Allele Dmel\gcm^ΔP1

General Information
Symbol	Dmel\gcm^ΔP1	Species	D. melanogaster
Name		FlyBase ID	FBal0045751
Feature type	allele	Associated gene	Dmel\gcm
Also Known As	gcm^P1

Allele class	loss of function allele, amorphic allele - genetic evidence
Mutagen	Delta2-3
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class	amorphic allele - genetic evidence (Jones et al., 1995) loss of function allele (Chotard et al., 2005)
Mutagen	Delta2-3 (Jones et al., 1995)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype	gcm^rA87 (Jones et al., 1995)
Nature of the lesion	Statement Reference Small 3.5kb deletion that specifically removes the entire glial-specific transcript. (Jones et al., 1995)
Cytology
Phenotypic Data
Phenotypic Class
	developmental rate defective (Sepp et al., 2001) increased cell death \| recessive (Booth et al., 2000) lethal \| recessive (Jones et al., 1995) neuroanatomy defective (Kinrade and Hidalgo, 2004, Huelsmeier et al., 2007) neuroanatomy defective \| recessive \| somatic clone (Awasaki et al., 2008)
Phenotype Manifest In
	abdominal 1 lateral pentascolopidial chordotonal organ lch5 (Jones et al., 1995) abdominal 2 lateral pentascolopidial chordotonal organ lch5 (Jones et al., 1995) abdominal 3 lateral pentascolopidial chordotonal organ lch5 (Jones et al., 1995) abdominal 4 lateral pentascolopidial chordotonal organ lch5 (Jones et al., 1995) abdominal 5 lateral pentascolopidial chordotonal organ lch5 (Jones et al., 1995) abdominal 6 lateral pentascolopidial chordotonal organ lch5 (Jones et al., 1995) abdominal 7 lateral pentascolopidial chordotonal organ lch5 (Jones et al., 1995) abdominal segment 1 (Sepp et al., 2001) abdominal segment 2 (Sepp et al., 2001) abdominal segment 3 (Sepp et al., 2001) abdominal segment 4 (Sepp et al., 2001) abdominal segment 5 (Sepp et al., 2001) abdominal segment 6 (Sepp et al., 2001) aCC neuron (Sepp et al., 2001) central nervous system (Jones et al., 1995) dMP2 neuron (Hidalgo and Booth, 2000) embryonic/larval glial cell (Jones et al., 1995, Booth et al., 2000, Huelsmeier et al., 2007) embryonic/larval glial cell \| precursor (Kim et al., 1998) embryonic/larval nervous system (Sepp et al., 2001) embryonic/larval neuron (Booth et al., 2000) fascicle \| embryonic stage (Hidalgo and Booth, 2000) intermediate longitudinal fascicle (Kinrade and Hidalgo, 2004) intersegmental nerve (Sepp et al., 2001) lch3 neuron (Sepp et al., 2001) lch5 neuron (Sepp et al., 2001) longitudinal connective (Hidalgo and Booth, 2000, Kinrade et al., 2001) neuropil associated CNS glial cell \| somatic clone (Awasaki et al., 2008) presumptive embryonic/larval central nervous system (Shandala et al., 2003, Booth et al., 2000) segmental nerve pioneer neuron (Sepp et al., 2001) sensory neuron (Sepp et al., 2001) support cell of the dorsal bipolar dendritic cell (Jones et al., 1995) ventral abdominal cluster (Sepp et al., 2001) ventral thoracic cluster (Sepp et al., 2001)
Detailed Description
	Statement Reference If somatic recombination is induced at mid-first-instar larval stage to generate labelled homozygous gcm[ΔP1] 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 gcm[ΔP1] clones. (Awasaki et al., 2008) Lateral glial cells are absent in homozygous mutant embryos. (Huelsmeier et al., 2007) gcm^ΔP1 larvae do not show defective gliogenesis in the optic lobe. (Chotard et al., 2005) In gcm^ΔP1 stage 12.1 embryos the vMP2/pCC fascicle extends normally, but the dMP2/MP1 fascicle extends outwards straight to the muscle (88.2% penetrance). In gcm^ΔP1 mutants at stage 14 only the vMP2/pCC fascicle is formed. (Kinrade and Hidalgo, 2004) Mutant embryos show strong pathfinding defects of axons in the central nervous system. (Shandala et al., 2003) 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. (Alfonso and Jones, 2002) 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. (Kinrade et al., 2001) 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). (Sepp et al., 2001) 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. (Booth et al., 2000) 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. (Hidalgo and Booth, 2000) Nearly all presumptive glia fail to differentiate into glia in homozygous embryos. (Kim et al., 1998) 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. (Jones et al., 1995)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement Reference gcm^ΔP1, robo³ has neuroanatomy defective phenotype, enhanceable by lea^{Scer\UAS.T:Hsap\MYC}/Scer\GAL4^15J2 (Kinrade and Hidalgo, 2004) gcm^ΔP1 has neuroanatomy defective phenotype, enhanceable by lea^{Scer\UAS.T:Hsap\MYC}/Scer\GAL4^15J2 (Kinrade and Hidalgo, 2004) gcm^ΔP1 has neuroanatomy defective phenotype, enhanceable by robo³ (Kinrade and Hidalgo, 2004)
Enhancer of
Statement Reference gcm^ΔP1 is an enhancer of neuroanatomy defective phenotype of robo³ (Kinrade and Hidalgo, 2004)
Phenotype Manifest In
Enhanced by
Statement Reference gcm^ΔP1, robo³ has dMP2 neuron phenotype, enhanceable by lea^{Scer\UAS.T:Hsap\MYC}/Scer\GAL4^15J2 (Kinrade and Hidalgo, 2004) gcm^ΔP1, robo³ has vMP2 neuron phenotype, enhanceable by lea^{Scer\UAS.T:Hsap\MYC}/Scer\GAL4^15J2 (Kinrade and Hidalgo, 2004) gcm^ΔP1 has dMP2 neuron phenotype, enhanceable by robo³ (Kinrade and Hidalgo, 2004) gcm^ΔP1 has fascicle phenotype, enhanceable by robo³ (Kinrade and Hidalgo, 2004) gcm^ΔP1 has intermediate longitudinal fascicle phenotype, enhanceable by robo³ (Kinrade and Hidalgo, 2004) gcm^ΔP1 has longitudinal connective phenotype, enhanceable by Df(3L)H99 (Kinrade et al., 2001) gcm^ΔP1 has medial longitudinal fascicle phenotype, enhanceable by robo³ (Kinrade and Hidalgo, 2004) gcm^ΔP1 has MP1 neuron phenotype, enhanceable by robo³ (Kinrade and Hidalgo, 2004) gcm^ΔP1 has pCC neuron phenotype, enhanceable by robo³ (Kinrade and Hidalgo, 2004) gcm^ΔP1 has vMP2 neuron phenotype, enhanceable by robo³ (Kinrade and Hidalgo, 2004)
Enhancer of
Statement Reference gcm^ΔP1 is an enhancer of dMP2 neuron phenotype of robo³ (Kinrade and Hidalgo, 2004) gcm^ΔP1 is an enhancer of fascicle phenotype of robo³ (Kinrade and Hidalgo, 2004) gcm^ΔP1 is an enhancer of intermediate longitudinal fascicle phenotype of robo³ (Kinrade and Hidalgo, 2004) gcm^ΔP1 is an enhancer of medial longitudinal fascicle phenotype of robo³ (Kinrade and Hidalgo, 2004) gcm^ΔP1 is an enhancer of MP1 neuron phenotype of robo³ (Kinrade and Hidalgo, 2004) gcm^ΔP1 is an enhancer of pCC neuron phenotype of robo³ (Kinrade and Hidalgo, 2004) gcm^ΔP1 is an enhancer of vMP2 neuron phenotype of robo³ (Kinrade and Hidalgo, 2004)
Additional Comments
Genetic Interactions
Statement Reference In gcm^ΔP1 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 gcm^ΔP1 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 gcm^ΔP1 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 gcm^ΔP1 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 gcm^ΔP1 robo³ double mutant embryos in which the longitudinal fascicles either collapse along the midline (63.3% penetrance when visualised with Avic\GFP^{Scer\UAS.T:Hsap\Myr2}) or misroute severely towards the periphery and exit the central nervous system (13.3% penetrance when visualised with Avic\GFP^{Scer\UAS.T:Hsap\Myr2}). However, when MP2 axons in these embryos misexpress lea^{Scer\UAS.T:Hsap\MYC}, under the control of Scer\GAL4^15J2, 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 lea^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^15J2 in a gcm^ΔP1 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 lea^{Scer\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). (Kinrade and Hidalgo, 2004) Axonal extension along the longitudinal pathways is severely affected. Longitudinal connectives are virtually missing, and every segment has connectives crossing the midline. (Kinrade et al., 2001)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Comments
Stocks ( 0 )

Notes on Origin
Discoverer

External Crossreferences & Linkouts
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Synonyms & Secondary IDs ( 5 )
Reported As
Symbol Synonym	gcm^D1 (Pereanu et al., 2007) gcm^P1 (Shandala et al., 2003, Huelsmeier et al., 2007) gcm^ΔP1 (Chotard et al., 2005, Banerjee et al., 2006, Awasaki et al., 2008) gcm^ΔPI (Alfonso and Jones, 2002) gcm^δP1 (Jones et al., 2004)
Name Synonym
Secondary FlyBase IDs

References ( 21 )

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List References by type	Research paper ( 20 ) Review ( 1 )
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Allele Dmel\gcmΔP1

Allele Dmel\gcm^ΔP1