|Also Known As||E(spl)b32.2, Df(3R)E(spl)b32.2, Df(3R)E(spl)grob32.2|
|Computed Breakpoints include||[96F9];[96F11]|
|Member of large scale dataset(s)|
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|Nature of the Aberration|
|Class of aberration (relative to progenitor)|
|Formalized genetic data||boss << bk1 << HLHmδ << bk2 hits gro|
|Genetic mapping information|
|Comments on Cytology|
|Gene Deletion & Duplication Data|
|Genes Deleted / Disrupted|
|Completely deleted / disrupted|
|Partially deleted / disrupted|
|Genes NOT Deleted / Disrupted|
|Genes NOT Duplicated|
|In combination with other aberrations|
|NOT in combination with other aberrations|
Df(3R)gro[b32.2] ; gro[+t10.4] intestinal stem cell (ISC) clones show an overproliferation of small ISC-like cells.
Wound closure does not appear to be compromised compared to controls in Df(3R)gro[b32.2]/+ wing discs which have been fragmented (a 90[o] sector has been dissected out of the posterior compartment, leaving a 3/4 anterior fragment) and then implanted into wild-type females (analysed at 24 and 48 hours after implantation). However, the Df(3R)gro[b32.2]/+ regenerating discs show significantly impaired proliferation compared to controls.
Df(3R)grob32.2 follicle cells clones carrying gro+t10.4 do not undergo extra cell divisions compared to wild type.
Somatic clones in the follical cells, do not have any detectable phenotype.
Homozygous clones develop densely packed microchaetae within the clone.
Homozygous clones in the leg form normal joints even when they span more than one segment and show differentiation of ectopic sensory organs.
Ventral mitotic clone in the wing causes thickening of the central component of wing vein LIII but does not affect vein differentiation in the opposite surface. Clones induced in a rhove-1 vn1 mutant background that cover the vein LV territory do not differentiate a vein.
Scer\GAL4da.G32-mediated coexpression of l(1)scScer\UAS.cHa and daScer\UAS.cGa cause increase of cells in the CNS: brain lobes are enlarged (protruding through the holes in the cephalic epidermis), the ventral cord shows regional enlargement and sensory organs contain a large number of neurons. Neural hyperplasia is also increased, epidermis, fore- and hindgut, tracheal tree and salivary glands are completely neuralised.
Complements the gro1 allele. Clones in the thorax generate dense clusters of bristles at the locations that the macrochaetae develop. The microchaetae differentiate at high density forming large fields of bristles. The phenotype suggests that the Dhyd\E(spl) complex genes are required for segregation of the SOPs but not for their further differentiation. Duplicated trichogens occasionally occur in these clones, associated with fused tormogens, due to close packing of SOPs, rather than changes in SOP progeny identity. Clones in the wing that reach the wing margin show a loss of sensory structures along the wing margin. Wing veins also appear thicker.
Df(3R)grob32.2 gro+t10.4 clones differentiate dense clumps of microchaetes that are frequently seen to be adjacent to one another. A small amount of epidermis differentiates and there are areas where bristles are intermingled with epidermal hairs. Small tufts of macrochaetes can be seen.
Expression of E(spl)m8-HLH[Scer\UAS.cNa] under the influence of Scer\GAL4da.G32 attenuates the mutant phenotype of Df(3R)grob32.2. A weaker attenuation is seen with E(spl)m5-HLH[Scer\UAS.cNa]. Simultaneous expression of E(spl)m8-HLH[Scer\UAS.cNa] or E(spl)m5-HLH[Scer\UAS.cNa] with E(spl)m8-HLH[1,bd-.Scer\UAS] driven by Scer\GAL4da.G32 causes severe neural hypoplasia in embryos and adults, and reduces the level of neural hyperplasia in Df(3R)grob32.2.
|Stocks ( 0 )|
|Notes on Origin|
|Balancer / Genotype Variants of the Aberration|
|Synonyms & Secondary IDs ( 12 )|
|Secondary FlyBase IDs|
|References ( 29 )|
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|Recent research papers ( 1 )|