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General Information
D. melanogaster
FlyBase ID
Feature type
Also Known As
H99, Df(H99), DfH99, Df(3)H99, Df(3R)H99, def(3L)H99, Df(1)H99, hidH99, Deficiency (3L)H99, Df(3 L) H99
Computed Breakpoints include
Sequence coordinates
Member of large scale dataset(s)
Nature of Aberration
Cytological Order
Class of aberration (relative to wild type)
Class of aberration (relative to progenitor)
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data

bk1 << W << bk2

Genetic mapping information
Comments on Cytology

The distal breakpoint corresponds to the 75B11-13 bands, and the proximal breakpoint is presumed to be within the 75C1' band (a new small band between 75C1 and 75C2).

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)

Sequence Crossreferences
DNA sequence
Protein sequence
Gene Deletion and Duplication Data
Genes Deleted / Disrupted
Genes NOT Deleted / Disrupted
Complementation Data
Molecular Data
Genes Duplicated
Complementation Data
Completely duplicated
Partially duplicated
Molecular Data
Completely duplicated
Partially duplicated
Genes NOT Duplicated
Complementation Data
Molecular Data
Affected Genes Inferred by Location
    Phenotypic Data
    In combination with other aberrations

    Df(3L)MM3/Df(3L)H99 animals have a defect in the programmed cell death of vCrz neurons: 11.8 +/- 1.6 neurons are present at 7 hours after puparium formation (APF) (these neurons are no longer present in wild-type animals at this stage) and 7.9 +/- 3.5 neurons are present at 16 hours APF.

    Df(3L)X25/Df(3L)H99 results in lethality.

    Df(3L)XR38/Df(3L)H99 animals have a defect in the programmed cell death of vCrz neurons: 14.3 +/- 1.0 neurons are present at 7 hours after puparium formation (these neurons are no longer present in wild-type animals at this stage). 0.4 +/- 0.8 surviving EW3-sib cells are seen in these animals (these cells die during embryogenesis in wild type).

    Df(3L)grim-A6C/Df(3L)H99 animals have a defect in the programmed cell death of vCrz neurons: 16 +/- 0 neurons are present at 7 hours after puparium formation (APF) (these neurons are no longer present in wild-type animals at this stage) and 16 +/- 0 neurons are present at 16 hours APF. 9.3 +/- 0.6 surviving EW3-sib cells are seen in these animals (these cells die during embryogenesis in wild type).

    The programmed cell death of bursCCAP neurons seen in the adult ventral nerve cord of wild type flies after eclosion is partially suppressed in Df(3L)H99/Df(3L)XR38 mutant homozygotes. An average of nine bursCCAP neurons are still present at 4-5 days.

    Df(3L)H99 strongly suppresses the axon scaffold phenotypes seen in Df(1)NetABΔ mutant stage 16 embryos. The defects in negative geotaxis behaviour are further enhanced compared to Df(1)NetABΔ alone, but the mechanical startle-induced locomotor reactivity phenotype is significantly rescued.

    In contrast to wild-type animals, abdominal neuroblasts are not eliminated after hatching in Df(3L)XR38/Df(3L)H99 larvae.

    Inferred to overlap with: Df(3L)XR38.

    Transient persistence of mushroom body neuroblasts is seen in the brains of young adult Df(3L)H99/Df(3L)XR38 animals (mushroom body neuroblasts are not seen in wild-type adults). The persisting adult mushroom body neuroblasts are only half the size of mushroom body neuroblasts present during earlier stages of development and they divide slowly, generating very few adult mushroom body neurons.

    At 30 hours after puparium formation (APF), Df(3L)H99/Df(3L)XR38 brains have more neuroblasts than wild-type controls (these mutant animals have the normal number of large, dpn-expressing neuroblasts at earlier, larval stages). Central brain neuroblasts aberrantly persist even at 48 hours APF in these animals, but their numbers are considerably reduced.

    Autophagy still occurs in Df(3L)H99/Df(3L)ED225 embryos.

    Inferred to overlap with: Df(3L)ED225.

    Df(3L)XR38/Df(3L)H99 mutants, that are rpr null, exhibit a rescue of apoptosis in Crz-expressing neurons of the ventral nerve cord, with approximately 7 pairs of Crz-expressing neurons surviving in these mutants, compared to none in wild-type.

    Anterior dMP2 and MP1 neurons survive in late stage Df(3L)H99/Df(3L)XR38 embryos (in contrast to wild-type embryos, where these neurons are lost by the late embryonic stage). 66% of anterior dMP2 neurons survive in late stage Df(3L)H99/Df(3L)X25 embryos (in contrast to wild-type embryos, where these neurons are lost by the late embryonic stage). Anterior MP1 neurons survive in late stage Df(3L)H99/Df(3L)X25 embryos (in contrast to wild-type embryos, where these neurons are lost by the late embryonic stage). Few anterior dMP2 and MP1 neurons survive in Df(3L)H99/Df(3L)X14 late stage embryos (similar to wild-type embryos, where these neurons are lost by the late embryonic stage).

    No affect is seen on amnioserosa disintegration in mutants.

    Df(3L)XR38/Df(3L)H99 animals have essentially normal salivary gland cell death; only 4.2% have persistent larval salivary glands at 20 hours after puparium formation. Df(3L)XR38/Df(3L)H99 pupae show normal larval midgut cell death.

    Df(3L)XR38/Df(3L)H99 flies are viable, emerge at the expected frequency and have no obvious visible defects. They have a shortened lifespan. Df(3L)XR38/Df(3L)H99 embryos and embryos derived from Df(3L)XR38/Df(3L)H99 females that lack both zygotic and maternal rpr show no changes in overall apoptosis. Salivary gland and midgut histolysis are not detectably altered in Df(3L)XR38/Df(3L)H99 pupae. X-ray induced apoptosis is significantly inhibited in Df(3L)XR38/Df(3L)H99 animals, although some ectopic cell death is seen. Df(3L)XR38/Df(3L)H99 males are sterile, although spermatogenesis appears normal and large numbers of motile sperm are present in the testes of mutant males. Sperm are not transferred to females when wild-type females are placed with Df(3L)XR38/Df(3L)H99 males for several days. The courtship index of Df(3L)XR38/Df(3L)H99 males is not significantly different from wild type. The major block in mating appears to be an inability of the males to bend their abdomens sufficiently for copulation. The thoracic and abdominal ganglia of the ventral nerve cord are enlarged in Df(3L)XR38/Df(3L)H99 adults. The abdominal ganglion shows the most extensive hyperplasia. 26.6 +/- 1.2 CCAP-expressing neurons persist in the ventral nerve cord 2-6 days after eclosion in Df(3L)XR38/Df(3L)H99 adults, compared to the wild-type number of 3 +/- 0.7. 65 +/- 3.8 EcR-A-expressing neurons persist in Df(3L)XR38/Df(3L)H99 adults, compared to 2.8 +/- 1.4 in 1-2 day old wild-type adults. Many neuroblasts are present in the abdominal neuromeres of Df(3L)XR38/Df(3L)H99 larvae, in contrast to wild type where most of these neuroblasts undergo apoptosis by the end of embryogenesis. There is a substantial increase in the number of BrdU-labelled cells in the larval abdominal neuromere compared to wild type and cells that have been labelled with BrdU during the larval stages are abundant in the adult ventral nerve cord.

    NOT in combination with other aberrations

    Df(3L)H99 heterozygotes do not present significant changes in the number of adult brain glial cells, as compared to controls.

    Df(3L)H99 heterozygotes do not exhibit a significant proportion of hyperplastic testes, as compared to controls.

    Wings of Df(3L)H99/+ adults are significantly larger than those of controls.

    Upon exposure to ionizing radiation, Df(3L)H99 wing disc clones show basal cell delamination, as compartment to controls.

    Df(3L)H99 embryonic ventral nerve cords have significantly increased numbers of DAC and CUT expressing neurons, compared to controls.

    Wing disc of Df(3L)H99 heterozygote third instar larvae are slightly bigger compared to controls.

    The dramatic increase in apoptosis (assessed by Caspase-3 staining) in the third instar larval wing disc characteristic for pcm14 homozygote mutants is strongly suppressed by combination with Df(3L)H99 in heterozygote state and the disc differentiation is also restored (the disturbed wg pattern is recovered). The reduced size of the third larval instar imaginal wing disc is strongly rescued too and the resulting disc size is intermediate between that of pcm14/pcm14 alone and that of Df(3L)H99/+ (which on its own gives rise to wing disc bigger than wild-type) and smaller than wild-type.

    In Spiroplasma-infected Df(3L)H99 female embryos, the CNS and PNS develops normally. In infected males, a remarkable neural malformation is observed.

    Heterozygous animals have a defect in the programmed cell death of vCrz neurons: 6.7 +/- 2.1 neurons are present at 7 hours after puparium formation (these neurons are no longer present in wild-type animals at this stage).

    The programmed cell death of bursCCAP neurons seen in the adult ventral nerve cord of wild type flies after eclosion is partially suppressed in Df(3L)H99/+ mutant homozygotes. An average of four bursCCAP neurons are seen at 3-5 days.

    Df(3L)H99 mutant embryos exhibit defects in the engulfment of apoptotic neurons. Small lysosomes are observed in the phagocytic glial cells, rather than the larger phagolysosomes seen in wild type.

    The amount of spermatogonial cysts death seen in Df(3L)H99/+ mutant males is similar to wild type controls.

    Minimal eye overgrowth is seen in Df(3L)H99 mutant clones (generated using the eyFLP method).

    Df(3L)H99 clones induced in third instar larval eye discs have an increased number of ommatidial cells compared to controls but ommatidial organisation is normal and a single R7 cell is found in each ommatidium.

    Mutant embryos show a modest increase in the number of adult muscle precursor cells per hemisegment compared to wild type. There is an increase in lateral, dorsolateral and dorsal adult muscle precursor cells, but the number of ventral adult muscle precursor cells is unaffected.

    In contrast to controls, no chromosomal breaks in the 75C1-2 region are found in chromosomes bearing the deficiency.

    Bristle morphogenesis is unaffected in Df(3L)H99 MARCM mutants.

    In contrast to controls, the amnioserosa of Df(3L)H99 embryos persists as an intact coherent tissue beyond the 4-lobe midgut stage and beyond the onset of somatic musculature innervation. This phenotype is frequently observed in mutant embryos that are greater than 24 hours old and still alive, indicating that the amnioserosa can persist at least 8 hours beyond its normal time of degeneration.

    In contrast to controls, Df(3L)H99 embryos show no acridine orange staining in the dorsal region of the asymmetric 4-lobe midgut stage.

    Df(3L)H99 embryos show no TUNEL-positive cells in the amnioserosa or other tissues.

    P1 neurons that are normally absent from the female brain are seen in the brains of females containing homozygous Df(3L)H99 MARCM clones.

    Wings mosaic for Df(3L)H99 are morphologically normal at eclosion, but melanized blemishes appear at random throughout the wing over 3-7 days.

    Df(3L)H99 mosaic wings retain Disc\RFPhs.DsRedT4.T:nls5-positive wing epithelial cells 4-11 days after eclosion, whereas control epithelial cells undergo apoptosis moments after eclosion.

    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.

    Heterozygous Df(3L)H99 does not affect the level of cell death in Crz-expressing neurons in the ventral nerve cord.

    Df(3L)H99/+ flies show eyes of wild-type size.

    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.

    Df(3L)H99 abdominal neuroblast clones continue to divide for at least 24 hours after wild-type clones have died.

    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.

    Levels of apoptosis in embryonic primordial germ cells are unaffected in Df(3L)H99 mutant embryos.

    The wing discs of Df(3L)H99/+ mutant third instar larvae exhibit reduced levels of apoptosis in response to X-ray induced irradiation with 4000 rads compared to controls.

    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.

    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.

    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.

    Df(3L)H99/+ heterozygotes show an incompletely penetrant phenotype of male terminalia rotation.

    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).

    Mutant animals show a small but significant increase in glial cells over controls.

    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.

    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.

    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.

    No mushroom body dfectes arew seen in mutants.

    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.

    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.

    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)

    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.

    Heterozygous adults have a significantly longer abdominal ganglion than wild type.

    Has no effect on the eye phenotype produced by activated arm constructs. (either armS44Y.GMR or armS56F.GMR).

    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.

    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.

    Homozygous embryos form normal salivary glands.

    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.

    Stigmatophore development is normal.

    Homozygous embryos show mild defects in germband retraction.

    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.

    th is epistatic to the mutant phenotype of Df(3L)H99.

    Homozygous embryos show wild-type midgut morphogenesis.

    Dominantly suppresses the KrIf-1/+ eye phenotype.

    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.

    Df(3L)H99/In(3L)WrvX1 transheterozygotes show supernumerary pigment cells in the developing eye, due to failure of apoptosis.

    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.

    Homozygous embryos do not show programmed cell death, resulting in supernumerary midline glia.

    Embryos contain supernumerary midline glia cells. These cells appear to be persistent mesectodermal cells that are present transiently in wild-type embryos.

    Four copies of P{grim-Cos} restores apoptosis to Df(3L)H99 embryos, rescue is dose-dependent. Embryos are still defective for head involution.

    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.

    Individuals display virtually no cell death during embryogenesis.

    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.

    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.

    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.

    Stocks (3)
    Notes on Origin
    Balancer / Genotype Variants of the Aberration
    Separable Components
    Other Comments
    Synonyms and Secondary IDs (21)
    Reported As
    Symbol Synonym
    Deficiency (3L)H99
    Df(3 L)H99
    (O'Neill and Rusan, 2022, Bhat et al., 2021, Kiely and Gilbert-Ross, 2021, Petrignani et al., 2021, Xie et al., 2021, Zhou et al., 2021, Blanco et al., 2020, Brown et al., 2020, Prieto-Godino et al., 2020, Wolfstetter et al., 2020, Asaoka et al., 2019, Hanyu-Nakamura et al., 2019, Harding and White, 2019, Jia et al., 2019, Park et al., 2019, West et al., 2018, Doyle et al., 2017, Foo et al., 2017, Khandelwal et al., 2017, Martins et al., 2017, Napoletano et al., 2017, Schott et al., 2017, Blumröder et al., 2016, Carrasco-Rando et al., 2016, Jussen et al., 2016, Lacin and Truman, 2016, Lee et al., 2016, Towler et al., 2016, Urbach et al., 2016, Arias et al., 2015, Arya et al., 2015, Barrios et al., 2015, Kale et al., 2015, Moris-Sanz et al., 2015, Waldron et al., 2015, Wang and Baker, 2015, Zhang et al., 2015, Butí et al., 2014, Fan et al., 2014, Sánchez-Higueras et al., 2014, Dichtel-Danjoy et al., 2013, Fox et al., 2013, Khan et al., 2013, Lee et al., 2013, Melzer et al., 2013, Shklyar et al., 2013, Yang et al., 2013, Davidson and Duronio, 2012, Ge et al., 2012, Lim et al., 2012, Ma et al., 2012, Verghese et al., 2012, Anh et al., 2011, Holland et al., 2011, Marinho et al., 2011, Maruyama et al., 2011, Suissa et al., 2011, Beam and Moberg, 2010, Benito-Sipos et al., 2010, Fan et al., 2010, Schreader et al., 2010, Siegrist et al., 2010, Andreyenkova et al., 2009, Chung et al., 2009, González and Busturia, 2009, Mohseni et al., 2009, Tanaka-Matakatsu et al., 2009, Tiwari and Roy, 2009, Wu et al., 2009, Bardet et al., 2008, Griswold et al., 2008, Kimura et al., 2008, Kurant et al., 2008, Miguel-Aliaga et al., 2008, Sanders and Arbeitman, 2008, Trinh et al., 2008, Xu et al., 2008, Guan et al., 2007, Krieser et al., 2007, Nguyen et al., 2007, Rogulja-Ortmann et al., 2007, Sato et al., 2007, Secombe et al., 2007, Sevrioukov et al., 2007, Tanaka-Matakatsu et al., 2007, Cela and Llimargas, 2006, Choi et al., 2006, Kuranaga et al., 2006, Lee et al., 2006, Leulier et al., 2006, Singh et al., 2006, Wells et al., 2006, Sano et al., 2005, Brodsky et al., 2004, Renault et al., 2004)
    (Pop et al., 2020, Sun et al., 2020, Park et al., 2019, Xu et al., 2018, Chung et al., 2017, Bhogal et al., 2016, Flegel et al., 2016, Shklover et al., 2015, Waldron et al., 2015, Bhaskar et al., 2014, Harumoto et al., 2014, Huang et al., 2014, Shklyar et al., 2014, Dichtel-Danjoy et al., 2013, Khan et al., 2013, Lee et al., 2013, Newquist et al., 2013, Newquist et al., 2013, Yacobi-Sharon et al., 2013, Olesnicky et al., 2012, Gilbert et al., 2011, Resnik-Docampo and de Celis, 2011, Tan et al., 2011, Bulchand et al., 2010, Figeac et al., 2010, Fishilevich et al., 2010, Karlsson et al., 2010, Mesquita et al., 2010, Forero et al., 2009, Koto et al., 2009, Joza et al., 2008, Montero et al., 2008, Abraham et al., 2007, Pfleger et al., 2007, Rogulja-Ortmann et al., 2007, Thummel, 2007, Tu et al., 2007, Abrams et al., 2006, Choi et al., 2006, Hays, 2006, Lim and Tomlinson, 2006, Peterson et al., 2006, Provost et al., 2006, Wichmann et al., 2006, Danial and Korsmeyer, 2004, Hay et al., 2004, Huh et al., 2004, Mellerick and Liu, 2004, Abrams et al., 2003, Bach et al., 2003, Bello et al., 2003, Claveria and Torres, 2003, De Falco et al., 2003, Fichelson and Gho, 2003, Mergliano and Minden, 2003, Gorski and Marra, 2002, Richardson and Kumar, 2002, Usui-Aoki et al., 2002, Yamamoto, 2002, Yoo et al., 2002, Bangs et al., 2000, Kumar and Doumanis, 2000, Daniel et al., 1999, Rodriguez et al., 1999, Wang et al., 1999, Chen et al., 1998, Hacohen et al., 1998, Hortsch et al., 1998, Peterson et al., 1998, Dong and Jacobs, 1997)
    deficiency (3L)H99
    Name Synonyms
    Secondary FlyBase IDs
      References (277)