C3147538T
C1601T
Q417term | Mad-PA; Q487term | Mad-PB
Q417term
Amino acid replacement: Q417term.
Nucleotide substitution: C1601T.
wing margin (with Mad11)
wing vein L2 (with Mad11)
wing vein L4 (with Mad11)
wing vein L5 (with Mad11)
Mad12/+ adults do not have any obvious wing phenotypes.
Mad12/+ third instar larvae have similar numbers of boutons to wild type.
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.
Heterozygotes climb sightly, but significantly, better than wild-type controls in a negative geotaxis assay.
Very few Mad12 mutant wing disc clones are recovered.
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.
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.
Homozygous cells in the morphogenetic furrow (in clones that encompass the morphogenetic furrow) can stil achieve proper apicobasal contraction.
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.
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.
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 average number of crystal cells per embryo is significantly reduced in homozygous stage 13-14 embryos compared to wild type.
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.
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.
Heterozygotes with Df(2L)C28 die as prepupae.
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.
Mad12 has lethal | recessive phenotype, non-enhanceable by lilliunspecified
Mad12 has decreased cell number | somatic clone phenotype, suppressible by Scer\GAL4FRT.Act5C/ykiS168A.UAS.Tag:V5
Mad12 has decreased cell number | somatic clone phenotype, suppressible by Scer\GAL4FRT.Act5C/ykiS250A.UAS.Tag:V5
Mad12/Mad[+] is a suppressor | partially of size defective | adult stage phenotype of Scer\GAL4A9, anchorGD3613
Mad12/Mad[+] is a suppressor | partially of visible | adult stage phenotype of Scer\GAL4A9, anchorGD3613
Mad12/Mad[+] is a suppressor of neuroanatomy defective | third instar larval stage phenotype of Ube3a35
Mad12/Mad[+] is a suppressor of neuroanatomy defective | third instar larval stage phenotype of brat2L-192-9/brat11
Mad12/Mad[+] is a suppressor of endocytosis defective | third instar larval stage phenotype of brat2L-192-9/brat11
Mad12/Mad[+] is a suppressor of locomotor behavior defective | adult stage phenotype of Scgδ840
Mad12 is a suppressor | partially of increased cell number | somatic clone phenotype of Scer\GAL4FRT.Act5C, ykiS168A.UAS.Tag:V5
Mad12 is a suppressor of increased cell number | somatic clone phenotype of Scer\GAL4FRT.Act5C, ykiS250A.UAS.Tag:V5
Mad12/Mad[+] is a suppressor of visible phenotype of Scer\GAL4A9, gbbUAS.cKa
Mad12/Mad[+] is a suppressor of visible phenotype of Scer\GAL4A9, dppUAS.cHa
Mad12 is a suppressor of visible phenotype of Scer\GAL4en-e16E, saxQ263D.UAS.cDa
Mad12/Mad[+] is a suppressor of visible phenotype of Scer\GAL4en-e16E, saxQ263D.UAS.cDa
Mad12 is a non-suppressor of planar polarity defective phenotype of Scer\GAL4hs.2sev, Tak1UAS.cMa
Mad12, Scer\GAL4A9, anchorGD3613 has size defective | adult stage phenotype
Mad12, Scer\GAL4A9, anchorGD3613 has visible | adult stage phenotype
Mad12/Mad[+], dpphr4 has partially lethal - majority die phenotype
Mad12/Mad[+], dpphr27 has partially lethal - majority die | maternal effect phenotype
Mad12/Mad[+], sax1 has lethal | dominant | maternal effect phenotype
Mad12/Mad[+], sax2 has lethal | dominant | maternal effect phenotype
Mad12/Mad[+], Smn73Ao has neuroanatomy defective | third instar larval stage phenotype
Mad12/Mad[+], Smnf01109 has neuroanatomy defective | third instar larval stage phenotype
Dcr-1Q1147X, Mad12/Mad[+] has decreased cell number | somatic clone | larval stage phenotype
Dcr-1Q1147X, Mad12/Mad[+] has decreased cell number | somatic clone | pupal stage phenotype
Dcr-1Q1147X/Dcr-1[+], Mad12 has decreased cell number | somatic clone | larval stage phenotype
DlUASp.cJa, Mad12, Scer\GAL4nos.PG has increased cell number phenotype
Mad12, Su(H)del47, ci94 has mitotic cell cycle defective | somatic clone | cell autonomous phenotype
Mad12, ci94 has mitotic cell cycle defective | somatic clone | cell autonomous phenotype
Mad12, Su(H)del47 has mitotic cell cycle defective | somatic clone | cell autonomous phenotype
Mad12, smo3 has decreased cell number | somatic clone phenotype
Mad12, dpphr27/dpp[+] has lethal | dominant | maternal effect phenotype
Madk00237/Mad12 has neuromuscular junction | third instar larval stage phenotype, non-enhanceable by Nrx-1273/Nrx-1273
Madk00237/Mad12 has terminal bouton | third instar larval stage phenotype, non-enhanceable by Nrx-1273/Nrx-1273
Madk00237/Mad12 has neuromuscular junction | third instar larval stage phenotype, non-enhanceable by Nlg1Δ46/Nlg1Δ46
Madk00237/Mad12 has terminal bouton | third instar larval stage phenotype, non-enhanceable by Nlg1Δ46/Nlg1Δ46
Mad12 has wing disc | somatic clone phenotype, suppressible by Scer\GAL4FRT.Act5C/ykiS168A.UAS.Tag:V5
Mad12 has wing disc | somatic clone phenotype, suppressible by Scer\GAL4FRT.Act5C/ykiS250A.UAS.Tag:V5
Mad12 is a non-enhancer | germline clone of germline cyst | germline clone phenotype of bamΔ86
Mad12/Mad[+] is a suppressor | partially of wing vein phenotype of Scer\GAL4A9, anchorGD3613
Mad12/Mad[+] is a suppressor | partially of wing phenotype of Scer\GAL4A9, anchorGD3613
Mad12/Mad[+] is a suppressor of NMJ bouton | supernumerary | third instar larval stage phenotype of Ube3a35
Mad12/Mad[+] is a suppressor of NMJ bouton | supernumerary | third instar larval stage phenotype of brat2L-192-9/brat11
Mad12 is a suppressor | partially of wing disc | somatic clone phenotype of ykiS168A.UAS.Tag:V5
Mad12 is a suppressor of wing disc | somatic clone phenotype of ykiS250A.UAS.Tag:V5
Mad12/Mad[+] is a suppressor of wing vein phenotype of Scer\GAL4A9, gbbUAS.cKa
Mad12/Mad[+] is a suppressor of wing phenotype of Scer\GAL4A9, dppUAS.cHa
Mad12/Mad[+] is a suppressor of wing phenotype of Scer\GAL4en-e16E, saxQ263D.UAS.cDa
Mad12/Mad[+] is a non-suppressor of adult heart phenotype of Scgδ840
Mad12 is a non-suppressor of germline cyst | germline clone phenotype of bamΔ86
Mad12 is a non-suppressor of eye phenotype of Scer\GAL4hs.2sev, Tak1UAS.cMa
Mad12 is a non-suppressor of eye photoreceptor cell phenotype of Scer\GAL4hs.2sev, Tak1UAS.cMa
Mad12 is a non-suppressor of phenotype of Src42ASu(Raf)1-1
Mad12, Scer\GAL4A9, anchorGD3613 has wing phenotype
Mad12/Mad[+], dpphr4 has embryo | maternal effect phenotype
Mad12/Mad[+], Smn73Ao has NMJ bouton phenotype
Mad12/Mad[+], Smnf01109 has NMJ bouton phenotype
Dcr-1Q1147X, Mad12/Mad[+] has female germline stem cell | somatic clone | larval stage phenotype
Dcr-1Q1147X, Mad12/Mad[+] has female germline stem cell | somatic clone | pupal stage phenotype
Dcr-1Q1147X/Dcr-1[+], Mad12 has female germline stem cell | somatic clone | larval stage phenotype
DlUASp.cJa, Mad12, Scer\GAL4nos.PG has female germline stem cell phenotype
Mad12, ci94 has eye disc | somatic clone | cell autonomous phenotype
Mad12, Su(H)del47 has eye disc | somatic clone | cell autonomous phenotype
Mad12, Su(H)del47, ci94 has eye disc | somatic clone | cell autonomous phenotype
MadB1/Mad12, brkXH has anterior-posterior compartment boundary of the wing disc | somatic clone phenotype
Mad12, smo3 has eye disc | somatic clone phenotype
Addition of Mad12/+ to animals expressing anchorGD3613 under the control of Scer\GAL4A9 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\GAL4A9 driver alone.
The progeny from Mad12/+ mothers and dpphr4/+ fathers present embryo ventralization in less than half of cases, and near lethality, as compared to controls; the progeny from Mad12/+ mothers and dpphr27/+ fathers, but not dpphr56/+ or dppe87/+ fathers, exhibit semi-lethality, as compared to controls.
The neuromuscular junction overgrowth phenotype (increased total number of boutons and increased number of satellite boutons) of brat11/brat2L-192-9 larvae is significantly suppressed by Mad12/+.
The reduced uptake of FM1-43 dye seen at the neuromuscular junction in brat11/brat2L-192-9 larvae is significantly suppressed by Mad12/+.
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/+.
A Mad12 mutant background partially suppresses the overgrowth seen when ykiS168A.Scer\UAS.T:SV5\V5 is expressed in wing disc clones under the control of Scer\GAL4Scer\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 ykiS250A.Scer\UAS.T:SV5\V5 is expressed in wing disc clones under the control of Scer\GAL4Scer\FRT.Act5C, returning the number of cells to control levels.
Homozygous Mad12 clones expressing cbtScer\UAS.cRa under the control of Scer\GAL4Act.PU do not survive in the wing pouch.
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 shgR69/+ 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/shgR69 transheterozygotes.
Mad12 mutant germline stem cells lacking one copy of Dcr-1Q1147X show clear stem cell maintenance defects when clones are generated during late larval/early pupal stages.
Dcr-1Q1147X 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 DlScer\UAS.P\T.cJa under the control of Scer\GAL4nos.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.
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.
Has no effect on the eye phenotype produced by activated arm constructs. (either armS44Y.GMR or armS56F.GMR).
Does not suppress the ability of Src42ASu(phl)1-1 to suppress the lethality of phl1/Y flies.
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.
Mad12/Mad1 is rescued by Scer\GAL4da.G32/MadUAS.N.YFP
Mad12 is rescued by MadαTub84B.PM
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.