TABLE 3.

Roles of cAMP signaling and pH response pathways in white-to-opaque switching^a

Strain	White-to-opaque switching frequency (%) at pH:
	4.0	5.0	6.0	7.0	7.5	8.0
WT	18.4 ± 2.9*	12.5 ± 0.9	13.8 ± 0.3*	5.4 ± 1.0*	<1.0	<1.3
cyr1/cyr1b	23.5 ± 3.3*	7.1 ± 4.1*	4.8 ± 1.3	2.4 ± 3.4	Growth defect	Growth defect
pde2/pde2	100.0	100.0	100.0*	93.8 ± 2.3	74.2 ± 1.8*	67.5 ± 1.2
phr1/phr1	2.7 ± 1.8*	0.2 ± 0.4	<0.2	0.2 ± 0.4	<0.3	<0.3
PHR1 reconstituted	9.4 ± 0.1*	5.9 ± 0.4*	2.9 ± 1.1*	0.9 ± 0.8*	<0.5	0.6 ± 1.0
phr2/phr2	Growth defect	Growth defect	0.9 ± 1.2	3.8 ± 3.2*	0.8 ± 1.1	<0.9
PHR2 reconstituted	5.8 ± 0.3	10.4 ± 2.3*	4.7 ± 0.8*	0.5 ± 0.8*	<0.5	<0.6
rim101/rim101	2.4 ± 0.7	6.0 ± 0.8*	1.7 ± 0.8	2.6 ± 0.6	3.8 ± 2.3	4.2 ± 0.2
RIM101 reconstituted	10.0 ± 2.8*	6.4 ± 1.3	4.6 ± 1.4*	0.7 ± 1.2*	<0.4	<0.4

^aThe WT was strain GH1013, an SC5314 background strain. White cells were plated onto Lee's glucose medium plates and incubated in air at 25°C for 7 days. Assays for the quantitation of white-to-opaque switching frequencies were performed. <, no opaque or opaque-sectored colonies were observed. PHR1, PHR2, or RIM101 reconstituted, a copy of the PHR1, PHR2, or RIM101 gene, respectively, was integrated into the original locus. *, statistically significant difference (Student's t test, P < 0.05; see footnote a of Table 1).

^bThe cyr1/cyr1 mutant grew extremely slowly. The switching frequencies were examined after 12 days of growth.