FlyBase Allele Report: Dmel\hpo[KC202]

General Information

Symbol

Dmel\hpo^KC202

Species

D. melanogaster

Name

FlyBase ID

FBal0190687

Feature type

allele

Associated gene

Dmel\hpo

Associated Insertion(s)

Carried in Construct

Key Links

Genomic Maps

JBrowse

Allele class

loss of function allele

Mutagen

Nature of the Allele

Allele class

loss of function allele

(Emoto et al., 2006, Udan et al., 2003)

Mutagen

FLPase

(Udan et al., 2003)

ethyl methanesulfonate

(Udan et al., 2003)

Progenitor genotype

Cytology

Description

The premature stop codon results in a protein truncated after the kinase domain, while the highly conserved dimerisation domain that mediates complex formation with sav is deleted.

(Udan et al., 2003)

Amino acid replacement: L?V.

(Udan et al., 2003)

Amino acid replacement: ??term.

(Udan et al., 2003)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

2R:19,495,139..19,495,139 [-]

Nucleotide change:

G19495139A

Reported nucleotide change:

G?A

Amino acid change:

W518term | hpo-PA; W518term | hpo-PB

Reported amino acid change:

W518

Comment:

A TGG to TAG nonsense mutation at hpo codon W518; one of two amino acid substitutions in mutant. The other is a Leu to Val amino acid substitution between the kinase and autoregulatory domains; the postion of the Leu to Val change was not specified.

(Udan et al., 2003)

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

Expression Data

Reporter Expression

Additional Information

Statement

Reference

Marker for

Reflects expression of

Reporter construct used in assay

Human Disease Associations

Disease Ontology (DO) Annotations

Models Based on Experimental Evidence ( 0 )

Disease

Evidence

References

Modifiers Based on Experimental Evidence ( 1 )

Disease

Interaction

References

exacerbates autism spectrum disorder

modeled by Abca3^GD3708

(Ueoka et al., 2020)

ameliorates neurodegenerative disease

modeled by FIG4^KK102943

(Kushimura et al., 2018)

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

eye

(Das Thakur et al., 2010)

haltere

(Udan et al., 2003)

head & cuticle

(Udan et al., 2003)

leg

(Udan et al., 2003)

mitotic spindle | somatic clone | third instar larval stage

(Keder et al., 2015)

photoreceptor neuron

(Udan et al., 2003)

thorax

(Udan et al., 2003)

type II neuroblast | somatic clone | third instar larval stage

(Keder et al., 2015)

wing

(Udan et al., 2003)

Detailed Description

Statement

Reference

hpo^KC202/+ adults are hyperactive when compared to controls.

(Ueoka et al., 2020)

hpo^KC202 homozygous mutant embryos do not display any significant increase in the frequency of hemisegments with abnormal number of neurons in the asymmetrically dividing RP2 neural lineage. However, the type II brain neuroblast somatic clones homozygous mutant for hpo^KC202 show defects in asymmetric cell division: mislocalization of asymmetrically distributed proteins as well as mitotic spindle orientation defects.

(Keder et al., 2015)

hpo^KC202 mutants produce overgrown adult eyes.

(Das Thakur et al., 2010)

hpo^KC202/+ heterozygotes exhibit wild-type dendritic tiling, with wild-type levels of dendritic crossing points per υm[2].

(Emoto et al., 2006)

hpo^KC202 mutants exhibit 'overgrowth' phenotypes. The adult head is enlarged, with larger eyes and an expanded, fold cuticle found on the head and antennae. hpo^KC202 mutant cells show overgrowth on the head cuticle, halteres, thorax, wings and legs. The position of pattern elements such as ommatidia, bristles and ocelli are relatively normal, with wild-type differentiation. hpo^KC202 mutant clones in adult eyes exhibit a considerable increase in the spacing between photoreceptor clusters in mutant regions as compared with wild-type. This is due to a large increase in the numbers of interommatidial cells, which are evident in hpo^KC202 mutant mid-pupal retina. These extra cells eventually differentiate into extra bristles and pigment cells. In contrast to the interommatidial cells, most hpo^KC202 mutant ommatidia have normal numbers of photoreceptor, cone and primary pigment cells. The sizes of all cell types in hpo^KC202 mutant eyes are normal, although the morphology of photoreceptors is often abnormal. The initial spacing of R8 cells and the number of photoreceptor cells per ommatidium is normal in hpo^KC202 mutant clones. Mutant somatic clone cells in eye discs (through the control of Scer\FLP1^ey.PB) that are almost completely mutant for hpo^KC202 undergo synchronised cell cycles in the morphogenetic furrow, and progress through the second mitotic wave. In contrast to wild-type, mutant hpo^KC202 cells fail to arrest in G1 and continue to proliferate after the second mitotic wave. This phenotype is cell autonomous as ectopic proliferation is restricted to uncommitted precursor cells and not observed in differentiating photoreceptor cells. In contrast to wild-type, hpo^KC202 mutant clones lack apoptotic cells.

(Udan et al., 2003)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

hpo^KC202 has visible | recessive phenotype, suppressible by Df(1)jub^I

(Das Thakur et al., 2010)

Enhancer of

Statement

Reference

hpo^KC202 is an enhancer of increased rate of movement | adult stage phenotype of Abca3^GD3708, Scer\GAL4^elav.PLu

(Ueoka et al., 2020)

Suppressor of

Statement

Reference

hpo^KC202/hpo[+] is a suppressor | partially of abnormal neuroanatomy | larval stage | somatic clone - tissue specific phenotype of Mitf^KK113614, Scer\GAL4^Act5C.PI

(Zhang et al., 2024)

hpo^KC202 is a suppressor of increased cell death phenotype of hid^unspecified

(Udan et al., 2003)

Other

Statement

Reference

hpo^KC202, trc¹/trc[+] has abnormal neuroanatomy phenotype

(Emoto et al., 2006)

hpo^KC202, trc²/trc[+] has abnormal neuroanatomy phenotype

(Emoto et al., 2006)

hpo^KC202/hpo[+], trc¹ has abnormal neuroanatomy phenotype

(Emoto et al., 2006)

hpo^KC202/hpo[+], trc² has abnormal neuroanatomy phenotype

(Emoto et al., 2006)

Scer\GAL4^αTub84B.PL, hpo^KC202, wg^l-17 has increased occurrence of cell division | somatic clone | cell autonomous | larval stage phenotype

(Udan et al., 2003)

Phenotype Manifest In

Suppressed by

Statement

Reference

hpo^KC202 has eye phenotype, suppressible by Df(1)jub^I

(Das Thakur et al., 2010)

Suppressor of

Statement

Reference

hpo^KC202/hpo[+] is a suppressor | partially of developing neuron | ectopic | larval stage | somatic clone - tissue specific phenotype of Mitf^KK113614, Scer\GAL4^Act5C.PI

(Zhang et al., 2024)

hpo^KC202/hpo[+] is a suppressor | partially of eye disc | larval stage | somatic clone - tissue specific phenotype of Mitf^KK113614, Scer\GAL4^Act5C.PI

(Zhang et al., 2024)

hpo^KC202/hpo[+] is a suppressor | partially of peripodial epithelium of eye disc | larval stage | somatic clone - tissue specific phenotype of Mitf^KK113614, Scer\GAL4^Act5C.PI

(Zhang et al., 2024)

hpo^KC202 is a suppressor of NMJ bouton | increased number | third instar larval stage phenotype of Abca3^GD3708, Scer\GAL4^elav.PLu

(Ueoka et al., 2020)

Other

Statement

Reference

hpo^KC202, trc¹/trc[+] has multidendritic dendrite phenotype

(Emoto et al., 2006)

hpo^KC202, trc²/trc[+] has multidendritic dendrite phenotype

(Emoto et al., 2006)

hpo^KC202/hpo[+], trc¹ has multidendritic dendrite phenotype

(Emoto et al., 2006)

hpo^KC202/hpo[+], trc² has multidendritic dendrite phenotype

(Emoto et al., 2006)

Additional Comments

Genetic Interactions

Statement

Reference

No significant increase in the proportion of hemisegments with abnormal number of neurons in the asymmetrically dividing RP2 neural lineage is is observed in cno²/+;hpo^KC202/+ double heterozygous embryos compared to either of the single heterozygotes or wild type.

(Keder et al., 2015)

A Df(1)djub^I/+ genetic background reduces the magnitude of hpo^KC202 eye phenotypes.

(Das Thakur et al., 2010)

Transheterozygotes for trc¹/hpo^MGH4 exhibit obvious iso-neuronal as well as hetero-neuronal tiling defects, including a significant increase in dendritic crossing-points compared to single mutants.

Transheterozygotes for trc²/hpo^MGH4 exhibit obvious iso-neuronal as well as hetero-neuronal tiling defects, including a significant increase in dendritic crossing-points compared to single mutants.

(Emoto et al., 2006)

hpo^KC202 mutant clones partially suppress the cell death observed in eye discs that ectopically express W^unspecified.

(Udan et al., 2003)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Comments

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

25090

y^d2 w¹¹¹⁸ P{ey-FLP.N}2; P{neoFRT}42D hpo^KC202/CyO, P{GAL4-Kr.C}DC3, P{UAS-GFP.S65T}DC7

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (1)

Reported As

Symbol Synonym

hpo^KC202

(Zhang et al., 2024, Neal et al., 2022, Ueoka et al., 2020, Azuma et al., 2018, Kushimura et al., 2018, Anderson et al., 2017, Ding et al., 2016, Sarov et al., 2016, Keder et al., 2015, Emoto et al., 2006)

Name Synonyms

Secondary FlyBase IDs

References (13)

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