Allele Dmel\gcmN7-4
| General Information | |||
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| Symbol | Dmel\gcmN7-4 | Species | D. melanogaster |
| Name | FlyBase ID | FBal0045750 | |
| Feature type | allele | Associated gene | Dmel\gcm |
| Also Known As | glide/gcmN7-4, glideN7-4 | ||
Map (
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| Allele class | loss of function allele, amorphic allele - genetic evidence | ||
| Mutagen | diepoxybutane | ||
Recent Updates
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| Description |
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| FB2013_03 | |||
| FB2013_02 | |||
| All updates | Click here to see a list of all updates to this record from FB2010_08 and on. | ||
Nature of the Allele
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| Allele class | |||
| Mutagen | |||
| Mutations Mapped to the Genome | |||
Type Location Additional Notes References point mutation evidence=experimental pr_change=C93S na_change=G9581315C | |||
| Associated Sequence Data | |||
| DDBJ
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EMBL / GenBank | DNA sequence Protein sequence Name | ||
| UniProtKB/Swiss-Prot | |||
| UniProtKB/TrEMBL | |||
| Progenitor genotype | |||
| Nature of the lesion | Statement Reference Nucleotide substitution: G to C. Amino acid replacement: C93S. | ||
| Cytology | |||
Phenotypic Data
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Phenotypic Class
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Phenotype Manifest In
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abdominal lateral pentascolopidial chordotonal organ lch5 & scolopidial ligament cell & stage 16 embryo mesothoracic tergum & macrochaeta | supernumerary (with gcmPyx) wing & neuron | supernumerary | somatic clone wing & thecogen cell | somatic clone | |||
Detailed Description
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Statement Reference Homozygous gcm[N7-4] neuroblast clones consistently show a loss of glial cells. However, axonal patterns in those clones appear normal. Stage 17 homozygous embryos show a complete loss of the blood brain barrier (assayed by studying dextran uptake in living embryos). The lch5 chordotonal organs of stage 16 gcmN7-4 mutant lack scolopidial ligament cells and ligament attachment cells. The resulting lch5 chordotonal organs are not fully stretched and have shorter than normal cap cells. Mutant cells lack most glial cells. In the ventral cord these cells are completely absent, occasionally 3 cells on average are seen throughout the whole ventral cord, compared to the 60 cells per neuromere seen in wild-type. This leads to major defects in axonal guidance and fasciculation, resulting in an overall lack of nerve cord condensation. Mutant embryos show a loss of some longitudinal fascicles. Only one or two most medial of the three Fas2 staining fascicles are seen in a number of segments. Moreover some axons abnormally cross the midline. Other phenotypers are also seen. Longitudinal connectives are thin and interrupted, commissures appear fused and the ventral cord fails to condense. Lateral glial cells of the embryonic central nervous system are almost entirely absent. Longitudinal connective shows breaks in stage 15 embryos. The subperineurial glial cells are absent from the embryonic CNS. The number of glial cells along wing vein L1 is drastically reduced in homozygous clones that affect the anterior wing margin. The few glial cells that are seen in the mutant territory are not themselves mutant (these wild-type glial cells are likely to have differentiated distally to the clone and subsequently migrated into the clone). Clones that affect wing vein L3 show similar effects. No homozygous mutant glial cells are ever seen in homozygous clones in the wing. Supernumerary neurons are also seen along the L3 vein in wing clones. One supernumerary neuron is seen when the L3-1, L3-3 or L3-v sensory organ alone is mutated, whereas no supernumerary neurons are seen in clones affecting the L3-2 sensory organ. Homozygous embryos exhibit a drastic reduction in the number of glial cells. Longitudinal fibres are partially or completely interrupted in several segments and the peripheral nerves exhibit defects. Embryos exhibit severe pathway defects and almost completely lack glia. | |||
External Data
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Interactions
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Phenotypic Class
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Suppressor of | |||
Statement Reference gcmN7-4/gcm[+] is a suppressor of increased cell number | embryonic stage phenotype of ago3, slmb00295 | |||
Phenotype Manifest In
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Suppressed by | |||
Statement Reference | |||
NOT suppressed by | |||
Statement Reference | |||
Suppressor of | |||
Statement Reference | |||
Additional Comments
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Genetic Interactions
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Statement Reference slmb[00295], ago[3], gcm[N7-4] triple mutants results in the absence of almost all glia, as observed in gcm[N7-4] single mutants. One copy of gcm[N7-4] suppresses the increased glial cell number phenotype observed in slmb[00295], ago[3] double mutants. | |||
Xenogenetic Interactions
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Statement Reference | |||
Complementation & Rescue Data
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| Rescued by | |||
| Comments | The addition of gcm+t5.6 to gcmN7-4 animals leads to the rescue of subperineural glia (SPG), and peripheral glia (PG). The addition of gcm+t7.6 to gcmN7-4 animals leads to the rescue of subperineural glia (SPG), peripheral glia (PG), central body glia (CBG) and some longitudinal glia. The addition of gcm+t9.6 to gcmN7-4 animals leads to the rescue of most glia. The addition of gcm+t12.6 to gcmN7-4 animals leads to the rescue of almost all glia, though gaps are still present along the longitudinal connectives. The extent of rescue in all of these cases is dose dependent. | ||
Stocks
( 1 ) | |||
| Kyoto | |||
Notes on Origin
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| Discoverer | |||
External Crossreferences & Linkouts
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| Other Crossreferences | |||
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Synonyms & Secondary IDs
( 8 ) | |||
| Reported As | |||
| Symbol Synonym | gcm gcmN7-4 gcmN7.4 gcmN17 glide/gcmN7-4 l(2)N7-4 N7-4 | ||
| Name Synonym | |||
| Secondary FlyBase IDs | |||
References
( 24 ) | |||
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Recent research papers ( 2 ) | |||
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Recent Updates
External Crossreferences & Linkouts