TABLE 2 .

pIV mutants defective for induction of the Psp response

Isolate	Amino acid substitution(s)	Φ(pspAp-lacZ) activity (%)a
14	S28P N88D D225G S274C S276P V281E	10
	I294V G339D L409I S417P E419V
34	L335Q, K381I	11
52	L188H, K381N, P396P, R424H	8
57	L373S, G399S	10
63	S18T S45T D100G D129D L199M L213S F249L L377H	10
69	M13I N128S V153A T355N	8
74	T42K D109G A303G	12
78	V56E A176T V238I T277R L278L P390L L392Q V416G K419R	8
104	K419I	12
115	L373S G399S	5
116	L85F V140D	6
117	F302Y V373A L426F	9
123	L222M G309A	9
124	P194M	4
132	K11N R78C G238C F411L S421N	8
181	N95I E150D L193L L276P	8
195	Q50R F255L LS356F	10

^aThe percentage of β-galactosidase activity in a strain with pBAD18-Kan encoding the mutant pIV, relative to wild-type pIV activity. Typically, a strain producing wild-type pIV had approximately 500 to 600 Miller units of β-galactosidase activity, whereas a strain with the empty pBAD18-Kan plasmid had approximately 30 Miller units of β-galactosidase activity.