|Feature type||allele||Associated gene||Dmel\Mad|
|Map ( GBrowse )|
|Allele class||amorphic allele - genetic evidence, loss of function allele|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Amino acid replacement: Q417@.
|Phenotype Manifest In|
Heterozygotes climb sightly, but significantly, better than wild-type controls in a negative geotaxis assay.
Mad/Mad mutant third instar larvae show increased uptake and transport of ingested fluorescently labeled fatty acids from the midgut lumen to the fat body compared to wild-type controls.
Clones of Mad-mutant cells cause premature differentiation of the adult midgut precursor cells into large, polyploid, enterocyte-like cells compared with wild-type cells.
Somatic clones of Mad homozygous cells in the developing retina at 42 hours APF have abnormal arrangements of inter-ommatidial cells including aberrant bristle-bristle contacts and abberant arrangements of secondary and tertiary pigment cells.
Homozygous cells in the morphogenetic furrow (in clones that encompass the morphogenetic furrow) can stil achieve proper apicobasal contraction.
Mad mutant germline stem cells (GSCs) show maintenance and cell division defects when clones are generated during adult stages. However no defects are seen when Mad clones are generated during the larval and pupal stages.
Mosaic female germaria containing germline stem cells in contact only with homozygous somatic cap cells do not show any defects in germline stem cell renewal.
G1 arrest is delayed in Mad eye disc cells; some mutant cells don't arrest at all in larger Mad clones.
Homozygous clones in the wing disc extrude from the wing epithelium.
When neutral marked clones are induced in the ovary, the proportion of germaria carrying marked somatic stem cells 3 weeks after clone induction is around 70% of that seen one week after clone induction. For Mad12 homozygous clones, the equivalent figure is under 25%, resulting in significantly fewer clones in the follicle cells.
Mad11/Mad12 transheterozygotes exhibit abnormal L4/L5 wing veins, with no L2 or crossveins and a large margin notch.
Clones of male Mad12 homozygous germline stem cells are still present in less than 1% of testes one week after clone induction and none are present two weeks after clone induction. This is in contrast to wild-type control clones, which are present in 82% of testes one week after clone induction and 64% two weeks after clone induction.
The evoked excitatory junctional potential (EJP) (measured at muscle 6 of segment A3) shows a decrease in amplitude in Mad1/Mad12 animals compared to wild type. Quantal content is reduced compared to wild type.
The average number of crystal cells per embryo is significantly reduced in homozygous stage 13-14 embryos compared to wild type.
Ovarioles carrying Mad12 GSC clones are not recovered, but ovarioles with mutant Mad12 germ cells in egg chambers are recovered, indicating that Mad12 GSCs can not be maintained before adulthood.
Homozygous clones induced before 72 hours after egg laying (AEL) show elimination of entire tarsal segments, whereas if clones are induced after 84 hours AEL, only dorsal leg pattern features are affected.
In somatic clones induced late in the third larval instar L3 bifurcates or terminates at the clone boundary. L2 was seen to loop round a small clone. In 50 clones, all were seen to disrupt vein formation in a cell autonomous manner.
When somatic clones are created in the glial cells of the developing eye, they contain fewer cells than equivalent wild-type clones. the total number glial cells remains the same as wild-type cells appear to compensate for the loss of mutant ones.
Encapsulation defects of 16-cell cysts are seen in ovaries containing homozygous follicle cell clones.
Clones induced in the pleura showed a sternite or tergite identity rarely - 6 cases out of several hundred clones. Other clones retain a pleural identity or display a weak phenotype such as mild sclerotinization. Clones at or near the dorsal midline show loss of tergal pigmentation. A partial loss of pigmentation is often observed in clones lateral to the anterior inflection of the pigment band.
20% of the dorsal branch fusion events are disrupted. The fusion cell extends a sprout but does not contact the appropriate fusion partner.
Gastric caecae frequently fail to elongate. Dorsal trunk and visceral branches of the developing trachea are essentially normal. Branching defects occur, ganglionic branches fail to fuse. Dorsal trunk is normal.
Embryos lacking maternal and zygotic Mad function (Mad10/Mad12 embryos derived from females with homozygous Mad12 germ line clones) show loss of dorsal tissue and expansion of the lateral denticle bands into dorsal regions. The phenotype is partially paternally rescuable.
MadEz/Mad12 flies have imaginal disc defects. All the progeny of MadEz/Mad12 females mated to wild-type males die as embryos. One-half of the embryos (presumptive genotype Mad12/+ have a weakly ventralised phenotype, and the other half (presumptive genotype MadEz/+) have a variably expressive dorsal-open phenotype.
Females with homozygous germ line clones lay very few eggs, all of which are unfertilised and smaller than normal. The ovaries of these females may contain no discernible ovarioles or may contain many degenerating egg chambers, the most mature of which are at stage 10.
Clonal analysis in the germarium reveals that mutant stem cells are lost more rapidly than wild type, though there is no effect on the formation of 16 cell cysts or their subsequent development. Stem cell half life is 0.25 weeks (wild type being 4.6 weeks). Stem cell division rate relative to control is 0.21. Cysts contain the normal 16 cells, including and oocyte.
Clonal analysis revealed that Mad function is autonomously required in the eye imaginal disc cells for proliferation and/or survival.
|NOT Enhanced by|
Mad12 has decreased cell number | somatic clone phenotype, suppressible by Scer\GAL4Scer\FRT.Act5C/ykiS168A.Scer\UAS.T:SV5\V5
Mad12 is a suppressor | partially of increased cell number | somatic clone phenotype of Scer\GAL4Scer\FRT.Act5C, ykiS168A.Scer\UAS.T:SV5\V5
Mad12 is a suppressor of increased cell number | somatic clone phenotype of Scer\GAL4Scer\FRT.Act5C, ykiS250A.Scer\UAS.T:SV5\V5
|NOT Suppressor of|
Mad12, Su(H)del47, ci94 has mitotic cell cycle defective | somatic clone | cell autonomous phenotype
|Phenotype Manifest In|
Mad12 has wing disc | somatic clone phenotype, suppressible by Scer\GAL4Scer\FRT.Act5C/ykiS168A.Scer\UAS.T:SV5\V5
|NOT Enhancer of|
Mad12 is a suppressor | partially of wing disc | somatic clone phenotype of ykiS168A.Scer\UAS.T:SV5\V5
|NOT Suppressor of|
The severe loss of climbing ability in a negative geotaxis assay which is seen in Scgδ mutants is suppressed if the flies are also carrying Mad/+. The dilated heart tube seen in Scgδ adults (detected as increased end-systolic and end-diastolic diameters as measured by optical coherence tomography) is is not rescued if the flies are carrying Mad/+.
A Mad mutant background partially suppresses the overgrowth seen when yki[S168A.Scer\UAS.T:SV5\V5] is expressed in wing disc clones under the control of Scer\GAL4[Scer\FRT.Act5C]. Suppression of growth is evident in the distal wing, but not in the proximal wing. A Mad mutant background suppresses the overgrowth seen when yki[S250A.Scer\UAS.T:SV5\V5] is expressed in wing disc clones under the control of Scer\GAL4[Scer\FRT.Act5C], returning the number of cells to control levels.
Homozygous Mad clones expressing cbt[Scer\UAS.cRa] under the control of Scer\GAL4[Act.PU] do not survive in the wing pouch.
Strong maternal effect lethality is observed when trans-heterozygous Mad sax females are crossed with wild-type males. Strong maternal effect lethality is observed when trans-heterozygous Mad sax females are crossed with wild-type males.
brk[XH]/brk[XH], Mad[B1]/Mad double mutant wing disc clones have normal apical-basal cell length.
Smn[73Ao]/Mad and Smn[f01109]/Mad double heterozygotes show a reduction in bouton number per muscle area at the third larval instar neuromuscular junction compared to wild type.
Mad/+ partially suppresses the abberant arangement of inter-ommatidial cells seen in the pupal and adult retinas of In(1)rst/Y animals. The retinas of shg[R69]/+ animals at 42 hours APF have only very occasional inter-ommatidial patterning defects (the occasional extra or misplaced cell). This phenotype is significantly enhanced in Mad/shg[R69] transheterozygotes.
Mad mutant germline stem cells lacking one copy of Dcr-1[Q1147X] show clear stem cell maintenance defects when clones are generated during late larval/early pupal stages. Dcr-1[Q1147X] mutant germline stem cells lacking one copy of Mad show clear stem cell maintenance defects when clones are generated during late larval/early pupal stages. Expressing Dl[Scer\UAS.P\T.cJa] under the control of Scer\GAL4[nos.PG] in Mad mutant GSCs during the larval/pupal stages results in an enlargement of the niche at 7 and 14 days after clone induction. No stem cell maintenance defects are observed. The number of Mad mutant GSCs in the enlarged niche increases from 7 days to 14 days.
Eye disc cells simultaneously mutant for Mad, ci and Su(H)[del47] continue proliferating instead of arresting in G1 ahead of the morphogenetic furrow. The same phenotype is seen in cells mutant for Mad and ci - the presence of Su(H)[del47] has no autonomous effect on G1 arrest. G1 arrest is delayed in Mad, Su(H)[del47] eye disc cells.
brkXH MadB1/Mad12 clones generated along the A/P boundary of the wing imaginal disc, using the FLP/FRT technique, show no defects in segregation behaviour. As with wild-type clones, these mutant clones stay in the compartment (anterior or posterior) in which they have been generated.
The weight of adp/Mad double heterozygous flies is not significantly different from that of control flies.
Has no effect on the eye phenotype produced by activated arm constructs. (either armS44Y.GMR or armS56F.GMR).
When Mad12, smo3 double mutant somatic clones are made in the developing eye, a small but significant reduction in the percentage of mutant cells is seen compared to Mad12 clones alone.
Shows a dominant maternal effect interaction with dpp; when Mad12/+ females are crossed to dpphr27/+ males, all progeny carrying dpphr27 die. This lethality is rescued by MadUbi-p63E.T:Hsap\MYC also partly by MedUbi-p63E.PD.
|Complementation & Rescue Data|
|Fails to complement|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 6 )|
(Gibson and Perrimon, 2005, Shen and Dahmann, 2005, Zhu and Xie, 2003, Marty et al., 2000, Rangarajan et al., 2001, Dorfman and Shilo, 2001, Jordan et al., 2000, Zhang et al., 1999, Yu et al., 1998, Xie and Spradling, 1998, Dudu et al., 2006, Corrigall et al., 2007, Grienenberger et al., 2003, O'Connor-Giles et al., 2008, Rodriguez, 2011)
(Bangi and Wharton, 2006, Takaesu et al., 2005, Chen and Schupbach, 2006, Kirilly et al., 2005, Christoforou et al., 2008, Firth and Baker, 2005, Oh and Irvine, 2011, Shcherbata et al., 2007, Wisotzkey et al., 2003, Cordero et al., 2007, Chang et al., 2008, Yu et al., 2009, Eivers et al., 2009, Bolivar et al., 2006, Ballard et al., 2010, Twombly et al., 2009, Eivers et al., 2011, Liu et al., 2011, Ball et al., 2010, Quijano et al., 2011, Stinchfield et al., 2012)
|Secondary FlyBase IDs|
|References ( 75 )|
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|List References by type|
|Recent research papers ( 7 )|