Aberration Dmel\Df(3R)Espl22

General Information
Symbol	Dmel\Df(3R)Espl22	Species	D. melanogaster
Name		FlyBase ID	FBab0002569
Feature type	chromosomal_deletion
Also Known As	E(spl)^Bx22, gro^BX22, Df(3R)E(spl)^BX22, Df(3R)BX22

Computed Breakpoints include	96F10-96F11;96F11
Deleted segment	96F10--96F11
Sequence coordinates
Member of large scale dataset(s)
Recent Updates
Description	What does this section display? This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms). What does this section not display? This section does not currently display links that were removed or gene model changes.
Update Feed	Click the icon below to subscribe to this FlyBase record and receive updates automatically through your feed reader.
FB2013_03
FB2013_02
All updates	Click here to see a list of all updates to this record from FB2010_08 and on.
Nature of the Aberration
Cytological Order
Progenitor	E(spl)m8-HLH¹ (Shepard et al., 1989, de Celis et al., 1991)
Mutagen	X ray (Preiss et al., 1988)
Class of aberration (relative to progenitor)	chromosomal_deletion (Preiss et al., 1988)
Breakpoints	[];[] (Preiss et al., 1988)
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data	bk1 << HLHm5 << gro << bk2
Genetic mapping information
Comments	Small deletion. (de Celis et al., 1991) about 14-kb deletion (4 to 17.5 kb); about 14-kb inversion (-10.5 to -7.6 and 4 kb)
Comments on Cytology
	Cytologically invisible deletion. (Preiss et al., 1988) Left limit of break 1 from polytene analysis (citation unavailable) Right limit of break 1 from inclusion of E(spl) (FBrf0055903) Left limit of break 2 from inclusion of E(spl) (FBrf0055903) Right limit of break 2 from polytene analysis (citation unavailable)
Sequence Crossreferences
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name
Gene Deletion & Duplication Data
Genes Deleted / Disrupted
Complementation Data
Completely deleted / disrupted	E(spl)m5-HLH (Ligoxygakis et al., 1998, Fischer-Vize et al., 1992) E(spl)m7-HLH (Ligoxygakis et al., 1998, Fischer-Vize et al., 1992) E(spl)m8-HLH (Ligoxygakis et al., 1998, Fischer-Vize et al., 1992, Jagla et al., 1997, Price et al., 1997) gro (Ligoxygakis et al., 1998, Fischer-Vize et al., 1992, de Celis and Ruiz-Gomez, 1995, Price et al., 1997)
Molecular Data
Genes NOT Deleted / Disrupted
Complementation Data
	yeti (Riede, 1996)
Molecular Data
Genes Duplicated
Complementation Data
Molecular Data
Genes NOT Duplicated
Complementation Data
Molecular Data
Related Comments

Phenotypic Data
In combination with other aberrations	Eggs from Df(3R)Espl22/Df(3L)10^H mothers exhibit an embryonic lethality significantly higher than from either Df(3L)10^H/+ or Df(3R)Espl22/+ mothers. 50-60% had no cuticle. Cuticles from 5-10% of unhatched embryos show a duplication of the posterior spiracle accompanied by disorganised denticle belts. (Chen et al., 1999)
NOT in combination with other aberrations	56% of heterozygous flies show duplication of the anterior postalar bristle. (Kaspar et al., 2008) The Df(3R)Espl22 chromosome does not act as a dominant suppressor of telomeric silencing (assayed using the effect of the chromosome on the eye colour phenotype of flies carrying "P{w^var}KR3-2", a stable "brown-red" variant of the P{3'WP-2,w^var}2Lt insertion). (Mason et al., 2004) Homozygous clones in the eye disc show a neurogenic phenotype. (Ligoxygakis et al., 1998) Phenotype manifest in: embryonic/larval dorsal vessel \| precursor Homozygous embryos have an increased number of cardiac precursor cells. (Jagla et al., 1997) Df(3R)Espl22 single mutant and Df(3R)Espl22, osa³⁰⁸ double mutant clones in the eye show excess neuronal differentiation. (Treisman et al., 1997) No effect on the faf eye phenotype. (Huang and Fischer-Vize, 1996) In clones in the wing, the phenotype depends on where the clone lies. In the anterior compartment all clones abutting the wing margin cause local overgrowth and pattern duplications. Those abutting the wing margin and restricted to dorsal or ventral surfaces cause overgrowth of both dorsal and ventral cells. Clones at the wing margin cause loss of sensory organs and mild scalloping of the margin. Clones double mutant for sgg^M11 and Df(3R)Espl22 in the anterior wing differentiate anterior bristles (as for clones of sgg^M11 single mutants), however double mutant clones in the posterior compartment differentiate hairs typical of the posterior wing margin. (de Celis and Ruiz-Gomez, 1995) Clones induced in the first larval instar generate single large patches that lack sensory bristles (macrochaetaes and microchaetes) in the notum. Clones induced in the late second or early third larval instar generate many small patches that lack sensory bristles in the notum. These areas correspond to areas of neural hyperplasia in the developing notum. Clones in the developing wing generate extra vein material. Clones in the developing eye cause the eye to be rough and scarred with highly disorganised ommatidia. (Tata and Hartley, 1995) The number of exit and dorsal roof glia in mutant embryos is higher than in wild-type embryos. (Nelson and Laughon, 1994) Embryos exhibit fused muscles in patterned arrangements, particularly in the more dorsal regions of the embryo. The birefringent is clearly correlated with the expansion of the CNS and PNS, and the loss of epidermis and the degree to which myoblast fusion occurs. Where myoblast fusion fails conspicuous clusters of mesodermal cells are formed and if epidermal territories are expanded cells in these clusters may be recruited to fusion. (Bate et al., 1993) Homozygotes display a wide dorsal shield that spans the width of the embryo with well formed telson and Filzkorper. One copy of P{ry⁺,HLHm5⁺,m6⁺,mX⁺,HLHm7⁺,E(spl⁺,gro⁺=E25R} is sufficient to rescue Df(3R)Espl22 to adulthood. Df(3R)Espl22/Df(3R)boss15 heterzygotes could be rescued to adulthood by the presence of the P{ry⁺,HLHm5⁺,m6⁺,mX⁺,HLHm7⁺=Ep} construct. (Delidakis et al., 1991) Strong to full phenotypic reversion: 250--450 facets per eye. Viable when heterozygous with a Dl allele. (Shepard et al., 1989) Intermediate neurogenic phenotype. P element construct carrying a wild type E(spl) gene copy partially rescues the neurogenic phenotype: less severe neural hyperplasia. (Preiss et al., 1988)
Stocks ( 2 )
Bloomington	3345 Df(3R)Espl22, tx¹/TM6B, Tb¹
Kyoto	106993 Df(3R)Espl22, tx¹/TM6B, Tb¹
Notes on Origin
Discoverer	Muskavitch.

Balancer / Genotype Variants of the Aberration

Separable Components

Other Comments
	Deletion of 14kb removing gro, HLHm5, HLHm7 and E(spl). (Tata and Hartley, 1995)
Synonyms & Secondary IDs ( 17 )
Reported As
Symbol Synonym	Df(2R)E(spl)BX22 (Price et al., 1997) Df(3R)^BX22 (Kahali et al., 2009) Df(3R)BX22 (Johannes and Preiss, 2002, Riede, 1996, Jimenez et al., 1997) Df(3R)E(spl)^BX22 (Goldstein et al., 1999, Ligoxygakis et al., 1998, de Celis and Ruiz-Gomez, 1995, Paroush et al., 1994, Kooh et al., 1993, Shepard et al., 1989) Df(3R)E(spl)^Bx22 (Jagla et al., 1997, Jagla et al., 1998) Df(3R)E(spl)BX22 Df(3R)Espl22 (Wehn and Campbell, 2006, Chao et al., 2007, Bejarano et al., 2007) Df (3R)Espl22 (Bonds et al., 2007) Df(3R)Espl²² (Venken, 2006) E(spl)^Bx22 (Wheeler et al., 2002) E(spl)^BX22 (Nagel and Preiss, 1999, Tata and Hartley, 1995, Fischer-Vize et al., 1992, Jennings et al., 1994, Delidakis et al., 1991, Shepard et al., 1989, Bate et al., 1993, Nelson and Laughon, 1994, Verheyen et al., 1996, Huang and Fischer-Vize, 1996, Abmayr et al., 1992, de Celis et al., 1991, Coyle-Thompson and Banerjee, 1993, Xu and Artavanis-Tsakonas, 1990, Preiss et al., 1988, Corbin et al., 1991, ) E(spl)^Drvbx22 (Long et al., 1996) E(spl)^r16 E(spl)BX22 (Aronson et al., 1997) gro^BX22 (Hasson et al., 2005, Cinnamon et al., 2004, Atchison et al., 2003, Kobayashi et al., 2001, Chen et al., 1999, Cavallo et al., 1998, Dubnicoff et al., 1997, Paroush et al., 1997, Chao et al., 2007, Cinnamon et al., 2008, Liotta et al., 2007, Walrad et al., 2011, Helman et al., 2011) Gro^BX22 (Walrad et al., 2010) groBX22 (Kaspar et al., 2008)
Name Synonym
Secondary FlyBase IDs
	FBal0003337
References ( 55 )

Generate a list of	All references relating to this aberration ( 55 )

List References by type	Research paper ( 53 ) Supplementary material ( 1 ) FlyBase analysis ( 1 )
Recent research papers ( 2 )
	Helman et al., 2011, Curr. Biol. 21(13): 1102--1110 Phosphorylation of Groucho Mediates RTK Feedback Inhibition and Prolonged Pathway Target Gene Expression. [FBrf0214255] Walrad et al., 2011, Mol. Biol. Cell 22(8): 1364--1374 Hairless is a cofactor for Runt-dependent transcriptional regulation. [FBrf0213441] Show all research papers ...