QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

Help viewing high resolution images Return to article

Fig. 3. Metaphase delay during mitosis 16 in pim mutants is caused by diplochromosomes. (A-E) Embryos were labeled with a DNA stain (red) and anti-phospho-histone H3 (PH3, green) at the stage of mitosis 16. (A-D) The number of PH3-positive mitotic cells in a defined epidermal region was counted in 10 embryos homozygous for pim¹ (B), dup^a1 (C), double mutant for both pim¹ and dup^a1 (D), as well as in pim⁺ embryos (A). The resulting average number of mitotic cells (E) in the mutant and the corresponding sibling embryos are indicated by white and black bars, respectively. dup encodes an initiation factor for DNA replication; dup^a1 homozygosity inhibits S phase 16 (Whittaker et al., 2000), as well as the accumulation of mitotic figures in pim¹ mutants during the subsequent mitosis (see text for further explanations). In metaphase cells with maximal PH3 labeling, chromosomes were arranged in metaphase plates in pim¹ dup^a1 double mutants (inset in D). In contrast, the single chromatid chromosomes present in dup^a1 mutants failed to congress into a plate (inset in C), as previously described (Parry et al., 2003). Bar, 25 µm (A-D). (F) Labeling with anti-cyclin B (green) and a DNA stain (red) demonstrates that progression through mitosis 16 is delayed before cyclin B degradation in pim¹ mutants. Bar, 10 µm.

Return to article