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Fig. 4. grp¹ mutants fail to regulate mitosis following incomplete replication. (A) grp¹ dup^a3 double mutants cannot delay the entry into M16 while dup^a3 mutants can. 7-7.5-hours-old embryos were fixed and stained to visualize PH3 and DNA. Ectodermal cells in the dup^a3 mutants are still arrested before M16 as indicated by the near absence of PH3-positive cells. By contrast, the corresponding region of grp¹ dup^a3 mutant embryos show robust PH3 signal, indicating that double mutants are unable to delay the entry into M16. (B) grp¹ dup^a1 double mutants fail to delay the progress through and eventual exit from M16 in contrast to Df/dup^a1. 8.5-9-hour-old embryos were fixed and stained with an antibody to PH3 and with Hoechst33258 to visualize DNA. Hemizygous Df/dup^a1 mutants are arrested in M16 and show a robust number of mitotic cells in the lateral ectoderm consistent with published results. By contrast, grp¹ dup^a1 mutants show a reduced number of mitotic cells. Hemizygous mutants (Df/dup^a1) were used due to decreased viability associated with dup^a1 chromosome. (C) grp¹ mutation restores nuclear density of dup^a1 mutants to wild-type levels. Nuclear density in Stage 12 embryos was quantified in thoracic segments 1, 2 and 3 and expressed in arbitrary units. Nuclear density is reduced in dup^a1 mutants; this is expected, as they have not completed M16. Nuclear density in grp¹ dup^a1 mutants resembles that of heterozygous controls, indicating that cells of the double mutant have completed cycle 16. Homozygous mutants were identified by the lack of ß-gal encoded by the balancer chromosome (not shown).

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