Allele Dmel\Mad¹²

General Information
Symbol	Dmel\Mad¹²	Species	D. melanogaster
Name		FlyBase ID	FBal0044916
Feature type	allele	Associated gene	Dmel\Mad

Map ( GBrowse )
Allele class	amorphic allele - genetic evidence, loss of function allele
Mutagen	ethyl methanesulfonate
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class	amorphic allele - genetic evidence (Raftery et al., 1995, Sekelsky et al., 1995, Wiersdorff et al., 1996) loss of function allele (Newfeld et al., 1997, Yu et al., 1998)
Mutagen	ethyl methanesulfonate (Sekelsky et al., 1995)
Mutations Mapped to the Genome

Type Location Additional Notes References point mutation 2L:3,147,538..3,147,538 evidence=experimental na_change=C3147538T phenotype=null pr_change=Q417@\|Mad-PA (Sekelsky et al., 1995)
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference Amino acid replacement: Q417@. (Takaesu et al., 2005) Point mutation. (Sekelsky et al., 1995)
Cytology
Phenotypic Data
Phenotypic Class
	decreased cell number \| adult stage \| somatic clone (Shcherbata et al., 2007) decreased cell number \| somatic clone (Rangarajan et al., 2001, Oh and Irvine, 2011) lethal \| embryonic stage \| maternal effect \| recessive (Hudson et al., 1998) lethal \| pupal stage \| recessive (Sekelsky et al., 1995) mitotic cell cycle defective \| cell autonomous \| somatic clone (Firth and Baker, 2005) neurophysiology defective (with Mad¹) (McCabe et al., 2004) visible \| somatic clone (Galindo et al., 2002, Kopp et al., 1999)
Phenotype Manifest In
	adult midgut precursor cell \| somatic clone (Mathur et al., 2010) crystal cell (Milchanowski et al., 2004) denticle belt (Das et al., 1998) egg (Wisotzkey et al., 1998) egg chamber (Wisotzkey et al., 1998) embryonic/first instar larval cuticle (Das et al., 1998) embryonic/first instar larval cuticle \| maternal effect (Hudson et al., 1998) embryonic/larval dorsal branch (Steneberg et al., 1999) embryonic/larval tracheal system (Waltzer and Bienz, 1999) embryonic/larval ventral anastomosis (Waltzer and Bienz, 1999) eye-antennal disc (Wiersdorff et al., 1996) eye disc \| cell autonomous \| somatic clone (Firth and Baker, 2005) fat body (with Mad⁷) (Ballard et al., 2010) female germline stem cell (Xie and Spradling, 1998) female germline stem cell \| adult stage \| somatic clone (Shcherbata et al., 2007) female germline stem cell \| somatic clone (Zhu and Xie, 2003) gastric caecum (Waltzer and Bienz, 1999) germarium (Jordan et al., 2000) imaginal disc \| maternal effect (Hudson et al., 1998) interommatidial bristle \| pupal stage P7 \| somatic clone (Cordero et al., 2007) leg \| somatic clone (Galindo et al., 2002) male germline stem cell \| germline clone (Kawase et al., 2004) ovariole (Wisotzkey et al., 1998) pleurum \| somatic clone (Kopp et al., 1999) secondary pigment cell \| pupal stage P7 \| somatic clone (Cordero et al., 2007) tarsal segment \| somatic clone (Galindo et al., 2002) tergite \| somatic clone (Kopp et al., 1999) tertiary pigment cell \| pupal stage P7 \| somatic clone (Cordero et al., 2007) wing disc \| somatic clone (Gibson and Perrimon, 2005, Oh and Irvine, 2011) wing margin (with Mad¹¹) (Takaesu et al., 2005) wing vein L2 (with Mad¹¹) (Takaesu et al., 2005) wing vein L2 \| cell autonomous \| somatic clone (Marquez et al., 2001) wing vein L3 \| cell autonomous \| somatic clone (Marquez et al., 2001) wing vein L4 (with Mad¹¹) (Takaesu et al., 2005) wing vein L5 (with Mad¹¹) (Takaesu et al., 2005)
Detailed Description
	Statement Reference Heterozygotes climb sightly, but significantly, better than wild-type controls in a negative geotaxis assay. (Goldstein et al., 2011) Very few Mad[12] mutant wing disc clones are recovered. (Oh and Irvine, 2011) Mad[12]/Mad[7] 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 Mad[12]-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 Mad[12] 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) Mad[12] 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[12] 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 Mad[12] eye disc cells; some mutant cells don't arrest at all in larger Mad[12] 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 the 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^{Scer\FRT.Act5C}/yki^{S168A.Scer\UAS.T:SV5\V5} (Oh and Irvine, 2011) Mad¹² has decreased cell number \| somatic clone phenotype, suppressible by Scer\GAL4^{Scer\FRT.Act5C}/yki^{S250A.Scer\UAS.T:SV5\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 of gravitaxis defective phenotype of Scgδ⁸⁴⁰ (Goldstein et al., 2011) Mad¹²/Mad[+] is a suppressor of visible phenotype of Scer\GAL4^A9, dpp^Scer\UAS.cHa (Bangi and Wharton, 2006) Mad¹²/Mad[+] is a suppressor of visible phenotype of Scer\GAL4^A9, gbb^Scer\UAS.cKa (Bangi and Wharton, 2006) Mad¹²/Mad[+] is a suppressor of visible phenotype of Scer\GAL4^en-e16E, sax^{Q263D.Scer\UAS.cDa} (Das et al., 1998) Mad¹²/Mad[+] is a suppressor of visible phenotype of tkv^SC143 (Das et al., 1998) Mad¹² is a suppressor \| partially of increased cell number \| somatic clone phenotype of Scer\GAL4^{Scer\FRT.Act5C}, yki^{S168A.Scer\UAS.T:SV5\V5} (Oh and Irvine, 2011) Mad¹² is a suppressor of increased cell number \| somatic clone phenotype of Scer\GAL4^{Scer\FRT.Act5C}, yki^{S250A.Scer\UAS.T:SV5\V5} (Oh and Irvine, 2011) Mad¹² is a suppressor of visible phenotype of Scer\GAL4^en-e16E, sax^{Q263D.Scer\UAS.cDa} (Waltzer and Bienz, 1999)
NOT Suppressor of
Statement Reference Mad¹² is a non-suppressor of planar polarity defective phenotype of Scer\GAL4^hs.2sev, Tak1^Scer\UAS.cMa (Mihaly et al., 2001)
Other
Statement Reference 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^{Scer\UAS.P\T.cJa}, Mad¹², Scer\GAL4^nos.PG has increased cell number phenotype (Shcherbata et al., 2007) Mad¹², ci⁹⁴ has mitotic cell cycle defective \| somatic clone \| cell autonomous phenotype (Firth and Baker, 2005) Mad¹², dpp^hr27/dpp[+] has lethal \| dominant \| maternal effect phenotype (Das et al., 1998) Mad¹², Scer\GAL4^Act.PU, cbt^Scer\UAS.cRa has cell lethal \| somatic clone phenotype (Rodriguez, 2011) Mad¹², smo³ has decreased cell number \| somatic clone phenotype (Rangarajan et al., 2001, Rangarajan et al., 2001) Mad¹², Su(H)^del47, ci⁹⁴ has mitotic cell cycle defective \| somatic clone \| cell autonomous phenotype (Firth and Baker, 2005) Mad¹², Su(H)^del47 has mitotic cell cycle defective \| somatic clone \| cell autonomous phenotype (Firth and Baker, 2005) Mad¹²/Mad[+], dpp^hr27 has lethal \| dominant phenotype (Das et al., 1998) 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 neuroanatomy defective \| third instar larval stage phenotype (Chang et al., 2008) Mad¹²/Mad[+], Smn^f01109 has neuroanatomy defective \| third instar larval stage phenotype (Chang et al., 2008)
Phenotype Manifest In
Suppressed by
Statement Reference Mad¹² has wing disc \| somatic clone phenotype, suppressible by Scer\GAL4^{Scer\FRT.Act5C}/yki^{S168A.Scer\UAS.T:SV5\V5} (Oh and Irvine, 2011) Mad¹² has wing disc \| somatic clone phenotype, suppressible by Scer\GAL4^{Scer\FRT.Act5C}/yki^{S250A.Scer\UAS.T:SV5\V5} (Oh and Irvine, 2011)
Enhancer of
Statement Reference Mad¹²/Mad[+] is an enhancer of inter-ommatidial 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 Dd^G0269 (Liu et al., 2011) Mad¹²/Mad[+] is a suppressor of wing phenotype of Scer\GAL4^A9, dpp^Scer\UAS.cHa (Bangi and Wharton, 2006) Mad¹²/Mad[+] is a suppressor of wing phenotype of Scer\GAL4^en-e16E, sax^{Q263D.Scer\UAS.cDa} (Das et al., 1998) Mad¹²/Mad[+] is a suppressor of wing phenotype of tkv^SC143 (Das et al., 1998) Mad¹²/Mad[+] is a suppressor of wing phenotype of tkv^TAJ3 (Hoodless et al., 1996) Mad¹²/Mad[+] is a suppressor of wing vein \| ectopic phenotype of tkv^SC143 (Das et al., 1998) Mad¹²/Mad[+] is a suppressor of wing vein phenotype of Scer\GAL4^A9, gbb^Scer\UAS.cKa (Bangi and Wharton, 2006) Mad¹² is a suppressor \| partially of wing disc \| somatic clone phenotype of yki^{S168A.Scer\UAS.T:SV5\V5} (Oh and Irvine, 2011) Mad¹² is a suppressor of wing disc \| somatic clone phenotype of yki^{S250A.Scer\UAS.T:SV5\V5} (Oh and Irvine, 2011)
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 eye phenotype of Scer\GAL4^hs.2sev, Tak1^Scer\UAS.cMa (Mihaly et al., 2001) Mad¹² is a non-suppressor of eye photoreceptor cell phenotype of Scer\GAL4^hs.2sev, Tak1^Scer\UAS.cMa (Mihaly et al., 2001) Mad¹² is a non-suppressor of germline cyst \| germline clone phenotype of bam^Δ86 (Casanueva and Ferguson, 2004) Mad¹² is a non-suppressor of phenotype of Src42A^Su(phl)1-1 (Zhang et al., 1999)
Other
Statement Reference 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^{Scer\UAS.P\T.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, smo³ has eye disc \| somatic clone phenotype (Rangarajan et al., 2001, Rangarajan et al., 2001) Mad¹², Su(H)^del47, 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/Mad[+], Smn^73Ao has NMJ bouton phenotype (Chang et al., 2008) Mad¹²/Mad[+], Smn^f01109 has NMJ bouton phenotype (Chang et al., 2008) Mad^B1/Mad¹², brk^XH has wing disc \| anterior/posterior compartment boundary \| somatic clone phenotype (Shen and Dahmann, 2005, Shen and Dahmann, 2005)
Additional Comments
Genetic Interactions
Statement Reference The severe loss of climbing ability in a negative geotaxis assay which is seen in Scgδ[840] mutants is suppressed if the flies are also carrying Mad[12]/+. The dilated heart tube seen in Scgδ[840] 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[12]/+. (Goldstein et al., 2011) The aberrant wing vein phenotype seen in Dd[G0269]/Y animals is suppressed by Mad[12]/+. (Liu et al., 2011) A Mad[12] 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[12] 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 Mad[12] 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 Mad[12] sax[1] females are crossed with wild-type males. Strong maternal effect lethality is observed when trans-heterozygous Mad[12] sax[2] females are crossed with wild-type males. (Twombly et al., 2009) brk[XH]/brk[XH], Mad[B1]/Mad[12] double mutant wing disc clones have normal apical-basal cell length. (Widmann and Dahmann, 2009) Smn[73Ao]/Mad[12] and Smn[f01109]/Mad[12] 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) Mad[12]/+ partially suppresses the abberant arangement of inter-ommatidial cells seen in the pupal and adult retinas of In(1)rst[3]/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[12]/shg[R69] transheterozygotes. (Cordero et al., 2007) Mad[12] 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[12] 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[12] 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[12] mutant GSCs in the enlarged niche increases from 7 days to 14 days. (Shcherbata et al., 2007) Eye disc cells simultaneously mutant for Mad[12], ci[94] 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[12] and ci[94] - the presence of Su(H)[del47] has no autonomous effect on G1 arrest. G1 arrest is delayed in Mad[12], 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 adp[60]/Mad[12] 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 & Rescue Data
Fails to complement	Mad^ES1 (Decotto and Ferguson, 2001) Mad^Ez (Hudson et al., 1998)
Rescued by	Mad¹² is rescued by Mad^αTub84B.PM (Marty et al., 2000)
Comments
Stocks ( 0 )

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 & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 6 )
Reported As
Symbol Synonym	Mad - (Mathur et al., 2010) Mad12 (Shcherbata et al., 2007) mad¹² (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) Mad¹² (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) MAD¹² (Goldstein et al., 2011, Mathur et al., 2010) Mad^- (Weiss et al., 2010)
Name Synonym
Secondary FlyBase IDs

References ( 75 )

Generate a list of	All references relating to this allele ( 75 )

List References by type	Research paper ( 72 ) Supplementary material ( 2 ) Letter ( 1 )
Recent research papers ( 7 )
	Stinchfield et al., 2012, Development 139(15): 2721--2729 Fat facets deubiquitylation of Medea/Smad4 modulates interpretation of a Dpp morphogen gradient. [FBrf0219593] Eivers et al., 2011, Sci. Signal. 4(194): ra68 Phosphorylation of Mad Controls Competition Between Wingless and BMP Signaling. [FBrf0216411] Goldstein et al., 2011, Hum. Mol. Genet. 20(5): 894--904 SMAD signaling drives heart and muscle dysfunction in a Drosophila model of muscular dystrophy. [FBrf0212934] Liu et al., 2011, Dev. Growth Differ. 53(6): 822--841 Negative modulation of bone morphogenetic protein signaling by Dullard during wing vein formation in Drosophila. [FBrf0214664] Oh and Irvine, 2011, Dev. Cell 20(1): 109--122 Cooperative Regulation of Growth by Yorkie and Mad through bantam. [FBrf0212763] Quijano et al., 2011, Genetics 189(3): 809--824 Wg Signaling via Zw3 and Mad Restricts Self-Renewal of Sensory Organ Precursor Cells in Drosophila. [FBrf0216675] Rodriguez, 2011, PLoS ONE 6(4): e18418 Drosophila TIEG Is a Modulator of Different Signalling Pathways Involved in Wing Patterning and Cell Proliferation. [FBrf0213463] Show all research papers ...

Allele Dmel\Mad12

Allele Dmel\Mad¹²