Table 3.

Mutations in RAM genes result in axial and bipolar budding defects

	Axial, %	Bipolar, %	Random, %
wt (vector)	3.0 ± 2.6	68.4 ± 1.4	28.6 ± 3.9
wt (pBUD4)	82.7 ± 2.0	4.5 ± 1.3	12.8 ± 3.0
hym1	59.2 ± 0.5	3.1 ± 1.6	38.1 ± 1.2
cbk1	54.6 ± 2.1	1.0 ± 0.1	44.4 ± 2.0
tao3	56.1 ± 2.9	3.1 ± 0.6	40.8 ± 2.3
kic1	40.1	2.3	57.7
mob2	43.6	3.9	52.5
bni1	85.9 ± 4.0	0.6 ± 0.5	13.6 ± 3.6
wt (vector)	0.0 ± 0.0	70.1 ± 2.6	29.9 ± 2.6
wt (pBUD4)	0.0 ± 0.0	75.8 ± 3.7	24.2 ± 3.7
hym1/hym1	1.0 ± 1.7	7.0 ± 2.6	92.0 ± 4.0
cbk1/cbk1	0.0 ± 0.0	8.6 ± 1.9	91.3 ± 2.0
tao3/tao3	0.3 ± 0.6	12.9 ± 3.0	86.8 ± 3.3
bni1/bni1	0.0 ± 0.0	9.6 ± 3.2	90.4 ± 3.2

Strains containing plasmid p2698 with BUD4 (pBUD4) or pRS316 (vector) were grown to midlogarithmic phase, sonicated for cell separation and stained with Calcofluor to visualize bud scars. Strains contain pBUD4 unless otherwise indicated. Upper rows show haploid strains, lower rows show diploid strains. For each sample, a minimum of 100 cells was counted from at least three independent fields. The strains used were wild-type (W303-1A and Y1028), hym1Δ (Y1614 and Y1622), cbk1Δ (Y1747 and Y2623), tao3Δ (Y3152 and Y3565), kic1Δ (Y3323 and Y3529), mob2Δ (Y3424 and Y3527), and bni1Δ (Y581 and Y2619).