Fig. 6. Hyperadhesive phenotype in optic placode following reduction of EGFR function. (A) Anti-FasII labeling of stage-15 wild-type embryo, lateral view. Optic placode has invaginated and split into Bolwig’s organ (Bo) and optic lobe (ol), the latter attached to the brain (br). (B) In embryo lacking EGFR (Egfr^f5) and carrying deficiency H99, which inhibits cell death, optic placode fails to invaginate and Bolwig’s organ remains attached to optic lobe (‘non-disjunction’). (C) Labeling of Bolwig’s organ with mab22C10 demonstrates that photoreceptor neurons remain arranged in a layered array, rather than transforming into spindle shaped cells as in wild type (compare with A). (D-F) Defects in visual system following application of 2-hour heat pulses (3°C) to EGFR temperature sensitive allele (Egfr^f1). All panels show heads of stage-15 embryos, labeled with anti-FasII antibody. Heat pulses between 3 and 6 hours (D) cause defects in head development, but leave the visual system intact. (E) Heat pulses around the time of optic placode invagination and disjunction (6-8 hours) result in non-disjunction phenotype of Bolwig’s organ and optic lobe (arrowhead), although usually milder than phenotype observed in Egfr null. Frequently phenotype is asymmetric: in the embryo shown in dorsal view, non-disjunction is prominent on right side, but absent from left side (arrow). (F) Heat pulses from 8-10 hours do not affect optic placode morphogenesis, but causes reduction in Bolwig’s neurons. Note small size of Bolwig’s organ, compared with wild type shown in G.

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