α-Speclm88 heterozygotes are viable.
α-Speclm88 homozygous and α-Specrg41/α-Speclm88 transheterozygous embryos show mild midline axon guidance defects, with on average less than one medial longitudinal fascicle ectopically crossing the midline per embryo. α-Speclm88/+ embryos do not show this defect.
Rescued to the adult stage by α-SpecRpS27A.PL.
α-Speclm88 has abnormal neuroanatomy | recessive phenotype, enhanceable by β-SpecG0198
α-Speclm88 is an enhancer of abnormal neuroanatomy phenotype of β-SpecG0198
α-Speclm88, Hsap\SNCAQUAS.cOa, Ncra\QFQF2.nSyb has lethal phenotype
α-Speclm88 has medial longitudinal fascicle | ectopic phenotype, enhanceable by β-SpecG0198
α-Speclm88 is an enhancer of medial longitudinal fascicle | ectopic phenotype of β-SpecG0198
β-SpecG0198/Y; α-Speclm88/+ embryos show a mild enhancement of the midline defects seen in β-SpecG0198/Y embryos. β-SpecG0198/Y; α-Speclm88/α-Speclm88 embryos causes an enhancement of the number of times the medial longitudinal fascicle ectopically cross the midline compared to either single mutant.
The expression of Hsap\SNCANcra\QUAS.cOa under the control of Ncra\QFQF2.nSyb in combination with heterozygosity for α-Speclm88 leads to lethality.