Fig. 1. Mutations in mks, a Cdc27 APC/C subunit gene at 65E, result in a metaphase arrest with overcondensed chromosomes. (A,E) Squashed preparations of wild-type larval neuroblasts in metaphase and late anaphase, respectively. (B-D,F-H) Overcondensed mitotic chromosomes in preparations of mks¹ cells. Most cells are diploid (B,C,F,G), although 1-2% are tetraploid (D,H). (C, arrows) A diploid cell in which sister chromatids are well separated. Anaphase cells were classified as cells that were always elongated and in which the chromosome distribution followed the direction of the elongation. They were distinguished from prometaphase cells, which did not show such elongation and had chromosomes in a random position. The proportion of anaphases is reduced compared to the wild type (Table 1A) and, when these do occur, they show lagging chromatids (F,G, arrowheads). (I) A molecular map of the 65E region indicating the sites of the P-insertions in mks¹ and mks². In situ hybridization shows the P-element responsible for the mks¹ mutation is inserted at 65E. Restriction endonuclease cleavage sites for HindIII (H), EcoRI (E), BamHI (B), BglII (Bg), SaccII (S), SpeI (Sp), ScaI (Sc) and XmnI (X) are indicated. Segments of chromosomal DNA inserted into the rescuing transformation plasmid, pR6.2 and its negative control, p76.2Bam (see Materials and Methods) are indicated below the map. (J) Estimation of mks transcripts relative to those of rpL17A in third instar larvae by RT-PCR (see Materials and Methods). Canton S (Can S) larvae were used as the wild type.