Amino acid replacement: G313D.
Amino acid replacement: V318M.
G8545584A
G313D | Nrg-PA; G313D | Nrg-PB; G313D | Nrg-PC; G313D | Nrg-PD; G313D | Nrg-PE; G313D | Nrg-PF; G313D | Nrg-PG; G313D | Nrg-PH; G313D | Nrg-PI
G313D
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
G8545601A
V319M | Nrg-PA; V319M | Nrg-PB; V319M | Nrg-PC; V319M | Nrg-PD; V319M | Nrg-PE; V319M | Nrg-PF; V319M | Nrg-PG; V319M | Nrg-PH; V319M | Nrg-PI
V318M
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
dorsal multidendritic neuron ddaD & axon | conditional ts
dorsal multidendritic neuron ddaD & dendritic tree | conditional ts
dorsal multidendritic neuron ddaE & axon | conditional ts
dorsal multidendritic neuron ddaE & dendritic tree | conditional ts
Nrgl3 mutant flies exhibit a stalling phenotype and, less frequently, in misguidance defects of ocellar and orbital bristle mechanosensory (BM) axons. Sometimes only one or a subset of axons seems to stall within a nerve, although other axons extend normally. In a few cases, BM axons separate from the epidermis without connecting with the orbital nerve, or project backwards or to an ectopic place. In a few cases, BM axons separate from the epidermis without connecting with the orbital nerve, or project backwards or to an ectopic place.
A temporal loss of Nrg, using the temperature-sensitive Nrgl3 mutant for 12.5% or 25% of pupal development during synapse formation and well as synapse maturation is able to disrupt the giant synapse anatomically and physiologically. In 50% of cases, the complete synaptic terminal is lacking when the temporal loss of function is induced during synapse formation.
When Nrgl3 mutants are exposed to nonpermissive temperatures during synapse formation (20-40% of pupal development) or during synaptic maturation (approximately 40-75% of pupal development), presynaptic terminals are absent or abnormally thin. When adults are exposed to nonpermissive temperatures, large vesicles in the giant fiber terminals are observed.
Overexpression of either Nrg167.Scer\UAS or NrgGPI.Scer\UAS in wing sensory neurons and two wing epithelial layers, mediated by Scer\GAL4MS1075, in an Nrgl3 background causes the same defective wing phenotypes that occur when these transgenes are expressed in a wild-type background.
Nrgl3 has abnormal neuroanatomy phenotype, enhanceable by Fas2[+]/Fas2e76
Nrgl3 has abnormal neuroanatomy phenotype, suppressible by Scer\GAL4MS1075/Hsap\L1CAMRSLE-.UAS
Nrgl3 has abnormal neuroanatomy phenotype, suppressible by Scer\GAL4MS1075/Mmus\L1camRSLE+.UAS
Nrgl3 has abnormal neuroanatomy phenotype, suppressible by Rnor\NrcamUAS.cKa/Scer\GAL4MS1075
Nrgl3 has abnormal neuroanatomy | temperature conditional phenotype, suppressible by Hsap\NCAM1140.UAS/Scer\GAL4MS1075
Nrgl3 has abnormal neuroanatomy phenotype, non-suppressible by Hsap\L1CAMH1.UAS/Scer\GAL4MS1075
Nrgl3 has abnormal neuroanatomy phenotype, non-suppressible by Hsap\L1CAMH38.UAS/Scer\GAL4MS1075
Nrgl3 has ocellar nerve phenotype, enhanceable by Fas2[+]/Fas2e76
Nrgl3 has mechanosensory neuron phenotype, non-enhanceable by Fas2[+]/Fas2e76
Nrgl3 has ocellar nerve phenotype, suppressible by Scer\GAL4MS1075/Hsap\L1CAMRSLE-.UAS
Nrgl3 has mechanosensory neuron phenotype, suppressible by Scer\GAL4MS1075/Hsap\L1CAMRSLE-.UAS
Nrgl3 has ocellar nerve phenotype, suppressible by Scer\GAL4MS1075/Mmus\L1camRSLE+.UAS
Nrgl3 has ocellar nerve phenotype, suppressible by Rnor\NrcamUAS.cKa/Scer\GAL4MS1075
Nrgl3 has mechanosensory neuron phenotype, suppressible | partially by Rnor\NrcamUAS.cKa/Scer\GAL4MS1075
Nrgl3 has ocellar nerve | temperature conditional phenotype, suppressible by Hsap\NCAM1140.UAS/Scer\GAL4MS1075
Nrgl3 has mechanosensory neuron | temperature conditional phenotype, suppressible by Hsap\NCAM1140.UAS/Scer\GAL4MS1075
Nrgl3 has mechanosensory neuron phenotype, suppressible | partially by Scer\GAL4MS1075/Hsap\L1CAMRSLE-.UAS
NrgGPI.UAS, Nrgl3, Scer\GAL4MS1075 has wing phenotype, suppressible by Egfr[+]/Egfrt1
Nrg167.UAS, Nrgl3, Scer\GAL4MS1075 has wing phenotype, suppressible by Egfr[+]/Egfrt1
Nrgl3 has mechanosensory neuron phenotype, non-suppressible by Hsap\L1CAMH1.UAS/Scer\GAL4MS1075
Nrgl3 has ocellar nerve phenotype, non-suppressible by Hsap\L1CAMH1.UAS/Scer\GAL4MS1075
Nrgl3 has mechanosensory neuron phenotype, non-suppressible by Hsap\L1CAMH38.UAS/Scer\GAL4MS1075
Nrgl3 has ocellar nerve phenotype, non-suppressible by Hsap\L1CAMH38.UAS/Scer\GAL4MS1075
Expression of Hsap\L1CAMRSLE-.Scer\UAS under the control of Scer\GAL4MS1075 suppresses the bristle mechanosensory (BM) axonal defects seen in Nrgl3 mutant flies.
Expression of Hsap\L1CAMH1.Scer\UAS under the control of Scer\GAL4MS1075 does not suppress the bristle mechanosensory (BM) axonal defects seen in Nrgl3 mutant flies.
Expression of Hsap\L1CAMH38.Scer\UAS under the control of Scer\GAL4MS1075 does not suppress the bristle mechanosensory (BM) axonal defects seen in Nrgl3 mutant flies.
Expression of Hsap\L1CAMRSLE-.Scer\UAS under the control of Scer\GAL4MS1075 in Nrgl3 mutant individuals rescues the axonal defects in OP axons, along with slightly reducing the level of BM axon defects.
Expression of Mmus\L1camRSLE+.Scer\UAS under the control of Scer\GAL4MS1075 in Nrgl3 mutant individuals rescues the axonal defects in OP axons.
Expression of Rnor\NrcamScer\UAS.cKa under the control of Scer\GAL4MS1075 in Nrgl3 mutant individuals rescues the axonal defects in OP axons, along with slightly reducing the level of BM axon defects.
Expression of Hsap\NCAM1140.Scer\UAS in a Nrgl3 background, under the control of Scer\GAL4MS1075 suppresses the Nrgl3 phenotype at the restrictive temperature, specifically OP axon alterations and BM axon guidance defects.
Nrgl3 is rescued by Scer\GAL4MS1075/Nrg180.UAS
Nrgl3 is not rescued by Nrg167.UAS/Scer\GAL4MS1075
Scer\GAL4MS1075-driven expression of neural-Nrg180.Scer\UAS in Nrgl3 mutant animals rescues both the pentrance and the expressivity of the OP and BM axon misguidance defects.
Scer\GAL4MS1075-driven expression of Nrg167.Scer\UAS in Nrgl3 mutant animals shows a synergistic increase in the expressivity of OP axon alterations (i.e. axonal alterations are much more severe in those individuals that display the phenotype).
Lefevre.