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FB2026_02
,
released June 18, 2026
Small 3.5kb deletion that specifically removes the entire glial-specific transcript.
abnormal neuroanatomy (with gcm1308)
abnormal neuroanatomy (with gcmG78)
In gcmΔP1 mutants, glial cells are absent from the embryonic central nervous system.
gcmΔP1 homozygous embryos exhibit a 93% reduction in the number of repo-positive glia.
gcmΔP1/gcmG78 transheterozygous embryos exhibit a 69% reduction in the number of repo-positive glia.
gcmΔP1/gcm1308 transheterozygous embryos exhibit a 76% reduction in the number of repo-positive glia.
If somatic recombination is induced at mid-first-instar larval stage to generate labelled homozygous gcmΔP1 mutant clones, the mutant cells are underrepresented compared with labelled wild-type controls in neuropil glia. In contrast, there is no significant difference in the cluster number or size of perineurial glia between control and gcmΔP1 clones.
Lateral glial cells are absent in homozygous mutant embryos.
gcmΔP1 larvae do not show defective gliogenesis in the optic lobe.
Mutant embryos show strong pathfinding defects of axons in the central nervous system.
A low level of glial cell development occurs in mutant embryos (there are an average of 2 repo-positive cells per hemisegment in the ventral nerve cord compared to 30 in wild type). These glial ells are typically, but not always, in the positions normally occupied by the longitudinal glia and nerve root glia.
In mutant embryos axon fascicles, which may normally extend along the longitudinal pathways, may cross the midline in at least one, usually several, segments. Longitudinal axon tracts are thinner.
In mutant embryos, axons stall in their approach to the CNS. Evidence for developmental stalling is seen, in which one segment in an embryo is more delayed compared to another segment beyond the normal range of segment-to-segment variation. Stalls in stage 14 embryo abdominal segments A1 to A6 are observed in 30% of hemisegments. Mutants have lch neuronal defects, where lch projections bifurcate just outside the CNS. Some lch neurons extend into the CNS along the anterior fascicle and the remainder migrate along a more posterior route. The aCC and ISN pioneer motor axons exit the CNS along abnormal trajectories compared to the highly stereotypes pathways observed in wild-type. In mutant embryos a disruption of the stereotypic pattern of fasciculation seen in sensory axons of the ventral and ventral' clusters is seen. In all hemisegments v cluster axons fail to carry out their early dorsal migrations. As a result, they fasciculate with their v' partners at more ventral positions. Also, sensory axons of the anterior fascicle stray anteriorly from motor bundles of the intersegmental nerve (ISN).
Axonal loss is seen in 56% of hemisegments with no glia in homozygous stage 16 embryos. Apoptotic neurons are seen in 89% of embryos, in which there are generally high numbers of apoptotic neurons (up to 16) frequently clustered in groups of 2-6.
The pCC growth cone extends and then stalls normally in mutant embryos, while the axon of dMP2 extends but may or may not contact vMP2. Eventually, the first fascicle does form at stage 13. The pCC/vMP2 and dMP2/MP1 fascicles are either missing or fused into a single thick fascicle in 93% of cases in stage 14 embryos. Longitudinal fascicles can be formed by stage 16/17, even if with fasciculation problems; longitudinal tracts are fuzzy, dramatically defasciculated, fused into a single fascicle or misrouted towards the muscle or across the midline.
Nearly all presumptive glia fail to differentiate into glia in homozygous embryos.
Embryos exhibit severe pathway defects and almost completely lack glia. Longitudinal glial are missing so longitudinal tracts are exposed to haemolymph and in some segments are thinner or missing. Transformation of the glial cell supporting the presumptive BD neuron of the PNS into a BD neuron. At the pentascolopidial lateral CH organ ligament support cells are transformed to CH neurons, at least 4 extra CH neurons are present.
gcmΔP1 has abnormal neuroanatomy phenotype, enhanceable by robo2UAS.Tag:MYC/Scer\GAL415J2
gcmΔP1, robo13 has abnormal neuroanatomy phenotype, enhanceable by robo2UAS.Tag:MYC/Scer\GAL415J2
gcmΔP1 has abnormal neuroanatomy phenotype, enhanceable by robo13
gcmΔP1 is an enhancer of abnormal neuroanatomy phenotype of robo13
gcmΔP1 has pCC neuron phenotype, enhanceable by robo13
gcmΔP1 has vMP2 neuron phenotype, enhanceable by robo13
gcmΔP1, robo13 has dMP2 neuron phenotype, enhanceable by robo2UAS.Tag:MYC/Scer\GAL415J2
gcmΔP1, robo13 has vMP2 neuron phenotype, enhanceable by robo2UAS.Tag:MYC/Scer\GAL415J2
gcmΔP1 has larval MP1 neuron phenotype, enhanceable by robo13
gcmΔP1 has dMP2 neuron phenotype, enhanceable by robo13
gcmΔP1 has intermediate longitudinal fascicle phenotype, enhanceable by robo13
gcmΔP1 has medial longitudinal fascicle phenotype, enhanceable by robo13
gcmΔP1 has larval longitudinal connective phenotype, enhanceable by Df(3L)H99
gcmΔP1 is an enhancer of larval MP1 neuron phenotype of robo13
gcmΔP1 is an enhancer of dMP2 neuron phenotype of robo13
gcmΔP1 is an enhancer of intermediate longitudinal fascicle phenotype of robo13
gcmΔP1 is an enhancer of medial longitudinal fascicle phenotype of robo13
gcmΔP1 is an enhancer of pCC neuron phenotype of robo13
gcmΔP1 is an enhancer of vMP2 neuron phenotype of robo13
In gcmΔP1 robo3 double mutants, some embryonic central nervous system Fas2-positive fascicles collapse across the midline, with full collapse observed in 12.5% of cases and collapse from one side of the embryo (i.e. one hemisegment) in 22.6% of cases. This phenotype is never observed in either mutant alone. In gcmΔP1 robo3 double mutants, 31% of Fas2-positive axons also misroute towards the muscle, which is a phenotype observed with less frequency in gcm mutants. In gcmΔP1 robo3 double mutant stage 12-13 embryos both dMP2/MP1 and vMP2/pCC fascicles are affected, as the vMP2/pCC fascicle collapses completely over the midline (100% penetrance) and the dMP2/MP1 fascicle either does not extend or misroutes towards the muscle (89%). In gcmΔP1 robo3 double mutant stage 14 embryos there is a synergistic effect on both fascicles: the vMP2/pCC fascicle is completely collapsed over the midline (96% penetrance) and the dMP2/MP1 fascicle is missing (97% penetrance). The effect of glial loss is excerbated in severe gcmΔP1 robo3 double mutant embryos in which the longitudinal fascicles either collapse along the midline (63.3% penetrance when visualised with Avic\GFPScer\UAS.T:Hsap\Myr2) or misroute severely towards the periphery and exit the central nervous system (13.3% penetrance when visualised with Avic\GFPScer\UAS.T:Hsap\Myr2). However, when MP2 axons in these embryos misexpress leaScer\UAS.T:Hsap\MYC, under the control of Scer\GAL415J2, in the MP2 neurons, they do not extend longitudinally. Instead, they either do not grow (36.6% penetrance) and remain stunted at the base of the commissures, or they leave the central nervous system and misroute towards the muscle (30.7% penetrance). Ectopic expression of leaScer\UAS.T:Hsap\MYC under the control of Scer\GAL415J2 in a gcmΔP1 mutant embryo results in three classes of anomaly: 1. lateral displacement in embryos that have a mild phenotype (the expressivity of the gcm phenotype is variable); 2. in embryos with a more severe phenotype, the axons that misexpress leaScer\UAS.T:Hsap\MYC project over a single, fused, Fas2-fascicle (35% penetrance); and 3. axons misroute to the muscle exiting the central nervous system (10% penetrance).
Axonal extension along the longitudinal pathways is severely affected. Longitudinal connectives are virtually missing, and every segment has connectives crossing the midline.