FlyBase Allele Report: Dmel\Rac1[L89.UAS]

General Information

Symbol

Dmel\Rac1^L89.UAS

Species

D. melanogaster

Name

FlyBase ID

FBal0038992

Feature type

allele

Associated gene

Dmel\Rac1

Associated Insertion(s)

Carried in Construct

P{UAS-Rac1.L89}

Also Known As

UAS-Rac1^L89, UAS-Rac^L89, UAS-RacL89

Key Links

Transgenic product class

dominant_negative_variant

(Luo et al., 1994)

missense_variant

(Luo et al., 1994)

Mutagen

in vitro construct

Nature of the Allele

Transgenic product class

dominant_negative_variant

(Luo et al., 1994)

missense_variant

(Luo et al., 1994)

Mutagen

in vitro construct

(Luo et al., 1994)

Progenitor genotype

Carried in construct

P{UAS-Rac1.L89}

Cytology

Description

A dominant-negative form of Rac1 (carries the amino acid replacement S89L) is expressed under the control of UASt regulatory sequences.

(Luo et al., 1994)

Allele components

Component

Use(s)

Regulatory region(s)

UASt

binary expression system - regulatory region

Encoded product / tool

Rac1

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

axon, with Scer\GAL4^elav-C155

(Kaufmann et al., 1998)

border follicle cell, with Scer\GAL4^slbo.2.6

(Assaker et al., 2010, Medioni and Noselli, 2005)

embryonic/larval plasmatocyte, with Scer\GAL4^{Col4a1-A109.1F2.P}

(Paladi and Tepass, 2004)

embryonic/larval plasmatocyte, with Scer\GAL4^gcm-rA87.P

(Paladi and Tepass, 2004)

embryonic/larval spiracle primordium, with Scer\GAL4^ems.HRE

(Lovegrove et al., 2006)

embryonic myoblast, with Scer\GAL4^Mef2.5xCD

(Beckett et al., 2008)

eye, with Scer\GAL4^LL54

(Lee and Luo, 1999)

larval abdominal intersegmental nerve, with Scer\GAL4^elav-C155

(Kaufmann et al., 1998)

larval abdominal intersegmental nerve, with Scer\GAL4^insc-Mz1407

(Luo et al., 1994)

myoblast, with Scer\GAL4^how-24B

(Luo et al., 1994)

neuroblast | increased number | somatic clone, with Scer\GAL4^wor.PA

(de Torres-Jurado et al., 2022)

photoreceptor cell & axon, with Scer\GAL4^GMR.PF

(Long et al., 2006)

PNS glial cell, with Scer\GAL4^repo

(Sepp and Auld, 2003)

polar follicle cell, with Scer\GAL4^slbo.2.6

(Medioni and Noselli, 2005)

presumptive embryonic salivary gland, with Scer\GAL4^fkh.PH

(Pirraglia et al., 2006)

Detailed Description

Statement

Reference

Expression of Rac1^L89.Scer\UAS driven by Scer\GAL4^slbo.2.6 results in the impairment of border cell migration during egg chamber development.

(Assaker et al., 2010)

Expression of Rac1^L89.Scer\UAS under the control of Scer\GAL4^Mef2.5xCD results in a small number of unfused myoblasts in the embryo.

(Beckett et al., 2008)

Expression of Rac1^L89.Scer\UAS under the control of Scer\GAL4^GMR.PF results in severe defects in the R-cell projection pattern in the optic lobe.

(Long et al., 2006)

Expression of Rac1^L89.Scer\UAS under the control of Scer\GAL4^ems.HRE eliminates the spiracular chamber.

(Lovegrove et al., 2006)

Most salivary gland cells invaginate in embryos expressing Rac1^L89.Scer\UAS under the control of Scer\GAL4^fkh.PH, forming a tube with a slightly expanded lumen compared to wild type. At the stage when wild-type salivary gland cells turn to migrate posteriorly, the mutant lumen is thinner at its midpoint than normal or is completely broken, while the gland proper remains intact. At later stages, the salivary gland proper separates into pieces in the mutant embryos, with one segment at the surface of the embryo and another piece internal. 100% of stage 14 mutant embryos show this broken salivary gland phenotype.

(Pirraglia et al., 2006)

Expression of Rac1^L89.Scer\UAS in border cells, driven by Scer\GAL4^slbo.2.6, inhibits the migration of border cell clusters to the oocyte. However, the apical cap of these egg chambers forms and is shed normally.

(Medioni and Noselli, 2005)

Embryos expressing Rac1^L89.Scer\UAS under the control of Scer\GAL4^gcm-rA87.P show a delay in macrophage migration; mutant embryos have a larger macrophage free area ventrally at stage 13 than wild-type embryos, and a ventral region devoid of macrophages also persists at later stages in the mutant embryos.

Expression of Rac1^L89.Scer\UAS under the control of Scer\GAL4^{Cg25C-A109.1F2.P} causes some clustering of macrophages at stage 17 and they extend more prominent cellular protrusions than normal.

(Paladi and Tepass, 2004)

Rac1^L89.Scer\UAS driven by Scer\GAL4^repo produces embryos that show ectopic lamellar like projections as well as failed inter-connection of the lateral line glia. The underlying sensory axonal tracts defasciculate. Misplacements od sensory appear to be associated with glia.

(Sepp and Auld, 2003)

When expression is driven by Scer\GAL4⁵⁴ the eye is deformed.

(Lee and Luo, 1999)

Expression of Rac1^L89.Scer\UAS by Scer\GAL4^prd.RG1 has no effect on cytokinesis or mitosis.

(Prokopenko et al., 1999)

Scer\GAL4^elav-C155-mediated expression causes early ISNb growth cone arrest, axons never reach distal muscle targets. Scer\GAL4^elav-C155-mediated expression slightly disrupts CNS axon pathway, gaps between segments suggest failure in axon extension. Coexpression of Rac1^Scer\UAS.cLa under the same Scer\GAL4 driver causes a massive failure in axon extension, dramatically enhancing the effect of Rac1^L89.Scer\UAS. Axons that do extend follow abnormal trajectories.

(Kaufmann et al., 1998)

Only 15% embryos die when in combination with Scer\GAL4^elav.PLu, surviving adults are completely viable. When in combination with Scer\GAL4¹⁴⁰⁷ one copy of Rac1^L89.Scer\UAS causes some axonal loss between the lateral and dorsal clusters, two copies causes greater loss. One copy of Rac1^Scer\UAS.cLa ameliorates this axonal loss. Scer\GAL4^how-24B causes excessive fusion of the segmentally repeated myoblast cells.

(Luo et al., 1994)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Rac1^L89.UAS, Scer\GAL4^GMR.PF has abnormal neuroanatomy phenotype, enhanceable by bur^e10/bur[+]

(Long et al., 2006)

Phenotype Manifest In