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. 1998 Dec 28;143(7):1789–1800. doi: 10.1083/jcb.143.7.1789

Figure 6.

Figure 6

Deletion of POM152 suppresses the ndc1-1 SPB duplication defect in the first cell cycle. (A) ndc1-1 or ndc1-1, pom152 null double mutant strains [HC5-31c and HC5-31c(1166), respectively; Table I] containing pURA3-NDC1 (pALR10-NDC1, see Materials and Methods) or lacking pURA3-NDC1 were transformed with either pRS315 (pLEU2) or pPM1-HA (pLEU2-POM152) and were streaked to a 15°C Leu− plate. All strains containing pURA3-NDC1 were able to grow at the nonpermissive temperature. The ndc1-1 strain lacking pURA3-NDC1 failed to grow. However, the ndc1-1, pom152 null double mutant strain grew at 15°C when it contained the pLEU2 vector (*). When a plasmid-borne copy of POM152 (pLEU2-POM152) was reintroduced, the double mutant strain exhibited the ndc1-1 cold-sensitive phenotype (**). (B) DNA content of wild-type (WT), ndc1-1, and ndc1-1, pom152 null double mutant (ndc1-1, pom152Δ) strains [HC14-10c, HC5-31c, and HC5-31c(1166), respectively; Table I]. Asynchronous cultures (0:00, dashed lines) were arrested in G1 (1c DNA content; G2 and M cells have 2c DNA content) by treatment with alpha-factor at the permissive temperature (0:00, bold line) (see Materials and Methods). Cells were released from this arrest into media at the nonpermissive temperature for ndc1-1 for 19.5 h (19:30).