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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
glide/gcmN7-4, glideN7-4
Key Links
Nature of the Allele
Mutations Mapped to the Genome
Additional Notes
Nucleotide change:


Amino acid change:

C93S | gcm-PA; C93S | gcm-PB

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

Nucleotide substitution: G to C. Amino acid replacement: C93S.

Expression Data
Reporter Expression
Additional Information
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Modifiers Based on Experimental Evidence ( 0 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Disease-implicated variant(s)
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description

Homozygous gcmN7-4 neuroblast clones consistently show a loss of glial cells. However, axonal patterns in those clones appear normal.

Mutant embryos show a slight fusion of the maxillary and mandibular segments.

Stage 17 homozygous embryos show a complete loss of the blood brain barrier (assayed by studying dextran uptake in living embryos).

gcmN7-4 mutants exhibit a marked increase in the number of crystal cells. This phenotype is not enhanced when combined with Df(2L)200.

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.

In early stage 17 gcmN7-4/Df(2L)132 embryos, some ventral longitudinal muscles bypass their target tendon cells, cross the ventral midline and attach to muscles on the opposite side. This phenotype is not seen in gcmN7-4 homozygotes.

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.

Homozygous clones do not show bristle phenotypes. gcmPyx/gcmN7-4 adults have the same phenotype as gcmPyx/+ flies (extra macrochaetae on the notum).

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.

The number of neuroblasts increases in gcmN7-4 embryos. In stage 11 embryos, the first division of the 6-4 stem cell divides to produce 2 neuroblasts, instead of one neuroblast and a glioblast. In gcmN7-4/gcm34 embryos many glioblasts are transformed into neuroblasts.

One-third of hemocytes are missing in mutant embryos. gcmN7-4/gcm34 embryos have fewer hemocytes than normal, and the hemocytes show little migration compared to wild-type.

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
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressor of

gcmN7-4/gcm[+] is a suppressor of increased cell number | embryonic stage phenotype of ago3, slmb00295

Phenotype Manifest In
Enhanced by
Suppressed by
NOT suppressed by
Enhancer of
Suppressor of

gcmN7-4/gcm[+] is a suppressor of glial cell | embryonic stage phenotype of ago3, slmb00295

Additional Comments
Genetic Interactions

slmb00295, ago3, gcmN7-4 triple mutants results in the absence of almost all glia, as observed in gcmN7-4 single mutants. One copy of gcmN7-4 suppresses the increased glial cell number phenotype observed in slmb00295, ago3 double mutants.

The formation of the maxillary-mandibular boundary is completely lost in gcmN7-4, Dfd16 double mutant embryos.

Xenogenetic Interactions
Complementation and Rescue Data

gcm+t36.5 and gcmT:Zzzz\FLAG each fully rescue the lethality of gcmN7-4/Df(2L)132 animals.

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.

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Stocks (1)
Notes on Origin
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (9)
References (28)