P-element at 30B
embryonic peripheral nervous system & glial cell | supernumerary
embryonic peripheral nervous system & neuron
peripheral nervous system & neuron
sensory neuron & abdominal segment 1
sensory neuron & abdominal segment 2
sensory neuron & abdominal segment 3
sensory neuron & abdominal segment 4
sensory neuron & abdominal segment 5
sensory neuron & abdominal segment 6
sensory neuron & abdominal segment 7
sensory neuron & abdominal segment 8
sensory neuron & abdominal segment 9
sensory neuron & abdominal segment 10
sensory neuron & abdominal segment 11
sensory neuron & mesothoracic segment
sensory neuron & metathoracic segment
sensory neuron & prothoracic segment
serotonin neuron & embryonic abdominal segment 8
numb1 clones generated in the larval eye disc do not result in ommatidial rotation phenotypes - planar cell polarity defects.
numb1 mutant embryos show peripheral glial cell migratory defects.
In mutant embryos the number of myocardial cells in segments A2 to A7 is reduced from six to four per hemisegment. The reduction of myocardial cells is paralleled by an increase in eve expressing pericardial cells from two to four in 80% of hemisegments, accompanied by a loss of DA1 and DO2 muscles.
The development of the EW2 and EW3 neurons of the NB7-3 lineage is dramatically altered in numb1 mutants, but there is only a mild effect on EW1 neuron development. Novel apoptosis within the NB7-3 lineage is seen in the mutant embryos. The identity of the A8 serotonergic neuron in the central nervous system has a change of identity in mutant embryos, having expression characteristics similar to EW1 cells (rather than characteristics similar to EW2 cells, as occurs in wild-type embryos).
The dorsal bipolar dendritic (dbd) and dorsal dendritic arbor (dda) neurons are absent in mutant embryos.
In mutant embryos a loss of cardioblasts is seen. An increase in the number of eve expressing pericardial cells is seen.
In mutant embryos Malpighian tubule tip cells are missing except in about 8% embryos, where one or two of the four tubules are allocated normally.
In mutant embryos the DO5A muscle is duplicated at the expense of DA3A in most segments.
Muscles DA1 and DO1 are sometimes missing in homozygous embryos. The number of eve-expressing pericardial cells is increased compared to wild-type.
Stage 15 numb1 homozygous embryos have 3-8 neurons per hemisegment (compared to approximately 35 in wild-type).
Homozygous embryos have supernumerary lateral adult muscle precursors and lack segmental border muscles.
The RP2sib neuron, vMP2 neuron and U neuron are all duplicated at the expense of their siblings. The number of EL neurons is strongly reduced. pCC/aCC are unaffected. This phenotype is the reciprocal of that shown for spdo, Dl, N and mam embryos. The phenotype of numb; spdo double mutants is identical to embryos lacking spdo alone. The eve+ EL neurons are completely rescued.
Homozygous embryos have severe defects in the muscle pattern, including the loss of the dorsal set of muscles (including DA1) and the loss of muscles LL1 and VA3. Transformations of muscles LT4 towards LT3, and VA2 to VA1 are seen. Duplication of muscle DO5 is seen. Each of the six persistent twi-expressing adult muscle precursors in an abdominal hemisegment is duplicated. The duplication of the lateral adult precursors is associated with a loss of the segment border muscle, while the duplication of the three dorsal precursors is associated with the loss of dorsal muscles. Embryos have an excess of pericardial cells.
Embryos exhibit an absence of dorsal md neurons, md neurons, they either do not form, or lose their ability to express ct, or die.
Severe loss of neurons in the peripheral nervous system, the IIb cell adopts the fate of its sister IIa cell.
Homozygous embryos exhibit less than 10% of neurons than that of wild type.
dMP2 is transformed to the vMP2 fate. In numb1 Dl3 and numb1 Df(1)N-81k1 double mutants all MP2 neurons develop as dMP2.
Severe neuronal loss caused by transformation of both neurons and sheath cells into outer support cells.
Sensory organ related md neurons are usually absent or transformed into support cells.
In every segment dMP2 is transformed into a vMP2 neuron that lacks odd expression and has an anterior axon projection. The physical asymmetry of the MP2 division is not altered, only the fate of the daughter cells.
Disrupts differentiation of peripheral sensory neurons and deletion of several ventral longitudinal muscle fibres leaving one (muscle 6) or occasionally two in the embryo. Organisation of the CNS neuropil is unaltered. RP3 innervates muscle 6 in most embryos but can occasionally fail to synapse. RP1 fails to synapse with the only longitudinal fibre, instead continues to grow distally.
Homozygous embryos lack most of the sensory neurons of the peripheral nervous system, including the lateral nerve cell clusters of the abdominal segments.
Number of peripheral sensory neurons in a thoracic or abdominal hemisegment is severely reduced. The es neurons and glial cells are transformed into support cells, ch organ morphology is not maintained and md neurons are removed. One pleural external transverse muscle is missing and the oblique muscles that transverse each segment have abnormal arrangements.
apparently null since the neuronal phenotype of homozygotes is indistinguishable from that of hemizygotes.
numb1 has abnormal neuroanatomy | recessive | embryonic stage phenotype, suppressible | partially by Df(3R)Espl-X10/Df(3R)Espl-X10
numb1 has abnormal neuroanatomy phenotype, suppressible by spdoG104/spdo[+]
numb1 has abnormal neuroanatomy phenotype, suppressible by Scer\GAL4eg-Mz360/BacA\p35UAS.cHa
numb[+]/numb1 is an enhancer of visible phenotype of NakUAS.cCa, Scer\GAL4sca-537.4
numb[+]/numb1, wtsx1 has abnormal neuroanatomy | embryonic stage phenotype
numb1 has PNS neuron | embryonic stage phenotype, suppressible | partially by Df(3R)Espl-X10/Df(3R)Espl-X10
numb1 has EW2 neuron phenotype, suppressible by spdoG104/spdo[+]
numb1 has EW3 neuron phenotype, suppressible by spdoG104/spdo[+]
numb1 has abdominal dorsal bipolar neuron dbp | embryonic stage phenotype, suppressible by spdoH7
numb1 has neuron phenotype, suppressible by Mmus\NumblUAS.Tag:MYC/Scer\GAL4h-1J3
numb1 has neuron phenotype, suppressible by Scer\GAL4h-1J3/Mmus\NumbUAS.Tag:MYC
numb[+]/numb1 is an enhancer of wing sensillum phenotype of NakUAS.cCa, Scer\GAL4sca-537.4
numb[+]/numb1 is an enhancer of head sensillum phenotype of NakUAS.cCa, Scer\GAL4sca-537.4
numb[+]/numb1 is an enhancer of adult mesothoracic sensillum phenotype of NakUAS.cCa, Scer\GAL4sca-537.4
numb[+]/numb1 is a suppressor | partially of scutellar bristle | ectopic phenotype of Scer\GAL4ptc-559.1, spdoUAS.cOa
numb[+]/numb1, wtsx1 has larval RP2 motor neuron | embryonic stage phenotype
CycAC8LR1, numb1 has pericardial cell phenotype
CycAC8LR1, numb1 has muscle cell of A1-7 dorsal acute muscle 1 phenotype
CycAC8LR1, numb1 has muscle cell of mesothoracic dorsal acute muscle 1 phenotype
There is a slightly reduced number of ectopic scutellar bristles in flies expressing spdoScer\UAS.cOa under the control of Scer\GAL4nub-AC-62 in a numb1/+ background.
Dominantly enhances the adult external sensory organ phenotype produced by NakScer\UAS.cCa expressed under the control of Scer\GAL4sca-537.4.
spdoH7/spdoH7 largely suppresses the reduction in neuron numbers seen in stage 15 numb1 homozygous embryos. The phenotype of double mutants with spdoH7 does not resemble the numb1 phenotype, but the spdo mutant phenotype. In the absence of numb two dbd glial cells are seen. In double mutants with spdoH7, the dbd glial cell is missing, as for spdo mutants.
Scer\GAL4h-1J3-mediated expression of Mmus\NumblScer\UAS.cZa rescues the neuronal loss phenotype.
Scer\GAL4h-1J3 induced expression of Mmus\NumbScer\UAS.cZa rescues the neuronal phenotype of numb1 embryos and rescues the two dorsal most es organs in abdominal hemisegments to wild type.
numb1 is rescued by numbfTRG00025.sfGFP-TVPTBF
numb796/numb1 is rescued by numb+t19.5
numb+t19.5 efficiently rescues the lethality associated with numb1/numb796. Adult mechanosensory organ development is almost completely normal in the rescued flies.
numb1/numb796 flies rescued by numb2del show a widespread "double socket" phenotype, in which the shaft cell is transformed to a second socket cell.
Stock contains a second-site deletion uncovering l(2)gl.
On the basis of CNS phenotype numb alleles form a series: numb2 > numb4 > numb1/numb3.
P-element reversion demonstrates the P-element insertion is responsible for the mutant phenotype.