Nucleotide substitution: C3666T. Amino acid replacement: P1054S.
C21558108T
C3666T
P1054S | Egfr-PA; P1103S | Egfr-PB
P1054S
Malpighian tubules in homozygous embryos are shorter than wild type, posterior tubules are more strongly affected than the anterior. Reduction in size of the tubules is due to reduction in cell number, not cell death.
Homozygotes show a weak Egfr phenotype: the cuticle is more intact than in stronger Egfr alleles, but shows reductions in the ventral plate and H piece of the anterior head skeleton. There are variable reductions in the number and size of ventral setae and occasional ventral or dorsal midline defects. Many embryos fail to complete germ band retraction.
Weak 'flb' phenotype when homozygous and hemizygous. Embryos produced from heteroallelic combination with Egfrt1 have a severe ventralised phenotype, reduction in size of their dorsal appendage. Individuals are fully viable over the pupal lethals Egfrtop-CA and Egfrtop-EC20 and show a reduction in viability over Egfrtop-EB.
Head skeleton is defective, germ band fails to retract and abdominal denticle belts are reduced in width.
Egfrtop-101 is a suppressor of phenotype of rhohs.sev
Mutation of Egfr that affects the gene function required for embryogenesis, a class II lesion. The allelic series for class II lesions: Egfrtop-101 < Egfrtop-JE14 = Egfrf4 < Egfrf6.
Germline clone analysis indicates that there is very little, if any, requirement for Egfr in the germline.
Weak mutation.
Class IIA allele. Class IIA alleles do not disrupt tissue specific gene functions. Class II alleles fully or partially complement the developmental defects of Egfrt1 and Egfrtop-CA. Substantially complements the postembryonic lethality of Egfrtop-EC20. Several combinations of Egfr alleles involving Egfrtop-101, Egfrf4, Egfrf8 and Egfrf6 demonstrate interallelic complementation.