FlyBase Allele Report: Dmel\repo[03702]

General Information

Symbol

Dmel\repo⁰³⁷⁰²

Species

D. melanogaster

Name

FlyBase ID

FBal0009484

Feature type

allele

Associated gene

Dmel\repo

Associated Insertion(s)

P{PZ}repo⁰³⁷⁰²

Carried in Construct

Also Known As

repo³⁷⁰², repo³, repo², repo-lacZ

Key Links

Genomic Maps

JBrowse

Allele class

amorphic allele - genetic evidence

loss of function allele

Mutagen

P-element activity

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Hosoya et al., 1995)

loss of function allele

(Halter et al., 1995)

Mutagen

P-element activity

(Campbell et al., 1994, Xiong et al., 1994)

Progenitor genotype

Associated Insertion(s)

P{PZ}repo⁰³⁷⁰²

Cytology

Description

Contrary to that reported in FBrf0074834, P{PZ} is inserted between base pairs 202 and 203 of the published sequence (FBrf0074834), in the 5' UTR, in opposite orientation to the repo transcript.

(Halter et al., 1995)

P-element insertion, in the opposite direction as repo transcription, within an intron.

(Xiong et al., 1994)

Allele components

Component

Use(s)

Inserted element

P{PZ}

enhancer trap

Encoded product / tool

lacZ

reporter enzyme

Tagged with

Tag:NLS(P)

nuclear protein localization tag

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

transposable_element_insertion_site

3R:18,236,199..18,236,200 [+]

(Kerr et al., 2014, Spradling et al., 1999, Harvie et al., 1998, Halter et al., 1995, BDGP Project Members, 1994-1999, Campbell et al., 1994, Xiong et al., 1994)

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

central nervous system

(Shklyar et al., 2014)

embryonic/larval glial cell

(Lee and Jones, 2005)

embryonic/larval plasmatocyte

(Shklyar et al., 2014)

glial cell

(Shklyar et al., 2014)

larval intersegmental nerve branch ISNb of A1-7

(Wright et al., 2010)

larval longitudinal connective | embryonic stage

(Yoshiura et al., 2012)

larval ventral nerve cord | embryonic stage

(Yoshiura et al., 2012)

phagocytic vesicle

(Shklyar et al., 2014)

Detailed Description

Statement

Reference

repo⁰³⁷⁰²/+ mutants exhibit significantly impaired long term memory performance 24 hours after spaced training in an aversive olfactory association paradigm, as compared to controls; but do not show significantly decreased anesthesia-resistant memory performance 24 hours after massed training in an aversive olfactory association paradigm, as compared to controls.

(Matsuno et al., 2015)

Glial cell organisation is impaired in repo⁰³⁷⁰² mutant embryos. A higher volume of apoptotic particles is seen in repo⁰³⁷⁰² mutant CNS compared to controls, and many more of these apoptotic particles are not engulfed by phagocytes, glia or macrophages than in wild type.

The volume of glial cells in repo⁰³⁷⁰² mutant embryos is half the normal glial volume but the normal number of glial cells is formed.

repo⁰³⁷⁰² mutant embryos exhibit defects in the engulfment of apoptotic particles by glia in the CNS; the glial cells contain fewer phagosomes and apoptotic particles become overloaded within the glial cell. The macrophages in repo⁰³⁷⁰² mutants contain a greater volume of phagosomes compared to controls.

repo⁰³⁷⁰² mutant glial cell are abnormally located in the CNS and lack appropriate contacts with each other. Unlike the barely motile wild type glia, repo⁰³⁷⁰² mutant glia exhibit increased motility and are able to engulf multiple apoptotic particles.

(Shklyar et al., 2014)

The eve-positive U neurons derived from neuroblast NB7-1 and the four eg-positive neurons derived from neuroblast NB7-3 adopt normal positions in mutant embryos. The fasciculation of Fas2-positive motor neurons is abnormal in a small proportion of segments and the ventral nerve cord is slightly extended at stage 16.

(Yoshiura et al., 2012)

In the periphery of homozygous repo⁰³⁷⁰² embryos, the intersegmental nerve b (ISNb) is normal, although there are rare stall phenotypes.

(Wright et al., 2010)

In stage 16 repo⁰³⁷⁰² homozygous embryos, the numbers of lateral glia are reduced and those that remain are disorganised, most peripheral glia are either missing or displaced and longitudinal glia are displaced towards the lateral edges of the ventral nerve cord.

(Lee and Jones, 2005)

Heterozygotes with repo¹ are semi-lethal.

(Xiong et al., 1994)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

repo⁰³⁷⁰² has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by Tre1^Δ10

(Yoshiura et al., 2012)

Suppressed by

Statement

Reference

repo⁰³⁷⁰² has abnormal neuroanatomy | embryonic stage phenotype, suppressible by Scer\GAL4^repo.PU/NimC4^UAS.GFP

(Shklyar et al., 2014)

repo⁰³⁷⁰² has abnormal neuroanatomy | embryonic stage phenotype, suppressible by drpr^I.UAS/Scer\GAL4^repo.PU/NimC4^UAS.GFP

(Shklyar et al., 2014)

NOT suppressed by

Statement

Reference

repo⁰³⁷⁰² has abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by drpr^I.UAS/Scer\GAL4^repo.PU

(Shklyar et al., 2014)

Other

Statement

Reference

Tre1^Δ10, repo⁰³⁷⁰² has abnormal neuroanatomy | embryonic stage phenotype

(Yoshiura et al., 2012)

Phenotype Manifest In

Enhanced by

Statement

Reference

repo⁰³⁷⁰² has larval longitudinal connective phenotype, enhanceable by Tre1^Δ10

(Yoshiura et al., 2012)

Suppressed by

Statement

Reference

repo⁰³⁷⁰² has glial cell phenotype, suppressible | partially by Scer\GAL4^repo.PU/NimC4^UAS.GFP

(Shklyar et al., 2014)

repo⁰³⁷⁰² has glial cell phenotype, suppressible by drpr^I.UAS/Scer\GAL4^repo.PU/NimC4^UAS.GFP

(Shklyar et al., 2014)

NOT suppressed by

Statement

Reference

repo⁰³⁷⁰² has glial cell phenotype, non-suppressible by drpr^I.UAS/Scer\GAL4^repo.PU

(Shklyar et al., 2014)

Other

Statement

Reference

Tre1^Δ10, repo⁰³⁷⁰² has U neuron phenotype

(Yoshiura et al., 2012)

Tre1^Δ10, repo⁰³⁷⁰² has EG neuron phenotype

(Yoshiura et al., 2012)

Additional Comments

Genetic Interactions

Statement

Reference

Expression of drpr^I.Scer\UAS under the control of Scer\GAL4^repo.PU does not rescue the glial phagocytosis defects seen in repo⁰³⁷⁰² mutant embryos; the morphology and localisation of the glia still appear abnormal, and there is an increase in apoptotic particles outside of the glial cells.

Expression of NimC4^{Scer\UAS.T:Avic\GFP} under the control of Scer\GAL4^repo.PU partially rescues the phagocytosis defects seen in repo⁰³⁷⁰² mutant embryos. The morphology and localisation of the glia still appear abnormal and the cells are overloaded with apoptotic particles. However, although the total volume of apoptotic particles in the CNS remains the same as in repo⁰³⁷⁰² mutant embryos alone, a higher proportion have been engulfed by phagocytes in the rescue embryos.

Co-expression of NimC4^{Scer\UAS.T:Avic\GFP} and drpr^I.Scer\UAS under the control of Scer\GAL4^repo.PU fully rescues the phagocytosis defects seen in repo⁰³⁷⁰² mutant embryos.

(Shklyar et al., 2014)

Tre1^Δ10 ; repo⁰³⁷⁰² double mutant embryos show abnormal positioning of eve-positive U neurons derived from neuroblast NB7-1 and the four eg-positive neurons derived from neuroblast NB7-3. The fasciculation of Fas2-positive motor neurons is abnormal in a high proportion of segments.

(Yoshiura et al., 2012)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

repo⁰⁰⁶⁹²

(BDGP Project Members, 1994-1999)

repo⁰²¹³⁸

(BDGP Project Members, 1994-1999)

Comments

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

11604

ry⁵⁰⁶ P{PZ}repo⁰³⁷⁰²/TM3, ry^RK Sb¹ Ser¹

Notes on Origin

Discoverer

A. Spradling.

(Xiong et al., 1994)

Comments

Complements: l(3)00643⁰⁰⁶⁴³. Complements: Dlc90F⁰⁴⁰⁹¹. Complements: quag⁰⁵⁰⁸⁹. Complements: sprd⁰⁵²⁸⁴. Complements: l(3)05822⁰⁵⁸²². Complements: sr^06915b. Complements: 14-3-3ε^j2B10. Complements: MED17^s2956.

(BDGP Project Members, 1994-1999)

Remobilisation of the P{PZ} generates viable revertants.

(Halter et al., 1995)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (7)

Reported As

Symbol Synonym

l(3)03702

(Spradling et al., 1999)

l(3)03702⁰³⁷⁰²

repo⁰³⁷⁰²

(Titus et al., 2023, Raymond et al., 2022, Coates et al., 2021, Aw et al., 2017, Matsuno et al., 2015, Shklyar et al., 2014, Yoshiura et al., 2012, Park et al., 2009, Spokony and Restifo, 2009, Christensen et al., 2008.12.28, Christensen et al., 2008.12.28)

repo²

(Sawamoto et al., 1996, Xiong et al., 1994)

repo³⁷⁰²

(Wright et al., 2010, Lee and Jones, 2005, Inbal et al., 2004)

repo³

(Shandala et al., 2003, Halter et al., 1995, Hosoya et al., 1995)

repo^PZ

(Kerr et al., 2014)

Name Synonyms

Secondary FlyBase IDs

References (27)

Report Sections

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