FlyBase Allele Report: Dmel\fzr[ie28]

General Information

Symbol

Dmel\fzr^ie28

Species

D. melanogaster

Name

FlyBase ID

FBal0140964

Feature type

allele

Associated gene

Dmel\fzr

Associated Insertion(s)

Carried in Construct

Key Links

Allele class

amorphic allele - genetic evidence

Mutagen

Delta2-3 transposase

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Jacobs et al., 2002)

Mutagen

Delta2-3 transposase

(Jacobs et al., 2002)

Progenitor genotype

fzr^G0418

(Jacobs et al., 2002)

Cytology

Description

Imprecise excision of P{lacW} has caused a deletion that removes the first two exons of rap, with the breakpoint being somewhere in intron 2.

(Jacobs et al., 2002)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

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 ( 0 )

Disease

Interaction

References

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

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

Detailed Description

Statement

Reference

Stage 13-14 embryos hemizygous for fzr^ie28 display increased myoblast proliferation and cell numbers, likely accounted for by an increased number of fusion competent cells (FCMs); and significantly reduced actin focus size together with absent or very small fusion pores at fusion sites between FCMs and the growing muscle, but no difference in the number of actin foci per hemisegment compared to wild-type controls. A defect in myoblast fusion starting at the second fusion wave (following muscle precursor formation) becomes evident at stages 16-17 manifesting as small muscles and an excess of mono-nucleated myoblasts. Alongside, stage 16-17 embryos show an altered heart morphology, with misaligned, crowded and supernumerary pericardial cells and heart cardioblasts. There are no defects in cell determination, differentiation, migration, recognition or adhesion in somatic muscles or the heart.

(Drechsler et al., 2018)

Peripheral glia fail to initiate their migration in mutant embryos and accumulate at the central nervous system-peripheral nervous system transition zone. The number of glial cells per hemisegment is increased in the mutant embryos compared to controls.

(Silies and Klämbt, 2010)

The epidermis of rap^ie28 embryos shows an extra mitotic division cycle, so that the cells go through 17 rounds of division instead of 16.

(Reber et al., 2006)

Mutant embryos undergo an extra cell division (mitosis 17). This extra division appears normal.

(Jacobs et al., 2002)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

fzr^ie28 has lethal | recessive phenotype, suppressible by Dp(1;3)DC472

(Manivannan et al., 2022)

fzr^ie28 has increased cell number | recessive | dorsal closure stage phenotype, suppressible by CycB²/CycB²

(Drechsler et al., 2018)

fzr^ie28 has abnormal neuroanatomy | embryonic stage phenotype, suppressible by Fas2^EB112

(Silies and Klämbt, 2010)

NOT suppressed by

Statement

Reference

fzr^ie28 has increased cell number | recessive | dorsal closure stage phenotype, non-suppressible by CycB[+]/CycB²

(Drechsler et al., 2018)

fzr^ie28 has abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by Nrg^l4

(Silies and Klämbt, 2010)

Other

Statement

Reference

CycA^C8LR1, fzr^ie28 has abnormal mitotic cell cycle | embryonic stage phenotype

(Reber et al., 2006)

Phenotype Manifest In

Suppressed by

Statement

Reference

fzr^ie28 has embryonic somatic muscle cell phenotype, suppressible by CycB²/CycB²

(Drechsler et al., 2018)

fzr^ie28 has embryonic myoblast | dorsal closure stage phenotype, suppressible by CycB²/CycB²

(Drechsler et al., 2018)

fzr^ie28 has glial cell phenotype, suppressible by Fas2^EB112

(Silies and Klämbt, 2010)

NOT suppressed by

Statement

Reference

fzr^ie28 has embryonic somatic muscle cell phenotype, non-suppressible by CycB[+]/CycB²

(Drechsler et al., 2018)

fzr^ie28 has embryonic myoblast | dorsal closure stage phenotype, non-suppressible by CycB[+]/CycB²

(Drechsler et al., 2018)

fzr^ie28 has glial cell phenotype, non-suppressible by Nrg^l4

(Silies and Klämbt, 2010)

Other

Statement

Reference

fzr^ie28, lmgA⁰³⁴²⁴ has embryonic somatic muscle cell phenotype

(Drechsler et al., 2018)

fzr^ie28, lmgA⁰³⁴²⁴ has embryonic myoblast | late embryonic stage phenotype

(Drechsler et al., 2018)

fzr^ie28, mr[+]/mr² has embryonic somatic muscle cell phenotype

(Drechsler et al., 2018)

fzr^ie28, mr[+]/mr² has embryonic myoblast | late embryonic stage phenotype

(Drechsler et al., 2018)

fzr^ie28, lmgA[+]/lmgA⁰³⁴²⁴ has embryonic somatic muscle cell phenotype

(Drechsler et al., 2018)

fzr^ie28, lmgA[+]/lmgA⁰³⁴²⁴ has embryonic myoblast | late embryonic stage phenotype

(Drechsler et al., 2018)

fzr^ie28, mr² has embryonic somatic muscle cell phenotype

(Drechsler et al., 2018)

fzr^ie28, mr² has embryonic myoblast | late embryonic stage phenotype

(Drechsler et al., 2018)

CycA^C8LR1, fzr^ie28 has embryonic epidermis phenotype

(Reber et al., 2006)

CycA^C8LR1, fzr^ie28 has mitotic anaphase phenotype

(Reber et al., 2006)

CycA^C8LR1, fzr^ie28 has mitotic telophase phenotype

(Reber et al., 2006)

Additional Comments

Genetic Interactions

Statement

Reference

fzr^ie28/+ ; mr²/+ and fzr^ie28/+ ; lmgA⁰³⁴²⁴/+ embryos at stages 16-17 show disrupted myoblast fusion but an overall wild-type muscle morphology, while myoblast fusion is completely abolished in fzr^ie28/+ ; mr²/mr² and fzr^ie28/+ ; lmgA⁰³⁴²⁴/lmgA⁰³⁴²⁴ embryos.

(Drechsler et al., 2018)

The number of glial cells in rap^ie28 CycA^C8LR1 double mutant embryos is the same as in wild-type embryos, but they fail to migrate.

The glial cell migration defects of rap^ie28 embryos are significantly suppressed by Fas2^EB112 (54.7% of hemisegments show normal migration, 27.9% of hemisegments show partial migration). However, the increase in glial cell number and the axonal defects seen in rap^ie28 embryos is not suppressed by Fas2^EB112.

The glial cell migration defects of rap^ie28 embryos are not suppressed by Nrg^l4.

(Silies and Klämbt, 2010)

The epidermis of rap^ie28; CycA^C8LR1 double mutant embryos shows an extra mitotic division cycle as with CycA^C8LR1 single mutant embryos. This is in contrast to CycA^C8LR1 single mutant embryos, where the 16th mitotic division does not occur. In addition to the extra round of mitosis, rap^ie28; CycA^C8LR1 double mutant embryonic epidermal cells show abnormal anaphase and telophase figures with chromatin bridges.

(Reber et al., 2006)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

fzr^{CR00643-TG4.2}

(Manivannan et al., 2022)

Partially rescued by

fzr^ie28 is partially rescued by Scer\GAL4^Mef2.PU/fzr^UAS.Tag:MYC

(Drechsler et al., 2018)

fzr^ie28 is partially rescued by Scer\GAL4^elav-C155/fzr^UAS.cSa

(Silies and Klämbt, 2010)

Not rescued by

fzr^ie28 is not rescued by Scer\GAL4^repo.PU/fzr^UAS.cSa

(Silies and Klämbt, 2010)

fzr^ie28 is not rescued by Scer\GAL4^gcm.PU/fzr^UAS.cSa

(Silies and Klämbt, 2010)

Comments

Expression of rap^Scer\UAS.cSa under the control of either Scer\GAL4^gcm.PU or Scer\GAL4^repo.PU fails to rescue the increase in glial cell number and glial cell migration defects seen in rap^ie28 embryos.

Expression of rap^Scer\UAS.cSa under the control of Scer\GAL4^elav-C155 does not rescue the increase in glial cell number seen in rap^ie28 embryos, but the glial cell migration defect is completely rescued in 49.6% of hemisegments and is partially rescued in 25.9% of hemisegments. The axonal growth defects seen in the central and peripheral nervous systems are also rescued.

Expression of rap^Scer\UAS.cSa under the control of Scer\GAL4^elav.PLu almost completely rescues both the glial cell migration defects (71.5% complete rescue, 19% partial rescue) and increase in glial cell number seen in rap^ie28 embryos. The axonal growth defects seen in the central and peripheral nervous systems are also rescued.

(Silies and Klämbt, 2010)

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

91686

w^* fzr^ie28/FM7c, P{ftz-lacC}YH1

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (3)

Reported As

Symbol Synonym

cdh1^rapie28

(Slack et al., 2007)

fzr^ie28

(Manivannan et al., 2022, Drechsler et al., 2018, Neuert et al., 2017, Meghini et al., 2016, Silies and Klämbt, 2010, Silies and Klämbt, 2010, Reber et al., 2006, Schaeffer et al., 2004, Shcherbata et al., 2004, Araki et al., 2003, Jacobs et al., 2002)

rap^ie28

Name Synonyms

Secondary FlyBase IDs

References (12)

Report Sections

Open Close