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General Information
Symbol
Dmel\spdoG104
Species
D. melanogaster
Name
FlyBase ID
FBal0090131
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Nucleotide change:

T30477235R

Amino acid change:

Y141term | spdo-PA

Reported amino acid change:

Y141term

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Amino acid replacement: Y141term.

Amino acid replacement: Y?term.

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 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

abdominal 1 basiconical sensillum dbd & embryonic glial cell

abdominal 2 basiconical sensillum dbd & embryonic glial cell

abdominal 3 basiconical sensillum dbd & embryonic glial cell

abdominal 4 basiconical sensillum dbd & embryonic glial cell

abdominal 5 basiconical sensillum dbd & embryonic glial cell

abdominal 6 basiconical sensillum dbd & embryonic glial cell

abdominal 7 basiconical sensillum dbd & embryonic glial cell

macrochaeta & mesothoracic tergum | somatic clone

Detailed Description
Statement
Reference

spdoG104 mutant MARCM clones in the type neuroblast lineages contain fewer intermediate progenitors and no primary neuroblasts, compared with control clones.

Mutant embryos have an increased number of "Ap" neurons in the NB5-6T lineage.

spdoG104 double mutant clones in the adult thorax exhibit external sensory cell loss and an excess of neurons.

The number of SELK neurons is normal in spdoG104 mutant animals.

Both vMP2 and dMP2 adopt odd-positive dMP2 fate and extend axons posteriorly in 75% of mutant embryos.

spdoG104 mutant embryos show a decrease in eve-positive pericardial cell number.

Both svp-positive pericardial cells per hemisegment normally adopt the cardioblast cell fate in spdoG104 mutant embryos.

spdoG104 somatic clones in the notum lack most bristles.

There appears to be a transformation in cell fate in the NB7-3 lineage in mutant embryos, such that GMC-1 produces two EW1 cells rather than a single EW1 cell and the GW cell (as assayed by molecular marker expression).

Each hemisegment in a spdoG104 homozygous embryo contains duplicated RP2 neurons, no U neurons and normal numbers of EL neurons.

Shows severe phenotype in trans to Df(3R)tll-g. spdo embryos display an approximate doubling of the number of neurons in the PNS, though the neurons are distributed among the four typical clusters in each segment and the overall morphology of the embryos is not affected. The two sibling cells of SOPIIb take the same, neuronal, fate. The md neurons are also increased in number, as are the dbd neurons. The dbd neuron is duplicated at the expense of its glial cell. For those neurons that have a lineage-related sibling, the non-neuronal cells adopt a neuronal fate in spdo mutants. Marker expression suggests that es neurons are transformed to md neurons in spdo mutants, similar to the transformation in N mutants. Lack of spdo causes a severe lack of glial cells in the CNS. The longitudinal tracts of the CNS are disrupted. The anterior and posterior commissures appear thicker and less condensed than normal.

The RP2 motoneuron duplicated at the expense of the RP2sib. The aCC motoneuron is duplicated at the expense of the pCC interneuron. The Usib fates are duplicated at the expense of the U neurons. The dMP2 is duplicated at the expense of the vMP2. No change was observable in EL cell fate. This phenotype is the reciprocal of that shown for numb mutants. Mutant embryos do not show excess neuroblast formation characteristic of N mutants. The phenotype of numb; spdo double mutants is identical to embryos lacking spdo alone. The eve+ EL neurons are completely rescued.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
NOT suppressed by
Suppressor of
Statement
Reference
Phenotype Manifest In
NOT Enhanced by
Suppressed by
NOT suppressed by
Statement
Reference
NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

spdoG104/spdo[+] is a suppressor | partially of EW2 neuron phenotype of numb1

spdoG104/spdo[+] is a suppressor | partially of EW3 neuron phenotype of numb1

NOT Suppressor of
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The neuroblast-depletion phenotype is still observed in the type II neuroblast lineages when spdoG104 mutant clones are induced in a α-Adaptin06694 mutant background.

spdoG104 suppresses the extra socket cell phenotype seen in AP-47SHE-11 thorax clones, instead producing the external sensory cell loss and excessive neurons seen in spdoG104 mutants alone.

numbTS4D.Scer\UAS induced ectopic neuroblast formation is abolished in spdoG104 mutant clones.

Expression of NScer\UAS.cBa under the control of Scer\GAL4pros.PMG in a spdoG104 mutant background restores vMP2 development in the majority of hemisegments.

Expression of fngScer\UAS.cKa under the control of Scer\GAL4pros.PMG in a spdoG104 mutant background restores vMP2 development in approximately 60% of hemisegments.

Expression of neurScer\UAS.cPa and DlScer\UAS.cLa under the control of Scer\GAL4twi.PG in a spdoG104 mutant background does not alter the number of eve-positive pericardial cells compared to spdoG104 mutant embryos.

Expression of NScer\UAS.cBa under the control of Scer\GAL4twi.PG in a spdoG104 background increases eve-positive pericardial cell number and decreases DA1 muscle numbers compared to embryos mutant for spdoG104.

Expression of NScer\UAS.cBa under the control of Scer\GAL4twi.PG in a numb2 and spdoG104 mutant background increases the number of eve-positive pericardial cells, and decreases the number of eve-positive DA1 muscles compared to embryos mutant for spdoG104. However, there is no change observed in this increased number of eve-positive pericardial cells between spdoG104 embryos also expressing NScer\UAS.cBa (under the control of Scer\GAL4twi.PG) alone, or in combination with numb2.

Expression of fngScer\UAS.cKa under the control of Scer\GAL4twi.PG in a spdoG104 background increases eve-positive pericardial cell number and decreases DA1 muscle numbers compared to embryos mutant for spdoG104.

Expression of fngScer\UAS.cKa under the control of Scer\GAL4twi.PG in a numb2 and spdoG104 mutant background increases the number of eve-positive pericardial cells, and decreases the number of eve-positive DA1 muscles compared to embryos mutant for spdoG104. However, there is no change observed in this increased number of eve-positive pericardial cells between spdoG104 embryos also expressing fngScer\UAS.cKa (under the control of Scer\GAL4twi.PG) alone, or in combination with numb2.

Co-expression of neurScer\UAS.cPa and DlScer\UAS.cLa under the control of Scer\GAL4twi.PG in a spdoG104 mutant background partially restore svp-positive pericardial cell development by promoting more asymmetric divisions of progenitor cells.

NScer\UAS.cBa over expression by Scer\GAL4twi.PG in a spdoG104 mutant background increases the frequency at which both daughter cells adopt the svp-positive pericardial cell fate.

fngScer\UAS.cKa over expression by Scer\GAL4twi.PG in a spdoG104 mutant background results in both daughter cells to adopting a svp-positive pericardial cell fate almost all of the time.

The bristle loss phenotype seen in spdoG104; sec153 double homozygous somatic clones in the notum is indistinguishable from that seen in single mutant somatic clones for either allele.

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

The transformation of neurons (RP2 to RP2sib; dMP2 to vMP2; Usib to U) seen in Nintra.GS.Scer\UAS; Scer\GAL4pros.PMG or NECN.Scer\UAS; Scer\GAL4pros.PMG embryos is unaffected by spdoG104/spdoG104. The neuronal transformation phenotypes seen in spdoG104 homozygous embryos are not suppressed by DlScer\UAS.cHa; Scer\GAL4pros.PMG.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Fails to complement
Partially rescued by
Comments

Expression of spdo1.T:Avic\GFP fully rescues Df(3R)ZZ27/spdoG104 mutant phenotypes.

Expression of spdo2.T:Avic\GFP fully rescues Df(3R)ZZ27/spdoG104 mutant phenotypes.

Expression of spdo3.T:Avic\GFP fully rescues Df(3R)ZZ27/spdoG104 mutant phenotypes.

Expression of spdoT:Avic\GFP.T:Disc\RFP-mCherry fully rescues Df(3R)ZZ27/spdoG104 mutant phenotypes.

Expression of spdoΔNm.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4insc-Mz1407 completely rescues the loss of type II neuroblasts in spdoG104 mutants.

Expression of spdoScer\UAS.cOa under the control of Scer\GAL4twi.PG in a spdoG104 mutant background rescues the loss of eve-positive pericardial cell numbers observed in spdoG104 mutant embryos.

spdoScer\UAS.cOa; Scer\GAL4sca-109-68 completely or almost completely rescues formation of U2 neurons and suppresses RP2 neuron duplication in spdoG104 homozygous embryos.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
References (26)