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Fig. 5. Different requirements for PBL and RHO1 in cell migration and cytokinesis. (A-C) eve expression in the wild type (A) and in embryos homozygously mutant for pbl3 (B) or pbl11D (C). Although a strong reduction of EVE-positive cells is seen in the pbl3 mutants (B), pbl11D mutants (C) exhibit a significantly higher number of EVE-positive hemisegments (see also Table 1). (D,E) Cytokinesis defects in pbl3 (D) and pbl11D (E) homozygous embryos. Ventral view of embryos at extended germband stage (stage 11) stained with antibodies against EVE. Segmental expression of eve in the central nervous system can be seen as described before (Cui and Doe, 1995; Weigmann and Lehner, 1995). The EVE-positive cells represent products of an incomplete cytokinesis of neuroblast 7-1. Inserts show confocal sections of anti-EVE and anti-NRT stained embryos to label cell outlines (both antibodies in red); note the presence of two nuclei in the neuroblasts. (F) Expression of Rho1N19 in the mesoderm affects cytokinesis, but not migration. twi::Gal4; UAS::Rho1N19 embryo stained with anti-EVE (blue) and anti-TWI (brown). Embryos expressing UAS::Rho1N19 exhibit normal mesoderm differentiation indicated by the normal pattern of EVE-positive cells. Formation of cellular protrusions in twi::Gal4; UAS::Rho1N19 embryos is normal (G; twi::CD2 (red), anti-TWI (green)). (H) Cytokinesis in such embryos is blocked as binucleated cells (arrowheads) can be seen in a different focal plane of the embryo shown in (G). (I,J) EVE expression in twi::Gal4; Dmef2::Gal4/UAS::Rho1N19 embryos at stage 10 (I) and 11 (J). Note some irregularity in the arrangement of EVE-expressing cells (arrowhead in J).





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