FlyBase Allele Report: Dmel\Mad[12]

Mad¹²/Mad^k00237 transheterozygotes show a significant reduction in the number of synaptic boutons at the third instar larval neuromuscular junction, as compared to controls.

(Banerjee et al., 2017)

Mad¹²/+ third instar larvae have similar numbers of boutons to wild type.

(Li et al., 2016)

Mad¹² mutant nuclei are small and tightly packed, unlike wild-type copper cell nuclei, which are polyploid and regularly spaced.

Eight days after induction of intestinal stem cell (ISC) clones, the number of cells in Mad¹² mutant clones is significantly higher than in wild-type clones. After injury by feeding bleomycin, mutant clones have more cells than both wild-type clones and mutant clones before injury.

Wild-type clones contain one stem cell, whereas approximately one-third of Mad¹² mutant clones show a gradual increase in ISC number over time.

One-stem-cell Mad¹² mutant clones contain more stem cells than wild-type clones, indicating that mutant ISCs divide more often than wild-type ones.

(Guo et al., 2013)

Heterozygotes climb sightly, but significantly, better than wild-type controls in a negative geotaxis assay.

(Goldstein et al., 2011)

Very few Mad¹² mutant wing disc clones are recovered.

(Oh and Irvine, 2011)

Mad¹²/Mad⁷ 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.

(Ballard et al., 2010)

Clones of Mad¹²-mutant cells cause premature differentiation of the adult midgut precursor cells into large, polyploid, enterocyte-like cells compared with wild-type cells.

(Mathur et al., 2010)

Somatic clones of Mad¹² 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.

(Cordero et al., 2007)

Homozygous cells in the morphogenetic furrow (in clones that encompass the morphogenetic furrow) can stil achieve proper apicobasal contraction.

(Corrigall et al., 2007)

Mad¹² mutant germline stem cells (GSCs) show maintenance and cell division defects when clones are generated during adult stages. However no defects are seen when Mad¹² clones are generated during the larval and pupal stages.

(Shcherbata et al., 2007)

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.

(Bolivar et al., 2006)

G1 arrest is delayed in Mad¹² eye disc cells; some mutant cells don't arrest at all in larger Mad¹² clones.

(Firth and Baker, 2005)

Homozygous clones in the wing disc extrude from the wing epithelium.

(Gibson and Perrimon, 2005)

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.

(Kirilly et al., 2005)

Mad¹¹/Mad¹² transheterozygotes exhibit abnormal L4/L5 wing veins, with no L2 or crossveins and a large margin notch.

(Takaesu et al., 2005)

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.

(Kawase et al., 2004)

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.

(McCabe et al., 2004)

The average number of crystal cells per embryo is significantly reduced in homozygous stage 13-14 embryos compared to wild type.

(Milchanowski et al., 2004)

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.

(Zhu and Xie, 2003)

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.

(Galindo et al., 2002)

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.

(Marquez et al., 2001)

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.

(Rangarajan et al., 2001)

Encapsulation defects of 16-cell cysts are seen in ovaries containing homozygous follicle cell clones.

(Jordan et al., 2000)

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.

(Kopp et al., 1999)

20% of the dorsal branch fusion events are disrupted. The fusion cell extends a sprout but does not contact the appropriate fusion partner.

(Steneberg et al., 1999)

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.

(Waltzer and Bienz, 1999)

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.

(Das et al., 1998)

Mad^Ez/Mad¹² flies have imaginal disc defects. All the progeny of Mad^Ez/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 Mad^Ez/+) have a variably expressive dorsal-open phenotype.

(Hudson et al., 1998)

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.

(Wisotzkey et al., 1998)

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.

(Xie and Spradling, 1998)

Clonal analysis revealed that Mad function is autonomously required in the eye imaginal disc cells for proliferation and/or survival.

(Wiersdorff et al., 1996)

Heterozygotes with Df(2L)C28 die as prepupae.

(Raftery et al., 1995)

Larval heterozygotes with Df(2L)JS17 exhibit reduced fat body, midgut defects and greatly reduced gastric caecae and dissected pupae exhibit absent or severely reduced imaginal discs.

(Sekelsky et al., 1995)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

NOT Enhanced by

Statement

Reference

Mad¹² has lethal | recessive phenotype, non-enhanceable by lilli^unspecified

(Su et al., 2001)

Suppressed by

Statement

Reference

Mad¹² has decreased cell number | somatic clone phenotype, suppressible by Scer\GAL4^FRT.Act5C/yki^{S168A.UAS.Tag:V5}

(Oh and Irvine, 2011)

Mad¹² has decreased cell number | somatic clone phenotype, suppressible by Scer\GAL4^FRT.Act5C/yki^{S250A.UAS.Tag:V5}

(Oh and Irvine, 2011)

Enhancer of

Statement

Reference

Mad¹²/Mad[+] is an enhancer | maternal effect of lethal | recessive | partially phenotype of sog^P129D

(Decotto and Ferguson, 2001)

Suppressor of

Statement

Reference

Mad¹²/Mad[+] is a suppressor | partially of abnormal size | adult stage phenotype of Scer\GAL4^A9, anchor^GD3613

(Wang et al., 2018)

Mad¹²/Mad[+] is a suppressor | partially of visible | adult stage phenotype of Scer\GAL4^A9, anchor^GD3613

(Wang et al., 2018)

Mad¹²/Mad[+] is a suppressor of abnormal neuroanatomy | third instar larval stage phenotype of Ube3a³⁵

(Li et al., 2016)

Mad¹²/Mad[+] is a suppressor of abnormal neuroanatomy | third instar larval stage phenotype of brat^2L-192-9/brat¹¹

(Shi et al., 2013)

Mad¹²/Mad[+] is a suppressor of abnormal locomotor behavior | adult stage phenotype of Scgδ⁸⁴⁰

(Goldstein et al., 2011)

Mad¹² is a suppressor | partially of increased cell number | somatic clone phenotype of Scer\GAL4^FRT.Act5C, yki^{S168A.UAS.Tag:V5}

(Oh and Irvine, 2011)

Mad¹² is a suppressor of increased cell number | somatic clone phenotype of Scer\GAL4^FRT.Act5C, yki^{S250A.UAS.Tag:V5}

(Oh and Irvine, 2011)

Mad¹²/Mad[+] is a suppressor of visible phenotype of Scer\GAL4^A9, gbb^UAS.cKa

(Bangi and Wharton, 2006)

Mad¹²/Mad[+] is a suppressor of visible phenotype of Scer\GAL4^A9, dpp^UAS.cHa

(Bangi and Wharton, 2006)

Mad¹² is a suppressor of visible phenotype of Scer\GAL4^en-e16E, sax^{Q263D.UAS.cDa}

(Waltzer and Bienz, 1999)

Mad¹²/Mad[+] is a suppressor of visible phenotype of tkv^SC143

(Das et al., 1998)

Mad¹²/Mad[+] is a suppressor of visible phenotype of Scer\GAL4^en-e16E, sax^{Q263D.UAS.cDa}

(Das et al., 1998)

NOT Suppressor of

Statement

Reference

Mad¹² is a non-suppressor of abnormal planar polarity phenotype of Scer\GAL4^hs.2sev, Tak1^UAS.cMa

(Mihaly et al., 2001)

Other

Statement

Reference

Mad¹², Scer\GAL4^A9, anchor^GD3613 has abnormal size | adult stage phenotype

(Wang et al., 2018)

Mad¹², Scer\GAL4^A9, anchor^GD3613 has visible | adult stage phenotype

(Wang et al., 2018)

Mad¹²/Mad[+], dpp^hr4 has partially lethal - majority die phenotype

(Quijano et al., 2016)

Mad¹²/Mad[+], dpp^hr27 has partially lethal - majority die | maternal effect phenotype

(Quijano et al., 2016)

Mad¹², Scer\GAL4^Act.PU, cbt^UAS.cRa has FlyBase_internaltransgene_features:cell lethal:cell lethal | somatic clone phenotype

(Rodriguez, 2011)

Mad¹²/Mad[+], sax¹ has lethal | dominant | maternal effect phenotype

(Twombly et al., 2009)

Mad¹²/Mad[+], sax² has lethal | dominant | maternal effect phenotype

(Twombly et al., 2009)

Mad¹²/Mad[+], Smn^73Ao has abnormal neuroanatomy | third instar larval stage phenotype

(Chang et al., 2008)

Mad¹²/Mad[+], Smn^f01109 has abnormal neuroanatomy | third instar larval stage phenotype

(Chang et al., 2008)

Dcr-1^Q1147X, Mad¹²/Mad[+] has decreased cell number | somatic clone | larval stage phenotype

(Shcherbata et al., 2007)

Dcr-1^Q1147X, Mad¹²/Mad[+] has decreased cell number | somatic clone | pupal stage phenotype

(Shcherbata et al., 2007)

Dcr-1^Q1147X/Dcr-1[+], Mad¹² has decreased cell number | somatic clone | larval stage phenotype

(Shcherbata et al., 2007)

Dl^UASp.cJa, Mad¹², Scer\GAL4^nos.PG has increased cell number phenotype

(Shcherbata et al., 2007)

Mad¹², Su(H)^del47, ci⁹⁴ has abnormal mitotic cell cycle | somatic clone | cell autonomous phenotype

(Firth and Baker, 2005)

Mad¹², ci⁹⁴ has abnormal mitotic cell cycle | somatic clone | cell autonomous phenotype

(Firth and Baker, 2005)

Mad¹², Su(H)^del47 has abnormal mitotic cell cycle | somatic clone | cell autonomous phenotype

(Firth and Baker, 2005)

Mad¹², smo³ has decreased cell number | somatic clone phenotype

(Rangarajan et al., 2001)

Mad¹²/Mad[+], dpp^hr27 has lethal | dominant phenotype

(Das et al., 1998)

Mad¹², dpp^hr27/dpp[+] has lethal | dominant | maternal effect phenotype

(Das et al., 1998)

Phenotype Manifest In

NOT Enhanced by

Statement

Reference

Mad^k00237/Mad¹² has neuromuscular junction | third instar larval stage phenotype, non-enhanceable by Nrx-1²⁷³/Nrx-1²⁷³

(Banerjee et al., 2017)

Mad^k00237/Mad¹² has terminal bouton | third instar larval stage phenotype, non-enhanceable by Nrx-1²⁷³/Nrx-1²⁷³

(Banerjee et al., 2017)

Mad^k00237/Mad¹² has neuromuscular junction | third instar larval stage phenotype, non-enhanceable by Nlg1^Δ46/Nlg1^Δ46

(Banerjee et al., 2017)

Mad^k00237/Mad¹² has terminal bouton | third instar larval stage phenotype, non-enhanceable by Nlg1^Δ46/Nlg1^Δ46

(Banerjee et al., 2017)

Suppressed by

Statement

Reference

Mad¹² has wing disc | somatic clone phenotype, suppressible by Scer\GAL4^FRT.Act5C/yki^{S168A.UAS.Tag:V5}

(Oh and Irvine, 2011)

Mad¹² has wing disc | somatic clone phenotype, suppressible by Scer\GAL4^FRT.Act5C/yki^{S250A.UAS.Tag:V5}

(Oh and Irvine, 2011)

Enhancer of

Statement

Reference

Mad¹²/Mad[+] is an enhancer of interommatidial cell | ectopic | pupal stage P7 phenotype of shg^R69

(Cordero et al., 2007)

Mad¹² is an enhancer of phenotype of dpp^e87

(Sekelsky et al., 1995)

Mad¹² is an enhancer of phenotype of dpp^hr56

(Sekelsky et al., 1995)

NOT Enhancer of

Statement

Reference

Mad¹² is a non-enhancer | germline clone of germline cyst | germline clone phenotype of bam^Δ86

(Casanueva and Ferguson, 2004)

Suppressor of

Statement

Reference

Mad¹²/Mad[+] is a suppressor | partially of wing vein phenotype of Scer\GAL4^A9, anchor^GD3613

(Wang et al., 2018)

Mad¹²/Mad[+] is a suppressor | partially of wing phenotype of Scer\GAL4^A9, anchor^GD3613

(Wang et al., 2018)

Mad¹²/Mad[+] is a suppressor of NMJ bouton | increased number | third instar larval stage phenotype of Ube3a³⁵

(Li et al., 2016)

Mad¹²/Mad[+] is a suppressor of NMJ bouton | increased number | third instar larval stage phenotype of brat^2L-192-9/brat¹¹

(Shi et al., 2013)

Mad¹²/Mad[+] is a suppressor | partially of wing vein phenotype of Dd^G0269

(Liu et al., 2011)

Mad¹² is a suppressor | partially of wing disc | somatic clone phenotype of yki^{S168A.UAS.Tag:V5}

(Oh and Irvine, 2011)

Mad¹² is a suppressor of wing disc | somatic clone phenotype of yki^{S250A.UAS.Tag:V5}

(Oh and Irvine, 2011)

Mad¹²/Mad[+] is a suppressor of wing vein phenotype of Scer\GAL4^A9, gbb^UAS.cKa

(Bangi and Wharton, 2006)

Mad¹²/Mad[+] is a suppressor of wing phenotype of Scer\GAL4^A9, dpp^UAS.cHa

(Bangi and Wharton, 2006)

Mad¹²/Mad[+] is a suppressor of wing phenotype of tkv^SC143

(Das et al., 1998)

Mad¹²/Mad[+] is a suppressor of wing vein | ectopic phenotype of tkv^SC143

(Das et al., 1998)

Mad¹²/Mad[+] is a suppressor of wing phenotype of Scer\GAL4^en-e16E, sax^{Q263D.UAS.cDa}

(Das et al., 1998)

Mad¹²/Mad[+] is a suppressor of wing phenotype of tkv^TAJ3

(Hoodless et al., 1996)

NOT Suppressor of

Statement

Reference

Mad¹²/Mad[+] is a non-suppressor of adult heart phenotype of Scgδ⁸⁴⁰

(Goldstein et al., 2011)

Mad¹² is a non-suppressor of germline cyst | germline clone phenotype of bam^Δ86

(Casanueva and Ferguson, 2004)

Mad¹² is a non-suppressor of eye phenotype of Scer\GAL4^hs.2sev, Tak1^UAS.cMa

(Mihaly et al., 2001)

Mad¹² is a non-suppressor of eye photoreceptor cell phenotype of Scer\GAL4^hs.2sev, Tak1^UAS.cMa

(Mihaly et al., 2001)

Mad¹² is a non-suppressor of phenotype of Src42A^Su(Raf)1-1

(Zhang et al., 1999)

Other

Statement

Reference

Mad¹², Scer\GAL4^A9, anchor^GD3613 has wing phenotype

(Wang et al., 2018)

Mad¹²/Mad[+], dpp^hr4 has embryo | maternal effect phenotype

(Quijano et al., 2016)

Mad¹²/Mad[+], Smn^73Ao has NMJ bouton phenotype

(Chang et al., 2008)

Mad¹²/Mad[+], Smn^f01109 has NMJ bouton phenotype

(Chang et al., 2008)

Dcr-1^Q1147X, Mad¹²/Mad[+] has female germline stem cell | somatic clone | larval stage phenotype

(Shcherbata et al., 2007)

Dcr-1^Q1147X, Mad¹²/Mad[+] has female germline stem cell | somatic clone | pupal stage phenotype

(Shcherbata et al., 2007)

Dcr-1^Q1147X/Dcr-1[+], Mad¹² has female germline stem cell | somatic clone | larval stage phenotype

(Shcherbata et al., 2007)

Dl^UASp.cJa, Mad¹², Scer\GAL4^nos.PG has female germline stem cell phenotype

(Shcherbata et al., 2007)

Mad¹², ci⁹⁴ has eye disc | somatic clone | cell autonomous phenotype

(Firth and Baker, 2005)

Mad¹², Su(H)^del47 has eye disc | somatic clone | cell autonomous phenotype

(Firth and Baker, 2005)

Mad¹², Su(H)^del47, ci⁹⁴ has eye disc | somatic clone | cell autonomous phenotype

(Firth and Baker, 2005)

Mad^B1/Mad¹², brk^XH has anterior-posterior compartment boundary of the wing disc | somatic clone phenotype

(Shen and Dahmann, 2005)

Mad¹², smo³ has eye disc | somatic clone phenotype

(Rangarajan et al., 2001)

Additional Comments

Genetic Interactions

Statement

Reference

Addition of Mad¹²/+ to animals expressing anchor^GD3613 under the control of Scer\GAL4^A9 partially suppresses the thickened wing vein phenotype and suppresses the increased wing size phenotype, to the extent that it is decreased compared to flies with Scer\GAL4^A9 driver alone.

(Wang et al., 2018)

The decreased number of synaptic boutons at the third instar larval neuromuscular of Mad¹²/Mad^k00237 transheterozygotes is not suppressed or enhanced by either Nrx-1²⁷³ or Nlg1^Δ46 homozygosity.

(Banerjee et al., 2017)

Mad¹²/+ suppresses the increase in total boutons (and satellite boutons) at the neuromuscular junction in Ube3a³⁵/Ube3a³⁵ third instar larvae.

(Li et al., 2016)

The progeny from Mad¹²/+ mothers and dpp^hr4/+ fathers present embryo ventralization in less than half of cases, and near lethality, as compared to controls; the progeny from Mad¹²/+ mothers and dpp^hr27/+ fathers, but not dpp^hr56/+ or dpp^e87/+ fathers, exhibit semi-lethality, as compared to controls.

(Quijano et al., 2016)

The neuromuscular junction overgrowth phenotype (increased total number of boutons and increased number of satellite boutons) of brat¹¹/brat^2L-192-9 larvae is significantly suppressed by Mad¹²/+.

The reduced uptake of FM1-43 dye seen at the neuromuscular junction in brat¹¹/brat^2L-192-9 larvae is significantly suppressed by Mad¹²/+.

(Shi et al., 2013)

The severe loss of climbing ability in a negative geotaxis assay which is seen in Scgδ⁸⁴⁰ mutants is suppressed if the flies are also carrying Mad¹²/+.

The dilated heart tube seen in Scgδ⁸⁴⁰ 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 Mad¹²/+.

(Goldstein et al., 2011)

The aberrant wing vein phenotype seen in Dd^G0269/Y animals is suppressed by Mad¹²/+.

(Liu et al., 2011)

A Mad¹² 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 Mad¹² 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.

(Oh and Irvine, 2011)

Homozygous Mad¹² clones expressing cbt^Scer\UAS.cRa under the control of Scer\GAL4^Act.PU do not survive in the wing pouch.

(Rodriguez, 2011)

Strong maternal effect lethality is observed when trans-heterozygous Mad¹² sax¹ females are crossed with wild-type males.

Strong maternal effect lethality is observed when trans-heterozygous Mad¹² sax² females are crossed with wild-type males.

(Twombly et al., 2009)

brk^XH/brk^XH, Mad^B1/Mad¹² double mutant wing disc clones have normal apical-basal cell length.

(Widmann and Dahmann, 2009)

Smn^73Ao/Mad¹² and Smn^f01109/Mad¹² double heterozygotes show a reduction in bouton number per muscle area at the third larval instar neuromuscular junction compared to wild type.

(Chang et al., 2008)

Mad¹²/+ partially suppresses the abberant arangement of inter-ommatidial cells seen in the pupal and adult retinas of In(1)rst³/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 Mad¹²/shg^R69 transheterozygotes.

(Cordero et al., 2007)

Mad¹² 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 Mad¹² 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 Mad¹² 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 Mad¹² mutant GSCs in the enlarged niche increases from 7 days to 14 days.

(Shcherbata et al., 2007)

Eye disc cells simultaneously mutant for Mad¹², ci⁹⁴ 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 Mad¹² and ci⁹⁴ - the presence of Su(H)^del47 has no autonomous effect on G1 arrest.

G1 arrest is delayed in Mad¹², Su(H)^del47 eye disc cells.

(Firth and Baker, 2005)

brk^XH Mad^B1/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.

(Shen and Dahmann, 2005)

The weight of adp⁶⁰/Mad¹² double heterozygous flies is not significantly different from that of control flies.

(Wisotzkey et al., 2003)

Has no effect on the eye phenotype produced by activated arm constructs. (either arm^S44Y.GMR or arm^S56F.GMR).

(Freeman and Bienz, 2001)

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.

(Rangarajan et al., 2001)

Does not suppress the ability of Src42A^Su(phl)1-1 to suppress the lethality of phl¹/Y flies.

(Zhang et al., 1999)

Shows a dominant maternal effect interaction with dpp; when Mad¹²/+ females are crossed to dpp^hr27/+ males, all progeny carrying dpp^hr27 die. This lethality is rescued by Mad^{Ubi-p63E.T:Hsap\MYC} also partly by Med^Ubi-p63E.PD.

(Das et al., 1998)

Heterozygosity for Mad¹² weakly suppresses the blistered wing phenotype of tkv^TAJ3.

(Hoodless et al., 1996)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

Mad^ES1

(Decotto and Ferguson, 2001)

Mad^Ez

(Hudson et al., 1998)

Rescued by

Mad¹²/Mad¹ is rescued by Scer\GAL4^da.G32/Mad^UAS.N.YFP

(Smith et al., 2012)

Mad¹² is rescued by Mad^αTub84B.PM

(Marty et al., 2000)

Comments

Images (0)

Mutant

Wild-type

Stocks (4)

Bloomington

58785

w^*; Mad¹² P{neoFRT}40A/CyO, P{GFP-un1}CyO

51286

y¹ w^*; smo³ Mad¹² P{neoFRT}40A/SM6a

51301

P{hsFLP}12, y¹ w^*; Mad¹² P{neoFRT}40A/CyO; ci⁹⁴/Dp(1;4)1021, sv^spa-pol

51302

P{hsFLP}12, y¹ w^*; Df(2L)del47, Mad¹² CIAPIN1^del47 Su(H)^del47 P{neoFRT}40A P{l(2)35Bg^+t6.8}2/CyO; ci⁹⁴/Dp(1;4)1021, y⁺, sv^spa-pol

Notes on Origin

Discoverer

Comments

Mad mutations can be placed in an allelic series based on relative severity of the maternal effect enhancement of weak dpp alleles: Mad¹ < Mad⁷ < Mad¹² < Mad¹⁰ < Mad⁵ < Mad³ < Mad² < Mad¹¹ < Mad⁶ < Mad⁴ < Mad⁸ < Mad⁹.

(Sekelsky et al., 1995)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (6)

Reported As

Symbol Synonym

MAD¹²

(Goldstein et al., 2011, Mathur et al., 2010)

Mad -

(Mathur et al., 2010)

Mad12

(Shcherbata et al., 2007)

Mad^-

(Weiss et al., 2010)

Name Synonyms

Secondary FlyBase IDs

References (94)

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