Table 1. Bc 407 {pHT1618’P _aphA3 -gusA} and Bc 407 ∆mfd {pHT1618’P _aphA3 -gusA} were subjected to sublethal NO treatment (125 μM) for 2 h, then plated on LB-X-glucuramidase plates supplemented with tetracycline (10 μg/mL).

Clone number	Position#	Transition+	Amino acid change in the GUS protein*
1	643	G:C to T:A	Gly to Val
2	643	G:C to T:A	Gly to Val
3	1646	C:G to G:C	Tyr to Stop
4	1646	C:G to G:C	Tyr to Stop
5	1646	C:G to G:C	Tyr to Stop
6	1646	C:G to G:C	Tyr to Stop
7	1646	C:G to G:C	Tyr to Stop
8	1646	C:G to G:C	Tyr to Stop
9	1646	C:G to G:C	Tyr to Stop
10	1646	C:G to G:C	Tyr to Stop
11	1651	A:T to C:G	Tyr to Ser
12	1651	A:T to C:G	Tyr to Ser
13	1651	A:T to C:G	Tyr to Ser
14	1651	A:T to C:G	Tyr to Ser
15	2377	G:C to T:A	Arg to Leu
16	2377	G:C to T:A	Arg to Leu
Control plasmid		No mutation
Control plasmidfrom ∆mfd in LB		No mutation
Control bluecolonies		No mutation

^#Base position on the gus gene.

⁺Change in base pair compared to non mutated gene.

^*Corresponding change in amino acid in the Gus protein.

The pHT1618’P_aphA3-gusA plasmid was isolated from white colonies (only the ∆mfd {pHT1618′P_aphA3-gusA} strain gave white colonies), used to transform E. coli TG1, and isolated from the E. coli transformants; the P_aphA3-gusA region was then sequenced. Position of mutations (from 1 to 2537 bp, corresponding to the sequenced fragment), base pair changes and the corresponding amino acid changes are indicated for each sequenced region. As controls, the corresponding regions in the initial plasmid, in the plasmid isolated from the ∆mfd {pHT1618′P_aphA3-gusA} strain grown for 2 h in LB medium, and in plasmids isolated from blue colonies after NO treatment were also sequenced.