Nucleotide substitution: G?A. Mutation is in the intron 1 splice donor site and prevents synthesis of the mature mRNA.
G19833609A
G?A
Position of mutation on reference sequence inferred by FlyBase curator based on author statement. Mutation is in the intron 1 splice donor site and prevents synthesis
of the mature mRNA.
trc2/+ heterozygotes exhibit wild-type dendritic tiling, with wild-type levels of dendritic crossing points per υm[2].
stan[+]/stanE59, trc2 has abnormal neuroanatomy | third instar larval stage phenotype
hpoKC202, trc2/trc[+] has abnormal neuroanatomy phenotype
hpoMGH4, trc2/trc[+] has abnormal neuroanatomy phenotype
hpoMGH4/hpo[+], trc2 has abnormal neuroanatomy phenotype
hpoKC202/hpo[+], trc2 has abnormal neuroanatomy phenotype
stan[+]/stanE59, trc2 has larval dorsal multidendritic neuron ddaC | third instar larval stage phenotype
stan[+]/stanE59, trc2 has dendrite | third instar larval stage phenotype
hpoKC202, trc2/trc[+] has multidendritic dendrite phenotype
hpoMGH4, trc2/trc[+] has multidendritic dendrite phenotype
hpoMGH4/hpo[+], trc2 has multidendritic dendrite phenotype
hpoKC202/hpo[+], trc2 has multidendritic dendrite phenotype
Transheterozygotes for trc2/hpoMGH4 exhibit obvious iso-neuronal as well as hetero-neuronal tiling defects, including a significant increase in dendritic crossing-points compared to single mutants.
Transheterozygotes for trc2/hpoKC202 exhibit obvious iso-neuronal as well as hetero-neuronal tiling defects, including a significant increase in dendritic crossing-points compared to single mutants.