paralytic | posterior | dominant | larval stage phenotype

(Horiuchi et al., 2005)

Phenotype Manifest In

NOT Enhanced by

Statement

Reference

Khc²⁷ has larval multidendritic neuron phenotype, non-enhanceable by Sod1^G85R

(Nemtsova et al., 2023)

Khc²⁷ has mitochondrion | larval stage phenotype, non-enhanceable by Sod1^G85R

(Nemtsova et al., 2023)

Khc²⁷ has axon | larval stage phenotype, non-enhanceable by Sod1^G85R

(Nemtsova et al., 2023)

Suppressed by

Statement

Reference

Khc²⁷/Khc⁶³ has larval brain | larval stage phenotype, suppressible by ens^UAS.Venus/Scer\GAL4^69B

(Métivier et al., 2019)

Khc²⁷/Khc^E177K has axon | third instar larval stage phenotype, suppressible | partially by ens^ΔC/Df(3L)ens^Δ3277

(Kelliher et al., 2018)

Khc²⁷/Khc^E177K has postsynaptic Golgi apparatus | ectopic | third instar larval stage phenotype, suppressible | partially by ens^ΔC/Df(3L)ens^Δ3277

(Kelliher et al., 2018)

Khc²⁷/Khc^E177K has abdominal dorsal multidendritic neuron ddaC | third instar larval stage phenotype, suppressible | partially by ens^ΔC/Df(3L)ens^Δ3277

(Kelliher et al., 2018)

NOT suppressed by

Statement

Reference

Khc²⁷ has larval multidendritic neuron phenotype, non-suppressible by Sod1^G85R

(Nemtsova et al., 2023)

Khc²⁷ has mitochondrion | larval stage phenotype, non-suppressible by Sod1^G85R

(Nemtsova et al., 2023)

Khc²⁷ has axon | larval stage phenotype, non-suppressible by Sod1^G85R

(Nemtsova et al., 2023)

NOT Suppressor of

Statement

Reference

Khc²⁷/Khc⁶³ is a non-suppressor of mitotic spindle | third instar larval stage phenotype of Scer\GAL4^69B, ens^UAS.Venus

(Métivier et al., 2019)

Khc²⁷/Khc⁶³ is a non-suppressor of larval brain | third instar larval stage phenotype of Scer\GAL4^69B, ens^UAS.Venus

(Métivier et al., 2019)

Khc²⁷/Khc⁶³ is a non-suppressor of larval neuroblast | third instar larval stage phenotype of Scer\GAL4^69B, ens^UAS.Venus

(Métivier et al., 2019)

Other

Statement

Reference

Khc²⁷, ens[+]/ens^ΔC has oocyte phenotype

(Sung et al., 2008)

Aplip1^EK4, Khc²⁷/Khc[+] has axon phenotype

(Horiuchi et al., 2005)

Aplip1^EK4, Khc²⁷ has axon phenotype

(Horiuchi et al., 2005)

Additional Comments

Genetic Interactions

Statement

Reference

Lipid droplet transport is delayed in Df(2L)Δhalo^AJ/+ embryos, but transport kinetics are similar to wild type in Khc²⁷/+ Df(2L)Δhalo^AJ/+ embryos.

(Arora et al., 2016)

Khc²⁷/+ ; ens^ΔC/+ double heterozygous females show some stratification of late oocytes, suggesting a defect in cytoplasmic streaming.

(Sung et al., 2008)

Aplip1^EK4/+; Khc²⁷/+ larvae show posterior paralysis in 86% of cases; these mutants also show axonal swelling. Expression of the Aplip1^+tHa transgene fully rescues the posterior paralysis phenotype of Aplip1^EK4/+; Khc²⁷/+ larvae and partially rescues the axonal swelling phenotype.

(Horiuchi et al., 2005)

Khc²⁷ suppresses the bicaudal phenotype of BicD^D.

(Navarro et al., 2004)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

Khc^pgs1

(Barbosa et al., 2007)

Khc^5.287

(Januschke et al., 2002)

Khc^7.288

(Januschke et al., 2002)

Khc^8.70

(Januschke et al., 2002)

Khc⁸

(Brendza et al., 1999)

Rescued by

Khc²⁷/Khc^E177K is rescued by Khc^{UASp.mTagBFP2}/Scer\GAL4^ppk.PG

(Kelliher et al., 2018)

Khc²⁷ is rescued by Khc^{1-975.αTub67C.GFP}

(Williams et al., 2014)

Khc²⁷ is rescued by Khc^{Δ521-641.αTub67C.GFP}

(Williams et al., 2014)

Khc²⁷ is rescued by Khc^+t7.5

(Cha et al., 2002)

Khc²⁷ is rescued by Khc^+t7.5

(Brendza et al., 2000)

Khc²⁷ is rescued by Khc^+t7.5

(Brendza et al., 2000)

Partially rescued by

Khc²⁷ is partially rescued by Khc^{UASp.mTagBFP2}/Scer\GAL4^elav.PLu

(Winding et al., 2016)

Khc²⁷ is partially rescued by Khc^{mutA.UASp.mTagBFP2}/Scer\GAL4^elav.PLu

(Winding et al., 2016)

Khc²⁷ is partially rescued by Khc^{1-849.αTub67C.GFP}

(Williams et al., 2014)

Not rescued by

Khc²⁷ is not rescued by Khc^{1-975.ΔIAK.αTub67C.GFP}

(Williams et al., 2014)

Khc²⁷ is not rescued by Khc^{1-700.αTub67C.GFP}

(Williams et al., 2014)

Khc²⁷ is not rescued by Khc^{231-975.αTub67C.GFP}

(Williams et al., 2014)

Khc²⁷ is not rescued by Khc^{330-975.αTub67C.GFP}

(Williams et al., 2014)

Khc²⁷ is not rescued by Khc^{1-938.αTub67C.GFP}

(Williams et al., 2014)

Comments

The lethality of Khc²⁷ mutant larvae is delayed by Scer\GAL4^elav.PLu-driven expression of Khc^{Scer\UAS.P\T.T:Equa\eqFP578-TagBFP2} or Khc^{mutA.Scer\UAS.P\T.T:Equa\eqFP578-TagBFP2}, although the latter is much less effective. All Khc²⁷ mutants die before pupariation regardless of the expression of either of the two transgenes.

(Winding et al., 2016)

The presence of Khc^{1-975.αTub67C.T:Avic\GFP} rescues the polarity defects (such as osk mRNA transport) found in Khc²⁷ mutants.

The presence of Khc^{1-975.αTub67C.T:Avic\GFP} rescues the nucleus mis-positioning defects found in Khc²⁷ mutants.

The presence of Khc^{1-975.αTub67C.T:Avic\GFP} rescues the absence of dorsal appendages found in Khc²⁷ mutants.

The presence of Khc^{1-849.αTub67C.T:Avic\GFP} rescues the absence of dorsal appendages found in Khc²⁷ mutants in 48% of cases. Only 3.5% of these mutants have two fully formed dorsal appendages.

The presence of Khc^{1-700.αTub67C.T:Avic\GFP} rescues the absence of dorsal appendages found in Khc²⁷ mutants in 33% of cases.

Khc²⁷ mutants expressing Khc^{330-975.αTub67C.T:Avic\GFP} exhibit nucleus mis-positioining in the oocyte and abnormalities in dorsal appendage formation.

Khc²⁷ mutants expressing Khc^{231-975.αTub67C.T:Avic\GFP} exhibit nucleus mis-positioining in the oocyte and abnormalities in dorsal appendage formation.

The presence of Khc^{1-975.αTub67C.T:Avic\GFP} rescues the actin spheres found close to mis-localized nuclei in Khc²⁷ mutants.

The presence of Khc^{1-975.ΔIAK.αTub67C.T:Avic\GFP} fails to rescue the actin spheres found close to mis-localized nuclei in Khc²⁷ mutants.

The presence of Khc^{1-849.αTub67C.T:Avic\GFP} fails to rescue the actin spheres found close to mis-localized nuclei in Khc²⁷ mutants.

Khc²⁷ mutants expressing Khc^{1-975.ΔIAK.αTub67C.T:Avic\GFP} exhibit a strong nucleus positioning phenotype. Accordingly, dorsal appendage formation is also affected in these flies.

The presence of Khc^{1-849.αTub67C.T:Avic\GFP} fails to rescue osk mRNA transport but does rescue the dynein transport defects found in Khc²⁷ mutants.

Oocytes expressing Khc^{1-700.αTub67C.T:Avic\GFP} exhibit a Dynein localization phenotype indistinguishable from that of Khc²⁷ mutants.

Khc^{Δ521-641.αTub67C.T:Avic\GFP}, Khc²⁷ mutants eggs exhibit normal dorsal appendages and no aberrant actin spheres.

(Williams et al., 2014)

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

67409

w¹¹¹⁸; Khc²⁷/CyO; P{UASp-Khc.401.MCP}3/TM3, Sb¹

Notes on Origin

Discoverer

Comments

Based on the ability of the allele to compromise Khc function, the following alleles can be ranked from strongest to weakest as follows: Khc²⁷ > Khc²³ = Khc¹⁷.

(Serbus et al., 2005)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (3)

Reported As

Symbol Synonym

Khc^27-1

(Nemtsova et al., 2023)

khc²⁷

(Li et al., 2023, Li et al., 2017, Nieuwburg et al., 2017, Gardiol and St Johnston, 2014, Fan et al., 2011, Krauss et al., 2009, Krauss et al., 2009, Boylan et al., 2008, Satoh et al., 2008, Sung et al., 2008, Barbosa et al., 2007, Dahlgaard et al., 2007, Cha et al., 2002, Januschke et al., 2002)

Name Synonyms

Secondary FlyBase IDs

References (53)

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