|Feature type||allele||Associated gene||Dmel\shg|
|Mutagen||in vitro construct - regulatory fusion, in vitro construct - coding region fusion|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Carried in construct|
(Wood et al., 2006, Schock and Perrimon, 2003, Simoes et al., 2006, Schock and Perrimon, 2002, Ma et al., 2003, Bai and Montell, 2002, Reed et al., 2004, Oda and Tsukita, 2001, McGill et al., 2009, Pastor-Pareja et al., 2004, Stramer et al., 2005, Mirkovic and Mlodzik, 2006, Ninov et al., 2007, Becam et al., 2005, Rodriguez-Diaz et al., 2008, Bischoff and Cseresnyés, 2009, Dyer et al., 2007, Mavrakis et al., 2009, Siekhaus et al., 2010, Sekyrova et al., 2010, Goldbach et al., 2010, Ninov et al., 2010, Martin et al., 2009, He et al., 2010, Abreu-Blanco et al., 2011, Mateus et al., 2011, Olguín et al., 2011, Simões et al., 2010, Olguín et al., 2011, Bosveld et al., 2012, Bosveld et al., 2012, Fichelson et al., 2012, Pereira et al., 2006, Ishihara and Sugimura, 2012, Huang et al., 2011, Mohseni et al., 2009, Haruta et al., 2010)
|Phenotype Manifest In|
shg[Ubi-p63E.T:Avic\GFP-rs] clones generated in the histoblasts are largely excluded from the expanding front of the histoblast nest, and are observed remaining in the center of the nest.
|Phenotype Manifest In|
shg[Ubi-p63E.T:Avic\GFP-rs] does not significantly change the impaired epidermal cell elongation phenotype seen during dorsal closure stages in embryos expressing Rab11[S25N.Scer\UAS] under the control of Scer\GAL4[en-e16E].
The cytokinesis defects that are seen in the spermatids of males expressing scra[GD9720] under the control of Scer\GAL4[bam.T:Hsim\VP16] are significantly suppressed by co-expression of shg[Ubi-p63E.T:Avic\GFP-rs] such that 39.1% of spermatids are mononucleate, 19.3% are binucleate and 41.6% have four nuclei.
|Complementation & Rescue Data|
Expression of shg[Ubi-p63E.T:Avic\GFP-rs] rescues the lethality of shg[R69]. The head, ventral epidermis and tracheal defects of shg[R69] are almost completely rescued by shg[Ubi-p63E.T:Avic\GFP-rs]. When shg[Ubi-p63E.T:Avic\GFP-rs] is present, shg[R69] mutant cell clones are able to grow in size in the epithelia. These epithelia developed normally into adult tissues. When shg[Ubi-p63E.T:Avic\GFP-rs] is present in the background, egg chambers containing shg[R69] mutant germ-line clones show normal development. Cellularization occurs normally in embryos mutant for both maternal and zygotic shg[R69] that carry shg[Ubi-p63E.T:Avic\GFP-rs]. Similarly, in the presence of shg[Ubi-p63E.T:Avic\GFP-rs], posterior invagination occurs normally, and the ectoderm initiates extension and maintains epithelial integrity in embryos mutant for both maternal and zygotic shg[R69].
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 1 )|
|Secondary FlyBase IDs|
|References ( 37 )|
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|Recent research papers ( 7 )|