Nucleotide substitution: G to C. Amino acid replacement: C93S.
G9581315C
C93S | gcm-PA; C93S | gcm-PB
lethal (with Df(2L)30A-C)
mesothoracic tergum & macrochaeta | supernumerary (with gcmPyx)
wing & neuron | supernumerary | somatic clone
wing & thecogen cell | somatic clone
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).
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.
gcmN7-4/gcm[+] is a suppressor of increased cell number | embryonic stage phenotype of ago3, slmb00295
gcmN7-4 has embryonic maxillary segment phenotype, enhanceable by Dfd16
gcmN7-4 has embryonic mandibular segment phenotype, enhanceable by Dfd16
gcmN7-4 has CNS glial cell phenotype, suppressible by gcm2UAS.cKa/Scer\GAL4l(3)31-1-31-1
gcmN7-4 has subperineurial glial cell phenotype, non-suppressible by Scer\GAL4insc-Mz1407/NΔ242.UAS
gcmN7-4 is an enhancer of embryonic maxillary segment phenotype of Dfd16
gcmN7-4 is an enhancer of embryonic mandibular segment phenotype of Dfd16
gcmN7-4/gcm[+] is a suppressor of glial cell | embryonic stage phenotype of ago3, slmb00295
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.