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General Information
Symbol
Dmel\numb1
Species
D. melanogaster
Name
FlyBase ID
FBal0013186
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
nb1
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

P-element at 30B

Insertion components
P{hsneo}numb1
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

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

Detailed Description
Statement
Reference

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).

92% of heterozygous flies show rhythmic locomotor activity, with a period of 24.4 +/- 0.1 hours. 93% of numb1/numbSW flies show rhythmic locomotor activity, with a period of 24.6 +/- 0.1 hours.

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.

11% of hemisegments show an RP2 to RP2sib cell fate transformation in numb1/numb796 embryos. 23% of hemisegments show an RP2 to RP2sib cell fate transformation in numb1/Df(2L)30A-C embryos. numb1 insc22 double mutant embryos lack an eve-positive cell in the RP2 position in 98% of hemisegments.

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.

Many muscles are absent in numb1/numb2 embryos, particularly in the dorsal region. Most myocardial cells are formed. The number of eve-expressing pericardial cells is double that of wild-type.

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.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement
Reference
Enhancer of
Statement
Reference

numb[+]/numb1 is an enhancer of visible phenotype of NakUAS.cCa, Scer\GAL4sca-537.4

Other
Statement
Reference
Phenotype Manifest In
Suppressed by
Statement
Reference

numb1 has EW2 neuron phenotype, suppressible | partially by spdoG104/spdo[+]

numb1 has EW3 neuron phenotype, suppressible | partially by spdoG104/spdo[+]

numb1 has embryonic peripheral nervous system & neuron phenotype, suppressible by spdoH7

numb1 has embryonic peripheral nervous system & glial cell | supernumerary phenotype, suppressible by spdoH7

numb1 has phenotype, suppressible by Nl1N-ts1

Enhancer of
Statement
Reference
Suppressor of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference

The proportion of hemisegments with abnormal number of neurons in the asymmetrically dividing RP2 neural lineage is significantly increased in wtsx1/+;numb1/+ double heterozygous embryos compared to either of the single heterozygotes or wild type.

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.

In numb1, CycAC8LR1 double mutant embryos the formation of one non-myogenic eve expressing cell per segment is seen, apparently at the expense of DA1 muscle formation.

spdoG104/+ partially rescues formation of the EW2 and EW3 neurons in numb1 embryos.

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.

Embryos homozygous for numb1 and Nl1N-ts1 at the nonpermissive temperature exhibit neuronal overproduction.

numb1; ttkosn double mutant overproduces neurons, indistinguishable from ttkosn mutant.

Xenogenetic Interactions
Statement
Reference

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.

Complementation and Rescue Data
Fails to complement
Rescued by
Partially rescued by

numb796/numb1 is partially rescued by numb2del

Comments

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.

Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer

Stock contains a second-site deletion uncovering l(2)gl.

Comments
Comments

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.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (8)
References (56)