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Fig. 4. pbl mutant embryos have a mesodermal cell migration defect. (A,B) Transverse sections of in situ hybridisations with a twi antisense RNA probe. (A) In late stage 10 wild-type embryos, the mesodermal cells have dissociated and migrated dorsally to form a uniform layer beneath the ectoderm (arrows indicate dorsalmost mesodermal cells, which lie adjacent to the dorsalmost epidermal cells). (B) In a similarly staged pbl²/pbl³ mutant embryo, the mesodermal cells appear aggregated and have failed to complete dorsolateral migration (arrows indicate the dorsalmost epidermal cells). (C) A stage 10, wild-type embryo stained for F-Actin. Mesodermal cells have formed a monolayer beneath the ectoderm. (D,E) Equivalently staged pbl²/pbl³ embryos, in which mesoderm spreading is defective. (F) A stage 10 pbl²/pbl³ embryo expressing GFP-Actin driven by twi-GAL4 visualised with an anti-GFP antibody. Similar to D,E, the spreading of the mesoderm is defective. (G) A stage 10, pbl²/pbl³ embryo co-expressing wild-type PBL and GFP-Actin with twi-GAL4 visualised with an anti-GFP antibody. The dissociation and migration of the mesodermal cells has been rescued, such that the mesodermal cells form a uniform layer beneath the ectoderm similar to wild type. (G') The same embryo showing multinucleate cells in the ectoderm (arrows).

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