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. 1998 Aug 4;95(16):9301–9306. doi: 10.1073/pnas.95.16.9301

Figure 2.

Figure 2

Mutations in either the ATP-binding site or the polo-box abolish the capacity of Plk to complement the cdc5–1 defect. A haploid cdc5–1 mutant strain, KKY921–2B (MATa cdc5–1 leu2 trp1 ura1) (12) was transformed with various YCplac111-GAL1-HA-PLK constructs or with YCplac111-CDC5. To examine the ability of Plk constructs to complement the cdc5–1 defect, transformants were cultured at 37°C in yeast extract/peptone + 2% galactose medium for 10 hr as described (19) and were subjected to flow cytometry analyses. Vector, YCplac111-GAL1; CDC5, YCplac111-CDC5; PlK, YCplac111-GAL1-HA-Plk; K82M, YCplac111-GAL1-HA-PlkK82M; PlkΔC, YCplac111-GAL1-HA-PlkΔC; W414F, YCplac111-GAL1-HA-PlkW414F. (A–F) A G1 population (1N arrow) and G2/M population (2N arrow) are indicated in the vector panel. Cells with a DNA content >2N are indicated by the 4N arrow (a broad cell population with the third 4N arrow). (G–L) The increase in forward scatter at the x axis reflects an increase in cell size. The broad, spread out pattern observed in the cdc5–1 mutant transformed with vector (G) results from a heterogeneous population of enlarged cells whereas wild-type cells (data not shown) and the cdc5–1 mutant complemented with Cdc5 (H) or Plk (I) expression produce a distinct bell-shaped pattern of forward scatter.