Aberration Dmel\Df(3L)H99

General Information
Symbol	Dmel\Df(3L)H99	Species	D. melanogaster
Name		FlyBase ID	FBab0022359
Feature type	chromosomal_deletion	Created / Updated	2006-08-22/2006-08-22

Formalized genetic data	bk1 << W << bk2
Sequence coordinates
Deleted segment	75C1--75C2
Duplicated segment
Computed Breakpoints include	75C1-75C2;75C1-75C2
Breakpoints Inherited
Nature of the Aberration
Cytological Order
Progenitor
Mutagen	γ ray (Abbott and Lengyel, 1991)
Class of aberration (relative to progenitor)	chromosomal_deletion (White et al., 1994, Grether et al., 1995)
Breakpoints	75C1-75C2;75C1-75C2 (White et al., 1994, Grether et al., 1995)
Causes alleles
Carries alleles
Transposon Insertions
Genetic mapping information
Comments
Comments on Cytology
	Left limit of break 1 from polytene analysis (FBrf0074787) Right limit of break 1 from inclusion of W (FBrf0054189) Left limit of break 2 from inclusion of W (FBrf0054189) Right limit of break 2 from polytene analysis (FBrf0074787)
Molecularly Mapped Breakpoints

Sequence Crossreferences
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name
Gene Deletion & Duplication Data
Genes Deleted / Disrupted
Complementation Data
Completely deleted / disrupted	skl (Choi et al., 2006) rpr (Choi et al., 2006, White et al., 1994, White and Steller, 1995, Grether et al., 1995, Zhou et al., 1995, White et al., 1996, Chen et al., 1996, Zhou et al., 1997, Staveley et al., 1998, Sawamoto et al., 1998, Dumstrei et al., 1998, Lohmann et al., 2002, DeFalco et al., 2003, Chandrasekaran and Beckendorf, 2003) grim (Chen et al., 1996, Zhou et al., 1997, Staveley et al., 1998, Sawamoto et al., 1998, Dumstrei et al., 1998, DeFalco et al., 2003) W (Choi et al., 2006, Abbott and Lengyel, 1991, Grether et al., 1995, White et al., 1996, Chen et al., 1996, Zhou et al., 1997, Staveley et al., 1998, Sawamoto et al., 1998, Dumstrei et al., 1998, Kurada and White, 1998, DeFalco et al., 2003)
Molecular Data
Genes NOT Deleted / Disrupted
Complementation Data
Molecular Data
Genes Duplicated
Complementation Data
Molecular Data
Genes NOT Duplicated
Complementation Data
Molecular Data
Related Comments

Phenotypic Data
In combination with other aberrations
NOT in combination with other aberrations	Df(3L)H99 abdominal neuroblast clones continue to divide for at least 24 hours after wild-type clones have died. (Cenci and Gould, 2005) Df(3L)H99 homozygous stage 17 embryos have 10-12 midline glial cells per segment compared to an average of 2.8 per segment in wild-type. (Bergmann et al., 2002) Df(3L)H99/+ heterozygotes show an incompletely penetrant phenotype of male terminalia rotation. (Macias et al., 2004) Df(3L)H99/Df(1)XR38 females have on average 10 "neurons medially located, just above antennal lobe" (mALs), compared to 5 in wild-type females. The number in males (~30) is unaffected. When single cell clones are made using Df(3L)H99 in the adult brain, females have on average 19 mALs. The number in males (~30) is unaffected. When homozygous clones are induced at the embryonic stage, or 4-5 days after egg collection, the mAL neurons in females retain a normal contralateral projection pattern, but show ipsilateral projections. Abnormally dispersed dendritic branching is also seen. (Kimura et al., 2005) Df(3L)H99/In(3L)W^rvX1 transheterozygotes show supernumerary pigment cells in the developing eye, due to failure of apoptosis. (Kurada and White, 1998) th is epistatic to the mutant phenotype of Df(3L)H99. (Wang et al., 1999) Anterior dMP2 and MP1 neurons survive in late stage Df(3L)H99 embryos (in contrast to wild-type embryos, where these neurons are lost by the late embryonic stage). Anterior dMP2 neurons do not survive in heterozygous late embryos (as occurs in wild-type embryos, where these neurons are lost by the late embryonic stage). Few anterior MP1 neurons survive in heterozygous late stage embryos (similar to wild-type embryos, where these neurons are lost by the late embryonic stage). (Miguel-Aliaga and Thor, 2004) No mushroom body dfectes arew seen in mutants. (Watts et al., 2003) One ectopic external sensory organ forms near each the vmda1 neuron and 2 or 3 form in the dorsal region of Df(3L)H99 homozygotes. In addition 5 ectopic external sensory organs are formed in the ventral region of abdominal segment 8 of these embryos. (Orgogozo et al., 2002) Photoreceptor apoptosis at the periphery of developing eyes at 42 hours after puparium formation is almost completely eliminated in Df(3L)H99 homozygous clones. Ectopic photoreceptor clusters form in these clones. (Lin et al., 2004) Pole cells derived from homozygous embryos are able to migrate into the embryonic gonads when transplanted into host embryos, and are found normally within the ovaries and testes of the resulting third-instar larvae. (Hayashi et al., 2004) Stigmatophore development is normal. (Hu and Castelli-Gair, 1999) Apoptosis does not occur in homozygous embryos and hemocytes retain their small size and spindle shape. Homozygous embryos show defects in head morphogenesis, particularly processes occurring late in morphogenesis. Head structures are abnormally large, and invagination and intercalation movements are deficient. Severe defects in the reduction of the lateral gnathocephalon are seen. The dorsal ridge remains at the posterior of the head, due to the failure of head invagination. The antennal and maxillary sensory organs are separated by 3 to 4 cells, in contrast to wild-type, where they are virtually fused. The ganglia of the stomatogastric nervous system contain significantly more cells than wild-type. The clypeolabrum is significantly larger than wild-type, and does not retract into the dorsal pouch during later stages of embryogenesis, but remains as a large protuberance on the surface of the embryo. The labral sensilla remain separated by a broad patch of clypeolabral cells, in contrast to wild-type. The optic lobe is abnormally large, and shows abnormal invagination. The separation of the dorsomedial brain from the surface epithelium does not take place. Eye disc tissue flanks the antennal and maxillary sensory complexes and completely encircles the larval eye; dorsally eye disc tissue continues as a wide rectangular domain and meets its contralateral counterpart in the dorsal midline. (Nassif et al., 1998) At 24 hours after puparium formation (APF), a glial cell is present in 95% of clusters of the thoracic microchaete lineage in the pupal notum within regions covered by homozygous clones, whereas clusters within the wild-type twin spot show a glial cell in only 8% of cases. In heterozygous parts of the notum, glial cells are visible in 73% of clusters at 24 hours APF. At 30 hours APF, glial cells are detected in 63% of clusters in the notum within homozygous clones, in 45% of clusters in heterozygous regions and in none of the clusters within homozygous twin spots. At 25 hours APF, axonal projections from sensory neurons inside homozygous clones in the notum are more advanced than those outside the clone. (Fichelson and Gho, 2003) Complete absence of all programmed cell deaths. Mitotic clones of cells in the eye demonstrates that deleted region does not have adverse effects on cell division, differentiation or survival. Apoptosis can be induced by X irradiation. Supernumerary neuroblasts are present in fully developed embryo suggesting that a block in cell death leads to an increase in the number of cells. (White et al., 1994) Dominantly suppresses the Kr^If-1/+ eye phenotype. (Carrera et al., 1998) Embryos contain supernumerary midline glia cells. These cells appear to be persistent mesectodermal cells that are present transiently in wild-type embryos. (Dong and Jacobs, 1997) Four copies of P{grim-Cos} restores apoptosis to Df(3L)H99 embryos, rescue is dose-dependent. Embryos are still defective for head involution. (Chen et al., 1996) Has no effect on the eye phenotype produced by activated arm constructs. (either arm^S44Y.GMR or arm^S56F.GMR). (Freeman and Bienz, 2001) Hemizygotes die before hatching and possess an improperly formed cephalopharyngeal skeleton, all components are present but do not show their normal spatial relationship to each other. (Abbott and Lengyel, 1991) Heterozygous adults have a significantly longer abdominal ganglion than wild type. (Usui-Aoki et al., 2002) Homozygotes are embryonic lethal but exhibit an absence of cell death. Stage 17 mutant embryos exhibit a thickening of the longitudinal and commissural bundles suggesting some of the excess neurons may send out axonal processes. The nerve cord fails to condense properly and retains a lengthened appearance. Ectopic midline cells are observed in homozygous embryos due to lack of midline cell death. Cell death is not required for the formation of macrophage precursors or for their subsequent migration throughout the embryo. However in the absence of dying cells macrophage precursors do not exhibit morphological differentiation or phagocytosis. (Zhou et al., 1995) Homozygous embryos do not show programmed cell death, resulting in supernumerary midline glia. (Noordermeer et al., 1998) Homozygous embryos form normal salivary glands. (Myat and Andrew, 2000) Homozygous embryos have defects in head involution but their segment polarity is normal. Embryos have significantly more epidermal tissue in the head and lateral epidermis than wild type. During germband retraction, excess cells form a lateral fold and ectopic folds near the maxillary and labial segments and towards the posterior. (Cox et al., 2000) Homozygous embryos lack all programmed cell death (PCD) that is normally induced in response to various death-inducing signals. Consequently embryos contain many additional cells in the nervous system and especially in the head region which has extra larval photoreceptor cells. (Grether et al., 1995) Homozygous embryos show mild defects in germband retraction. (Li et al., 1999) Homozygous embryos show wild-type midgut morphogenesis. (Bilder et al., 1998) In 68% of hemisegments in the developing embryo have between six and 10 cells at the position of the NB7-3 cluster (compared to 4 in wild-type) (Novotny et al., 2002) In Df(3L)H99 mutants, stage 16 female gonads appear masculinized; male-specific somatic gonadal precursors persist and join the posterior of female gonads, as in wild-type male embryos. (DeFalco et al., 2003) In homozygous Df(3L)H99 embryos, the maxillary cirri primordium and the anterior boundary of the dorsal ridge, between the mandibular and maxillary segments, are missing. The optic lobe primordium is also missing. The Df(3L)XR38/Df(3L)H99 combination deletes only the rpr gene. In embryos of this genotype, the boundary between the maxillary and mandibular segments is largely abolished. In Df(3L)H99 mutant embryos, the boundaries between segments A6 and A7 and between A7 and A8 are partially fused. (Lohmann et al., 2002) In mutant embryos, head morphogenesis stalls at stage 13 or 14 of development while e.g. abdomen development proceeds normally. PNS structures in the head are abnormal. The Bolwig\'s organ is abnormal, with increased numbers of photoreceptors and defasciculation of the Bolwig\'s nerve. (Namba and Minden, 1999) Individuals display virtually no cell death during embryogenesis. (White and Steller, 1995) Mutant animals show a small but significant increase in glial cells over controls. (Sen et al., 2004) Neuroblast specific clones in the central abdomen result in a dramatic expansion of all three postembryonic neuroblast (pNB) lineages from a combined mean of 5.4 neurons for wild-type clones to 34 neurons per Df(3L)H99 clone in larvae. In contrast to wild-type abdominal lineages at 96 hours after larval hatching, the mutant clones still retain a single pNB that often labels with phosphorylated His3 protein. The maximum number of mitoses seen at any one time per Df(3L)H99 clone is two (representing divisions of the pNB and one ganglion mother cell) as occurs in wild-type clones. Df(3L)H99 pNB clones in the thorax are wild type in size. (Bello et al., 2003) The distribution of interface glia along the connectives is normal. The morphology of the ventral nerve cord is almost normal, though more midline cells than normal express sli. (Kinrade et al., 2001) The overall morphology of homozygous female germline clones is indistinguishable from wild-type, and DNA fragmentation still occurs in homozygous stage 12 and 13 nurse cells. (Foley and Cooley, 1998) The ventral crustacean cardioactive peptide immunoreactive (vCCAP-IR) neurons of the ventral nervous system do not die in heterozygous flies, in contrast to wild-type. (Draizen et al., 1999) When homozygous mutant clones are made aristae aristae are abnormal. They have ectopic branches, typically intermediate in size and located at the most proximal positions along the central core. These branches rea found very close to each without the wild-type regular spacing. the distal-most tips are also abnormal, having multiple smaller extensions rather than the normal three branched forked pattern. (Cullen and McCall, 2004) Cell death is reduced in Df(3L)H99 heterozygous third-instar larva at 6 hours after irradiation. By 18 and 24 hours after irradiation however, cell death appears as robust as in wild-type at similar stages. (Wichmann et al., 2006) Heterozygous Df(3L)H99 does not affect the level of cell death in Crz-expressing neurons in the ventral nerve cord. (Choi et al., 2006) The central nervous system is wider than in wild-type in late Df(3L)H99 embryos, but it has a fairly normal appearance. The commissures and longitudinal connectives are broadened and the junctions between them are thickened due to additional axons, but their pattern is not altered compared to wild type. The three Fas2-positive longitudinal connectives form, and apart from a variably "bumpy" appearance, they look similar to wild type. The peripheral transverse, segmental and intersegmental nerves appear normal as well as the four nerve branches (SNa-d). The nerves appear to be of normal thickness. The glia pattern, apart from a moderate displacement of some cells is also surprisingly normal and the number of repo-positive glial cells is normal in the mutant embryos. Most neuroblast lineages contain more cells than normal in Df(3L)H99 embryos and a specific set of these lineages show segment-specific characteristics. The extra cells can be specified as neurons with extended wild-type-like or abnormal axonal projections, but are not specified as glia. (Rogulja-Ortmann et al., 2007) Df(3L)H99/+ flies show eyes of wild-type size. (Singh et al., 2006)
Position Effect Variegation Data

Stocks ( 3 )
Bloomington	1576 Df(3L)H99, kni^ri-1 p^p/TM3, Sb¹ 9926 y¹ w^*; P{lacW}Ark^CD4/CyO; TM3, Sb¹/Df(3L)H99, kni^ri-1 p^p
Kyoto	106395 Df(3L)H99, kni^ri-1 p^p/TM3, Sb¹
Notes on Origin
Discoverer

Balancer / Genotype Variants of the Aberration

Separable Components

Other Comments

Synonyms & Secondary IDs ( 13 )
Reported As
Symbol Synonym	Df(1)H99 (Orgogozo et al., 2004, Orgogozo et al., 2002) Df(3)H99 (Anderson et al., 2005, Kozlova and Thummel, 2003, Tanentzapf and Tepass, 2003, Huh and Hay, 2002, Meier et al., 2000, Li et al., 1999) Df(3L)H99 (Rogulja-Ortmann et al., 2007, Singh et al., 2006, Choi et al., 2006, Wells et al., 2006, Cela and Llimargas, 2006, Kuranaga et al., 2006, Renault et al., 2004, Secombe et al., 2007) df(3L)H99 (Dumstrei et al., 2002) Df(3L)hid^H99 (Draizen et al., 1999) Df(3L)hidH99 (White et al., 1996) Df(3R)H99 (Haberman et al., 2003, Dumstrei et al., 1998, Bilder et al., 1998, Zhou et al., 1995, Sugiyama et al., 2007) Df(H99) (Moreno et al., 2002, Hsu et al., 2004) DfH99 (Sedore and Cronmiller, 2004, Baena-Lopez and Garcia-Bellido, 2006) H99 (Rogulja-Ortmann et al., 2007, Provost et al., 2006, De Falco et al., 2003, Hay et al., 2004, Danial and Korsmeyer, 2004, Huh et al., 2004, Bach et al., 2003, Mergliano and Minden, 2003, Yoo et al., 2002, Abrams et al., 2003, Claveria and Torres, 2003, Bello et al., 2003, Fichelson and Gho, 2003, Richardson and Kumar, 2002, Kumar and Doumanis, 2000, Gorski and Marra, 2002, Yamamoto, 2002, Usui-Aoki et al., 2002, Bangs et al., 2000, Wang et al., 1999, Daniel et al., 1999, Chen et al., 1998, Peterson et al., 1998, Hortsch et al., 1998, Hacohen et al., 1998, Dong and Jacobs, 1997, Rodriguez et al., 1999, Hays, 2006, Peterson et al., 2006, Abraham et al., 2007, Tu et al., 2007, Wichmann et al., 2006, Choi et al., 2006, Abrams et al., 2006, Lim and Tomlinson, 2006, Pfleger et al., 2007) hid^H99 (Werz et al., 2005, White et al., 1994) hid-H99 (Abbott and Lengyel, 1991) W^hid-H99 (Abbott and Lengyel, 1991)
Name Synonym
Secondary FlyBase IDs

References ( 146 )

Generate a list of	All references relating to this aberration ( 146 )

List References by type	Research paper ( 115 ) Supplementary material ( 1 ) Review ( 15 ) Erratum ( 1 ) Abstract ( 13 ) FlyBase analysis ( 1 )
Recent research papers ( 15 )
	Pfleger et al., 2007, Fly 1(2): 95--105 Mutation of the gene encoding the ubiquitin activating enzyme Uba1 causes tissue overgrowth in Drosophila. [FBrf0200069] Rogulja-Ortmann et al., 2007, Development 134(1): 105--116 Programmed cell death in the embryonic central nervous system of Drosophila melanogaster. [FBrf0194301] Secombe et al., 2007, Genes Dev. 21(5): 537--551 The Trithorax group protein Lid is a trimethyl histone H3K4 demethylase required for dMyc-induced cell growth. [FBrf0193047] Sugiyama et al., 2007, Genetics 176(2): 927--936 Involvement of the mitochondrial protein translocator component Tim50 in growth, cell proliferation and the modulation of respiration in Drosophila. [FBrf0200675] Abrams et al., 2006, Development 133(18): 3517--3527 Fork head and Sage maintain a uniform and patent salivary gland lumen through regulation of two downstream target genes, PH4αSG1 and PH4αSG2. [FBrf0195124] Baena-Lopez and Garcia-Bellido, 2006, Proc. Natl. Acad. Sci. USA 103(37): 13734--13739 Control of growth and positional information by the graded vestigial expression pattern in the wing of Drosophila melanogaster. [FBrf0193315] Cela and Llimargas, 2006, Development 133(16): 3115--3125 Egfr is essential for maintaining epithelial integrity during tracheal remodelling in Drosophila. [FBrf0192922] Choi et al., 2006, Development 133(11): 2223--2232 Programmed cell death mechanisms of identifiable peptidergic neurons in Drosophila melanogaster. [FBrf0190281] Kuranaga et al., 2006, Cell 126(3): 583--596 Drosophila IKK-related kinase regulates nonapoptotic function of caspases, via degradation of IAPs. [FBrf0194448] Lim and Tomlinson, 2006, Development 133(18): 3529--3537 Organization of the peripheral fly eye: the roles of Snail family transcription factors in peripheral retinal apoptosis. [FBrf0195310] Mettler et al., 2006, Development 133(3): 429--437 Timing of identity: spatiotemporal regulation of hunchback in neuroblast lineages of Drosophila by Seven-up and Prospero. [FBrf0190310] Provost et al., 2006, Genetics 172(1): 207--219 Loss-of-function mutations in a glutathione S-transferase suppress the prune-Killer of prune lethal interaction. [FBrf0190760] Singh et al., 2006, Development 133(23): 4771--4781 Lobe and Serrate are required for cell survival during early eye development in Drosophila. [FBrf0192707] Wells et al., 2006, Curr. Biol. 16(16): 1606--1615 Compensatory proliferation in Drosophila imaginal discs requires Dronc-dependent p53 activity. [FBrf0192041] Wichmann et al., 2006, Proc. Natl. Acad. Sci. USA 103(26): 9952--9957 Ionizing radiation induces caspase-dependent but Chk2- and p53-independent cell death in Drosophila melanogaster. [FBrf0194209] Show all research papers ...
Recent reviews (0)
	All reviews listed in FlyBase were published before 2006 Show reviews ...