FlyBase Allele Report: Dmel\Nrg[l4]

Nrg^l4/Nrg^l4 embryos display a synaptic defect similar to that seen in mir-8^Δ/mir-8^Δ (ISNb motor axons innervation defect at m6/7), though with reduced penetrance.

(Lu et al., 2014)

Synaptic retractions are seen in Nrg^l4 mutant third instar larval motorneuron clones at low frequency. Approximately 50% of axons end in "bulb-like" structures within nerve bundles and are not connected to a postsynaptic muscle. Large axonal swellings are also seen in the same axon proximal toward the cell body of the motoneuron. Similar rates of innervation are seen for all four major classes of motorneurons (SNc/d, SNb, SNa and ISN) as controls.

Flies expressing Nrg^+t25 in a Nrg^l4 mutant background establish a normal function of the adult Giant Fibre (GF)-Trochanteral Muscle (TTMn) circuit. There are no significant differences in average response latencies or following frequencies after a train of stimulations at 100 Hz when compared to wild type. No obvious morphological defects are seen at GF terminals.

Expression of Nrg^167ΔFIGQY in a Nrg^l4 mutant background does not result in a significant increase in synaptic retraction in third instar larvae compared to controls. NMJ length is similar to controls, as are bouton number and area.

Flies expressing Nrg^167ΔFIGQY in a Nrg^l4 mutant background establish a normal function of the adult Giant Fibre (GF)-Trochanteral Muscle (TTMn) circuit. There are no significant differences in average response latencies or following frequencies after a train of stimulations at 100 Hz when compared to wild type. No obvious morphological defects are seen at GF terminals.

Expression of Nrg^180ΔFIGQY in a Nrg^l4 mutant background does not result in a significant increase in synaptic retraction in third instar larvae compared to controls. NMJ length and bouton number are increased compared to controls. The bouton area is significantly reduced compared to controls.

Flies expressing Nrg^180ΔFIGQY in a Nrg^l4 mutant background are unable to establish a normal function of the Giant Fibre (GF)-Trochanteral Muscle (TTMn) circuit; there are significant increases in average response latencies and a decrease in following frequencies after a train of stimulations at 100Hz when compared to wild type. Morphological defects are seen at GF terminals. The GFs are present at the synaptic target area, however large areas of the synaptic terminals are either thinner or swollen and often contain large vacuole-like structures. Synaptic gap junctions are still present in animals that do not show any functional response.

Expression of Nrg^180YF in a Nrg^l4 mutant background does not result in a significant increase in synaptic retraction in third instar larvae compared to controls. NMJ length and bouton number are slightly increased compared to controls. The bouton area is not significantly different from controls.

Flies expressing Nrg^180YF in a Nrg^l4 mutant background are unable to establish a normal function of the Giant Fibre (GF)-Trochanteral Muscle (TTMn) circuit; there are significant increases in average response latencies and a decrease in following frequencies after a train of stimulations at 100 Hz when compared to wild type. Morphological defects are seen at GF terminals. The GFs are present at the synaptic target area, however large areas of the synaptic terminals are either thinner or swollen and often contain large vacuole-like structures. Synaptic gap junctions are still present in animals that do not show any functional response.

Expression of Nrg^180YD in a Nrg^l4 mutant background results in a significant increase in synaptic retraction in third instar larvae compared to controls. NMJ length and bouton number are increased compared to controls. The bouton area is not significantly different from controls.

Flies expressing Nrg^180YD in a Nrg^l4 mutant background are unable to establish a normal function of the Giant Fibre (GF)-Trochanteral Muscle (TTMn) circuit; there are significant increases in average response latencies and a decrease in following frequencies after a train of stimulations at 100 Hz when compared to wild type. Morphological defects are seen at GF terminals. The GFs are present at the synaptic target area, however large areas of the synaptic terminals are either thinner or swollen and often contain large vacuole-like structures. Synaptic gap junctions are still present in animals that do not show any functional response.

Expression of Nrg^180YA in a Nrg^l4 mutant background results in a significant increase in synaptic retraction in third instar larvae compared to controls. NMJ length and bouton number are increased compared to controls. The bouton area is not significantly different from controls.

Flies expressing Nrg^180YA in a Nrg^l4 mutant background are unable to establish a normal function of the Giant Fibre (GF)-Trochanteral Muscle (TTMn) circuit; there are significant increases in average response latencies and a decrease in following frequencies after a train of stimulations at 100 Hz when compared to wild type. Morphological defects are seen at GF terminals. The GFs are present at the synaptic target area, however large areas of the synaptic terminals are either thinner or swollen and often contain large vacuole-like structures. Synaptic gap junctions are still present in animals that do not show any functional response.

Expression of Nrg^180ΔC in a Nrg^l4 mutant background results in a significant increase in synaptic retraction in third instar larvae compared to controls. NMJ length is increased compared to controls. NMJ length and bouton number are increased compared to controls. The bouton area is significantly reduced compared to controls.

Expression of Nrg^180ΔPDZ in a Nrg^l4 mutant background does not result in a significant increase in synaptic retraction in third instar larvae compared to controls. NMJ length is similar to controls, as are bouton number and area.

Flies expressing Nrg^180ΔPDZ in a Nrg^l4 mutant background establish a normal function of the adult Giant Fibre (GF)-Trochanteral Muscle (TTMn) circuit. There are no significant differences in average response latencies or following frequencies after a train of stimulations at 100 Hz when compared to wild type. No obvious morphological defects are seen at GF terminals.

Flies expressing Nrg^180ΔC in a Nrg^l4 mutant background are unable to establish a normal function of the Giant Fibre (GF)-Trochanteral Muscle (TTMn) circuit; there are significant increases in average response latencies and a decrease in following frequencies after a train of stimulations at 100 Hz when compared to wild type. Morphological defects are seen at GF terminals. The GFs are present at the synaptic target area, however large areas of the synaptic terminals are either thinner or swollen and often contain large vacuole-like structures. Synaptic gap junctions are still present in animals that do not show any functional response.

(Enneking et al., 2013)

The synaptic Giant Fibre (GF) to Trochanteral Muscle (TTMn) connection is severely weakened in flies expressing Nrg^180ΔFIGQY in a Nrg^l4 mutant background. The GF synapse is unable to follow multiple stimuli given at 100 Hz in a 1:1 ratio and Response Latency is increased. Synaptic terminals are morphologically defective and reduced in size.

(Kudumala et al., 2013)

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.

(Hijazi et al., 2009)

In Nrg^l4 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.

(Banerjee et al., 2006)

29% of dorsal da neuron E (ddaE) and 38% of ddaD neurons show ectopic branches on their axons in Nrg^l4 embryos. The dendritic branches of ddaD cover a smaller field and have fewer terminals than wild-type ddaD neurons.

Nrg^l4 ddaE clones form ectopic branches on their axons.

(Yamamoto, 2006)

Nrg^l10/Nrg^l4 females are viable at 18[o]C but are inviable at 25[o]C.

Nrg^l4/Nrg⁸⁴⁹ and Nrg^l4/Nrg⁸⁹² females show reduced sexual receptivity compared to wild-type controls when mated to wild-type males.

(Carhan et al., 2005)

Fluorescent dye injected into the body cavity of Nrg^l4 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.

(Schwabe et al., 2005)

In the epidermis of about 80% of stage 15 Nrg^l4 mutant embryos, occasional clusters of septa are formed, often basal in their position.

(Faivre-Sarrailh et al., 2004)

Nrg^l4 mutants exhibit disruption of the paracellular barrier in the embryonic salivary gland. In Nrg^l4 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. Nrg^l4/Nrg^l4 somatic clones generated in larvae (approx. 72 hours after egg laying) do not survive in adult tissues.

(Genova and Fehon, 2003)

Fas2 expressing axons appear normal in homozygous embryos.

(Speicher et al., 1998)

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.

(Hall and Bieber, 1997)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Nrg^l4 has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by Fas3^A142/Fas3^A142

(Lu et al., 2014)

Suppressed by

Statement

Reference

Nrg^l4 has abnormal neuroanatomy | somatic clone | P-stage phenotype, suppressible by Scer\GAL4^ppk.PU/Rab5^S43N.UAS

(Zhang et al., 2014)

Nrg^180ΔFIGQY, Nrg^l4 has abnormal neurophysiology | adult stage phenotype, suppressible by Hsap\L1CAM^RSLE-.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has abnormal neuroanatomy | adult stage phenotype, suppressible by Hsap\L1CAM^RSLE-.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has abnormal neurophysiology | adult stage phenotype, suppressible by Hsap\L1CAM^L120V.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has abnormal neuroanatomy | adult stage phenotype, suppressible by Hsap\L1CAM^L120V.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has abnormal neurophysiology | adult stage phenotype, suppressible by Hsap\L1CAM^H38.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has abnormal neuroanatomy | adult stage phenotype, suppressible by Hsap\L1CAM^H38.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has abnormal neurophysiology | adult stage phenotype, suppressible | partially by Hsap\L1CAM^C264Y.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has abnormal neuroanatomy | adult stage phenotype, suppressible | partially by Hsap\L1CAM^C264Y.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has abnormal neurophysiology | adult stage phenotype, suppressible by Hsap\L1CAM^4A.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has abnormal neuroanatomy | adult stage phenotype, suppressible by Hsap\L1CAM^4A.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

NOT suppressed by

Statement

Reference

Nrg^180ΔFIGQY, Nrg^l4 has abnormal neuroanatomy | adult stage phenotype, non-suppressible by Hsap\L1CAM^UAS.1180/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has abnormal neurophysiology | adult stage phenotype, non-suppressible by Hsap\L1CAM^H1.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has abnormal neuroanatomy | adult stage phenotype, non-suppressible by Hsap\L1CAM^H1.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has abnormal neurophysiology | adult stage phenotype, non-suppressible by Hsap\L1CAM^H210Q.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has abnormal neuroanatomy | adult stage phenotype, non-suppressible by Hsap\L1CAM^H210Q.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has abnormal neurophysiology | adult stage phenotype, non-suppressible by Hsap\L1CAM^R184Q.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has abnormal neuroanatomy | adult stage phenotype, non-suppressible by Hsap\L1CAM^R184Q.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has abnormal neurophysiology | adult stage phenotype, non-suppressible by Hsap\L1CAM^UAS.1180/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Enhancer of

Statement

Reference

Nrg^l4/Nrg[+] is an enhancer of abnormal neuroanatomy | larval stage phenotype of Nak^RNAi.UAS, Scer\GAL4^elav-C155

(Yang et al., 2011)

NOT Suppressor of

Statement

Reference

Nrg^l4 is a non-suppressor of abnormal neuroanatomy | embryonic stage phenotype of fzr^ie28

(Silies and Klämbt, 2010)

Phenotype Manifest In

Enhanced by

Statement

Reference

Nrg^l4 has larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype, enhanceable by Fas3^A142/Fas3^A142

(Lu et al., 2014)

Nrg^l4 has embryonic/larval neuromuscular junction | embryonic stage phenotype, enhanceable by Fas3^A142/Fas3^A142

(Lu et al., 2014)

Nrg^l4 has axon | embryonic stage phenotype, enhanceable by Fas3^A142/Fas3^A142

(Lu et al., 2014)

Suppressed by

Statement

Reference

Nrg^l4 has dendritic tree | somatic clone | P-stage phenotype, suppressible by Scer\GAL4^ppk.PU/Rab5^S43N.UAS

(Zhang et al., 2014)

Nrg^l4 has larval dorsal multidendritic neuron ddaC | somatic clone | P-stage phenotype, suppressible by Scer\GAL4^ppk.PU/Rab5^S43N.UAS

(Zhang et al., 2014)

Nrg^180ΔFIGQY, Nrg^l4 has giant fiber neuron | adult stage phenotype, suppressible by Hsap\L1CAM^RSLE-.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has adult neuromuscular junction phenotype, suppressible by Hsap\L1CAM^RSLE-.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has giant fiber neuron | adult stage phenotype, suppressible by Hsap\L1CAM^L120V.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has adult neuromuscular junction | adult stage phenotype, suppressible by Hsap\L1CAM^L120V.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has giant fiber neuron | adult stage phenotype, suppressible by Hsap\L1CAM^H38.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has adult neuromuscular junction | adult stage phenotype, suppressible by Hsap\L1CAM^H38.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has giant fiber neuron | adult stage phenotype, suppressible | partially by Hsap\L1CAM^C264Y.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has adult neuromuscular junction | adult stage phenotype, suppressible | partially by Hsap\L1CAM^C264Y.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has giant fiber neuron | adult stage phenotype, suppressible by Hsap\L1CAM^4A.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has adult neuromuscular junction | adult stage phenotype, suppressible by Hsap\L1CAM^4A.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

NOT suppressed by

Statement

Reference

Nrg^180ΔFIGQY, Nrg^l4 has giant fiber neuron | adult stage phenotype, non-suppressible by Hsap\L1CAM^UAS.1180/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has adult neuromuscular junction phenotype, non-suppressible by Hsap\L1CAM^UAS.1180/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has giant fiber neuron | adult stage phenotype, non-suppressible by Hsap\L1CAM^H1.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has adult neuromuscular junction | adult stage phenotype, non-suppressible by Hsap\L1CAM^H1.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has giant fiber neuron | adult stage phenotype, non-suppressible by Hsap\L1CAM^H210Q.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has adult neuromuscular junction | adult stage phenotype, non-suppressible by Hsap\L1CAM^H210Q.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has giant fiber neuron | adult stage phenotype, non-suppressible by Hsap\L1CAM^R184Q.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Nrg^180ΔFIGQY, Nrg^l4 has adult neuromuscular junction | adult stage phenotype, non-suppressible by Hsap\L1CAM^R184Q.UAS/Scer\GAL4^shot-OK307

(Kudumala et al., 2013)

Enhancer of

Statement

Reference

Nrg^l4/Nrg[+] is an enhancer of dendritic arborizing neuron | larval stage phenotype of Nak^RNAi.UAS, Scer\GAL4^elav-C155

(Yang et al., 2011)

Nrg^l4/Nrg[+] is an enhancer of dendrite | larval stage phenotype of Nak^RNAi.UAS, Scer\GAL4^elav-C155

(Yang et al., 2011)

Nrg^l4 is an enhancer of larval longitudinal connective phenotype of Nrt⁵

(Speicher et al., 1998)

Nrg^l4 is an enhancer of symmetrical commissure phenotype of Nrt⁵

(Speicher et al., 1998)

Nrg^l4 is an enhancer of dMP2 neuron phenotype of Nrt⁵

(Speicher et al., 1998)

Nrg^l4 is an enhancer of larval MP1 neuron phenotype of Nrt⁵

(Speicher et al., 1998)

Nrg^l4 is an enhancer of SP1 neuron phenotype of Nrt⁵

(Speicher et al., 1998)

Nrg^l4 is an enhancer of axon | embryonic stage phenotype of Nrt¹

(Speicher et al., 1998)

NOT Enhancer of

Statement

Reference

Nrg^l4, Scer\GAL4^GMR.PF is a non-enhancer of eye photoreceptor cell phenotype of Scer\GAL4^GMR.PF, ed^UAS.cBa

(Islam et al., 2003)

Suppressor of

Statement

Reference

Nrg^l4, Scer\GAL4^GMR.PF is a suppressor of cone cell phenotype of Scer\GAL4^GMR.PF, ed^UAS.cBa

(Islam et al., 2003)

NOT Suppressor of

Statement

Reference

Nrg^l4 is a non-suppressor of glial cell phenotype of fzr^ie28

(Silies and Klämbt, 2010)

Nrg^l4, Scer\GAL4^GMR.PF is a non-suppressor of eye photoreceptor cell phenotype of Scer\GAL4^GMR.PF, ed^UAS.cBa

(Islam et al., 2003)

Other

Statement

Reference

Nrg^l4, Nrt^rP668 has axon | embryonic stage phenotype

(Speicher et al., 1998)

Additional Comments

Genetic Interactions

Statement

Reference

Fas3^A142/Fas3^A142 significantly enhances intersegmental nerve branch ISNb motor axon innervation defects (at m6/7) seen in Nrg^l4/Nrg^l4 embryos.

(Lu et al., 2014)

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.

(Yang et al., 2011)

The glial cell migration defects of rap^ie28 embryos are not suppressed by Nrg^l4.

(Silies and Klämbt, 2010)

The addition of Nrg^l4/+ significantly suppresses the loss of cone cell phenotype seen in ed^Scer\UAS.cBa, Scer\GAL4^GMR.PF animals but has no effect on photoreceptor loss.

(Islam et al., 2003)

Nrg^l4 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 Nrt^Scer\UAS.cSa expressed under the control of Scer\GAL4^Mz1277. Nrt^rP668 Nrg^l4 double mutant embryos have defects in Fas2 expressing axons. Nrt^R20F Nrg^l4 embryos have essentially normal Fas2 expressing axons.

(Speicher et al., 1998)

Xenogenetic Interactions

Statement

Reference

Expression of Hsap\L1CAM^{RSLE-.Scer\UAS} under the control of Scer\GAL4^OK307 suppresses the Giant Fibre (GF)-Trochanteral Muscle (TTM) synaptic defects seen in flies expressing Nrg^180ΔFIGQY in a Nrg^l4 mutant background; there is an increase in following frequencies after a train of stimulations at 100Hz and response latency is decreased. All flies observed show TTM responses upon GF stimulation. The morphology of the synaptic terminals is restored.

Expression of Hsap\L1CAM^{Scer\UAS.1180} under the control of Scer\GAL4^OK307 does not suppress the Giant Fibre (GF)-Trochanteral Muscle (TTM) synapse functional and morphological defects seen in flies expressing Nrg^180ΔFIGQY in a Nrg^l4 mutant background.

Expression of Hsap\L1CAM^H1.Scer\UAS under the control of Scer\GAL4^OK307 does not suppress the Giant Fibre (GF)-Trochanteral Muscle (TTM) synapse functional and morphological defects seen in flies expressing Nrg^180ΔFIGQY in a Nrg^l4 mutant background.

Expression of Hsap\L1CAM^{H210Q.Scer\UAS} under the control of Scer\GAL4^OK307 does not suppress the Giant Fibre (GF)-Trochanteral Muscle (TTM) synapse functional and morphological defects seen in flies expressing Nrg^180ΔFIGQY in a Nrg^l4 mutant background.

Expression of Hsap\L1CAM^{R184Q.Scer\UAS} under the control of Scer\GAL4^OK307 does not suppress the Giant Fibre (GF)-Trochanteral Muscle (TTM) synapse functional and morphological defects seen in flies expressing Nrg^180ΔFIGQY in a Nrg^l4 mutant background.

Expression of Hsap\L1CAM^{L120V.Scer\UAS} under the control of Scer\GAL4^OK307 significantly suppresses the Giant Fibre (GF)-Trochanteral Muscle (TTM) synapse functional and morphological defects seen in flies expressing Nrg^180ΔFIGQY in a Nrg^l4 mutant background.

Expression of Hsap\L1CAM^H38.Scer\UAS under the control of Scer\GAL4^OK307 significantly suppresses the Giant Fibre (GF)-Trochanteral Muscle (TTM) synapse functional and morphological defects seen in flies expressing Nrg^180ΔFIGQY in a Nrg^l4 mutant background.

Expression of Hsap\L1CAM^{C264Y.Scer\UAS} under the control of Scer\GAL4^OK307 significantly suppresses the Giant Fibre (GF)-Trochanteral Muscle (TTM) synapse functional and morphological defects seen in flies expressing Nrg^180ΔFIGQY in a Nrg^l4 mutant background. Half of the tested GF to TTM connections are functionally normal, while the other half are functionally impaired.

Expression of Hsap\L1CAM^4A.Scer\UAS under the control of Scer\GAL4^OK307 significantly suppresses the Giant Fibre (GF)-Trochanteral Muscle (TTM) synapse functional and morphological defects seen in flies expressing Nrg^180ΔFIGQY in a Nrg^l4 mutant background.

(Kudumala et al., 2013)

Complementation and Rescue Data

Fails to complement

Nrg^ibx

(Carhan et al., 2005)

Nrg⁸⁹²

(Carhan et al., 2005)

Nrg^l10

(Hall and Bieber, 1997)

Nrg^l7

(Hall and Bieber, 1997)

Rescued by

Nrg^l4 is rescued by Nrg^ΔIg3-4

(Zhang et al., 2014)

Nrg^l4 is rescued by Nrg^+t25

(Zhang et al., 2014)

Nrg^l4 is rescued by Nrg^180ΔC

(Zhang et al., 2014)

Nrg^l4 is rescued by Nrg^180ΔFIGQY

(Zhang et al., 2014)

Nrg^l4 is rescued by Nrg^180ΔPDZ

(Zhang et al., 2014)

Nrg^l4 is rescued by Nrg^UAS.180.cEa/Nrg^180YF/Scer\GAL4^shot-OK307

(Enneking et al., 2013)

Nrg^l4 is rescued by Nrg^UAS.180.cEa/Nrg^180YA/Scer\GAL4^shot-OK307

(Enneking et al., 2013)

Nrg^l4 is rescued by Nrg^UAS.180.cEa/Nrg^180ΔFIGQY/Scer\GAL4^shot-OK307

(Enneking et al., 2013)

Nrg^l4 is rescued by Nrg^+t25

(Enneking et al., 2013)

Nrg^l4 is rescued by Nrg^167ΔFIGQY

(Enneking et al., 2013)

Partially rescued by

Nrg^l4 is partially rescued by Nrg^{180ΔICD.UAS.Tag:FLAG}/Scer\GAL4^ppk.PU

(Zhang et al., 2014)

Nrg^l4 is partially rescued by Nrg^180ΔFIGQY

(Enneking et al., 2013)

Not rescued by

Nrg^l4 is not rescued by Nrg^ΔIg3-4

(Enneking et al., 2013)

Comments

Expression of Nrg^+t25 fully rescues Nrg^l4 mutant embryonic lethality. The axonal and NMJ defects seen in Nrg^l4 mutant larval motorneuron clones are also fully rescued and similar rates of innervation are seen for all four major classes of motorneurons (SNc/d, SNb, SNa and ISN) as controls.

Expression of Nrg^167ΔFIGQY fully rescues Nrg^l4 mutant embryonic lethality. The axonal and NMJ defects seen in Nrg^l4 mutant larval motorneuron clones are also fully rescued and similar rates of innervation are seen for all four major classes of motorneurons (SNc/d, SNb, SNa and ISN) as controls.

Expression of Nrg^180ΔFIGQY fully rescues Nrg^l4 mutant embryonic lethality. The axonal and NMJ defects seen in Nrg^l4 mutant larval motorneuron clones are only partially rescued and similar rates of innervation are seen for all four major classes of motorneurons (SNc/d, SNb, SNa and ISN) as controls.

Expression of Nrg^ΔIg3-4 fails to rescue Nrg^l4 mutant embryonic lethality. The axonal and NMJ defects seen in Nrg^l4 mutant larval motorneuron clones are also not rescued and similar rates of innervation are seen for all four major classes of motorneurons (SNc/d, SNb, SNa and ISN) as controls.

Expression of Nrg^{Scer\UAS.180.cEa} under the control of Scer\GAL4^OK307 significantly rescues the electrophysiological and morphological defects seen at the adult Giant Fibre (GF)-Trochanteral Muscle (TTMn) synapse when Nrg^180YF is expressed in a Nrg^l4 mutant background. Rescue is also seen when Nrg^{Scer\UAS.180.cEa} is expressed presynaptically (Scer\GAL4^c17) or postsynaptically (Scer\GAL4^{shakB.lethal.4.1}), and also when Scer\GAL4^c42.2 is expressed presynaptically only after the connection between the GF and the TTMn has been established.

Expression of Nrg^{Scer\UAS.180.cEa} under the control of Scer\GAL4^OK307 significantly rescues the electrophysiological and morphological defects seen at the adult Giant Fibre (GF)-Trochanteral Muscle (TTMn) synapse when Nrg^180YA is expressed in a Nrg^l4 mutant background. Rescue is also seen when Nrg^{Scer\UAS.180.cEa} is expressed presynaptically (Scer\GAL4^c17) or postsynaptically (Scer\GAL4^{shakB.lethal.4.1}), but not when Scer\GAL4^c42.2 is expressed presynaptically only after the connection between the GF and the TTMn has been established.

Expression of Nrg^{Scer\UAS.180.cEa} under the control of Scer\GAL4^OK307 significantly rescues the electrophysiological and morphological defects seen at the adult Giant Fibre (GF)-Trochanteral Muscle (TTMn) synapse when Nrg^180ΔFIGQY is expressed in a Nrg^l4 mutant background. Rescue is also seen when Nrg^{Scer\UAS.180.cEa} is expressed presynaptically (Scer\GAL4^c17) or postsynaptically (Scer\GAL4^{shakB.lethal.4.1}), but not when Scer\GAL4^c42.2 is expressed presynaptically only after the connection between the GF and the TTMn has been established.

(Enneking et al., 2013)

Nrg^l4 fails to complement the reduced female receptivity phenotype of Nrg^ibx and of Nrg⁸⁹².

Nrg^l4 fails to complement the reduced female receptivity phenotype of Nrg⁸⁹².

(Carhan et al., 2005)

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Mutant

Wild-type

Stocks (3)

Bloomington

5708

Nrg^l4/FM7c

36284

y¹ w^* Fas2^EB112 Nrg^l4 P{FRT(w^hs)}101/FM7a; Dr¹/TM3, Sb¹

Kyoto

108384

Nrg^l4/FM7c

Notes on Origin

Discoverer

Lefevre.

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (10)

Reported As

Symbol Synonym

Nrg¹⁴

(Luedke et al., 2024, Resnik-Docampo et al., 2021, Godenschwege et al., 2006, Read et al., 2005, Schwabe et al., 2005, Genova and Fehon, 2003)

Nrg¹

(Goossens et al., 2011, Faivre-Sarrailh et al., 2004)

Nrg^l4

(Popodi et al., 2010-, Mao and Freeman, 2009)

RA35

(Eeken et al., 1985)

l(1)7Fa⁴

l(1)RA35

(Spradling et al., 1994, Hortsch and Goodman, 1993, Bieber et al., 1989)

nrg¹⁴

(Kaur et al., 2019, Kakad et al., 2018, Siegenthaler et al., 2015, Lu et al., 2014, Zhang et al., 2014, Enneking et al., 2013, Kudumala et al., 2013, Yang et al., 2011, Hijazi et al., 2009, Stork et al., 2009, Moyer and Jacobs, 2008, Stork et al., 2008)

nrg¹

(Clements et al., 2021, Banerjee et al., 2006, Yamamoto, 2006, Carhan et al., 2005, Islam et al., 2003, Jenkins et al., 2001, Bouley et al., 2000, Speicher et al., 1998, Hall and Bieber, 1997)

nrg^I4

(Deligiannaki et al., 2015)

nrg^l4

(Silies and Klämbt, 2010)

Name Synonyms

Secondary FlyBase IDs

References (39)

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