|Feature type||allele||Associated gene||Dmel\Nrg|
|Also Known As||Nrg1, Nrg14, l(1)RA35|
|Allele class||amorphic allele - genetic evidence, loss of function allele|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Caused by aberration|
|Phenotype Manifest In|
axon & nerve
cell cortex & cortical cytoskeleton
dorsal multidendritic neuron ddaD & axon
dorsal multidendritic neuron ddaD & dendritic tree
dorsal multidendritic neuron ddaE & axon
dorsal multidendritic neuron ddaE & axon | somatic clone
embryonic epidermis & pleated septate junction
embryonic salivary gland & epithelial cell
lateral cord surface glia & nucleus
scolopidium & abdominal lateral pentascolopidial chordotonal organ lch5
septate junction & peripheral glial cell
Dextran dye can penetrate in the nerve cord after it has been injected into 22 hour mutant embryos, indicating a defect in the integrity of the nerve cord paracellular barrier.
In Nrgl4 homozygotes lateral pentascolopidial chordotonal organs have a disorganised morphology and rounded, rather than fusiform scolopales. Unlike in wild-type embryos, lateral pentascolopidial chordotonal organs in these embryos fail to exclude a 10kDa dextran dye. Ultrastructural analyses of peripheral nerves in these mutants at late stages of embryogenesis show that, while glial membranes are present around these nerves, the associated septate junctions linking inner and outer glial sheath cells are missing. and the inner and outer glial membranes are abnormally far apart. In addition, axons are often missing from bundles and replaced by protrusions from the inner glial cells.
29% of dorsal da neuron E (ddaE) and 38% of ddaD neurons show ectopic branches on their axons in Nrgl4 embryos. The dendritic branches of ddaD cover a smaller field and have fewer terminals than wild-type ddaD neurons. Nrgl4 ddaE clones form ectopic branches on their axons.
Nrg[l10]/Nrg[l4] females are viable at 18[o]C but are inviable at 25[o]C. Nrg[l4]/Nrg and Nrg[l4]/Nrg females show reduced sexual receptivity compared to wild-type controls when mated to wild-type males.
Fluorescent dye injected into the body cavity of Nrgl4 embryos penetrates into the nerve cord after the stage at which the nerve cord is sealed in wild-type embryos, showing that formation of the blood-brain barrier if defective. The surface glial cell shape and cortical actin distribution is only mildly disrupted.
In the epidermis of about 80% of stage 15 Nrgl4 mutant embryos, occasional clusters of septa are formed, often basal in their position.
Nrgl4 mutants exhibit disruption of the paracellular barrier in the embryonic salivary gland. In Nrgl4 homozygous mutants the adherens junction remains intact, with the regular spacing of plasma membranes maintained. However, the septae normally located between these membranes are reduced in number or absent. Nrgl4/Nrgl4 somatic clones generated in larvae (approx. 72 hours after egg laying) do not survive in adult tissues.
Homozygous embryos show a general disorganisation of the peripheral nervous system cell bodies. The aCC and SNb motoneurons often show a stalled phenotype, failing to extend normally, and SNb motoneurons sometimes show abnormal contacts with their targets.
|NOT Suppressor of|
|Phenotype Manifest In|
Nrgl4/Nrg[+] is an enhancer of dendrite | larval stage phenotype of NakdsRNA.Scer\UAS, Scer\GAL4elav-C155
Nrgl4/Nrg[+] is an enhancer of dendritic arborizing neuron | larval stage phenotype of NakdsRNA.Scer\UAS, Scer\GAL4elav-C155
|NOT Enhancer of|
|NOT Suppressor of|
Nrgl4, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF is a non-suppressor of eye photoreceptor cell phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, edScer\UAS.cBa
Nrg[l4] dominantly enhances the shortening of dendritic length and the reduction in the number of dendritic endpoints of dorsal dendritic arborisation neurons which is seen in larvae expressing Nak[dsRNA.Scer\UAS] under the control of Scer\GAL4[elav-C155].
The addition of Nrgl4/+ significantly suppresses the loss of cone cell phenotype seen in edScer\UAS.cBa, Scer\GAL4GMR.PF animals but has no effect on photoreceptor loss.
Nrgl4 Nrt5 double mutant embryos have a severe CNS phenotype, with thinning or complete interruption of the longitudinal connectives, and fusion of the commissures. Defects in Fas2 expressing neurons similar to those seen in Nrt5 single mutants are seen, although with much higher expressivity and penetrance. Axons of the dMP2 and MP1 neurons either stall or delay their extension considerably in 29% of cases. The ventral unpaired medial (VUM) neurons show misguidance phenotypes in 15% of cases, and anomalies in the trajectory of the SP1 axon are observed rarely. The pCC and vMP2 axons grow normally in most hemisegments, and the aCC and U neurons are normal. These defects are rescued by NrtScer\UAS.cSa expressed under the control of Scer\GAL4Mz1277. NrtrP668 Nrgl4 double mutant embryos have defects in Fas2 expressing axons. NrtR20F Nrgl4 embryos have essentially normal Fas2 expressing axons.
|Complementation & Rescue Data|
|Fails to complement|
|Stocks ( 2 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 10 )|
|Secondary FlyBase IDs|
|References ( 26 )|
|Generate a list of|
|List References by type|
|Recent research papers ( 1 )|