|Feature type||allele||Associated gene||Dmel\Rac1|
|Mutagen||in vitro construct - regulatory fusion|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Carried in construct|
(Medioni and Noselli, 2005, Kaufmann et al., 1998, Sepp and Auld, 2003, Prokopenko et al., 1999, Magie et al., 2002, Luo et al., 1994, Paululat et al., 1999, Lee and Luo, 1999, Long et al., 2006, Lovegrove et al., 2006, Pirraglia et al., 2006, Paladi and Tepass, 2004, Beckett et al., 2008, Assaker et al., 2010)
|Phenotype Manifest In|
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.
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.
Expression of Rac1L89.Scer\UAS under the control of Scer\GAL4GMR.PF results in severe defects in the R-cell projection pattern in the optic lobe.
Expression of Rac1L89.Scer\UAS under the control of Scer\GAL4ems.HRE eliminates the spiracular chamber.
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.
Expression of Rac1L89.Scer\UAS in border cells, driven by Scer\GAL4slbo.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.
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.
Rac1L89.Scer\UAS driven by Scer\GAL4repo 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.
Scer\GAL4elav-C155-mediated expression causes early ISNb growth cone arrest, axons never reach distal muscle targets. Scer\GAL4elav-C155-mediated expression slightly disrupts CNS axon pathway, gaps between segments suggest failure in axon extension. Coexpression of Rac1Scer\UAS.cLa under the same Scer\GAL4 driver causes a massive failure in axon extension, dramatically enhancing the effect of Rac1L89.Scer\UAS. Axons that do extend follow abnormal trajectories.
Only 15% embryos die when in combination with Scer\GAL4elav.PLu, surviving adults are completely viable. When in combination with Scer\GAL41407 one copy of Rac1L89.Scer\UAS causes some axonal loss between the lateral and dorsal clusters, two copies causes greater loss. One copy of Rac1Scer\UAS.cLa ameliorates this axonal loss. Scer\GAL4how-24B causes excessive fusion of the segmentally repeated myoblast cells.
|Phenotype Manifest In|
Rac1L89.Scer\UAS, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF has photoreceptor cell & axon phenotype, enhanceable by bure10/bur[+]
Rac1L89.Scer\UAS, Scer\GAL4fkh.PH has presumptive embryonic salivary gland phenotype, suppressible by shg[+]/shg2
Co-expression of Rab11[S25N.Scer\UAS.P\T.T:Avic\GFP-YFP] with Rac1[L89.Scer\UAS] driven by Scer\GAL4[slbo.2.6] enhances the border follicle cell migration phenotype associated with Rac1[L89.Scer\UAS] expression.
The R-cell axon projection defects caused by expression of Rac1L89.Scer\UAS under the control of Scer\GAL4GMR.PF are enhanced by bure10/+.
|Complementation & Rescue Data|
|Stocks ( 4 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 6 )|
|Secondary FlyBase IDs|
|References ( 15 )|