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. 2011 Aug;193(15):3822–3831. doi: 10.1128/JB.00360-11

Fig. 2.

Fig. 2.

(A) Inactivation of the apnC gene by insertional inactivation via homologous recombination. The transformation construct contains a selection marker (Cmr; 800 bp) (shaded) that is flanked by homologous sequences on both the 5′ and 3′ ends. KO, knockout. (B) Testing of the full segregation of the apnC mutation by PCR using primers specific to the flanking region of the construct inserted into apnC (sequence position 15074 in EMBL/GenBank/DDBJ accession no. EF672686). (C) HPLC analysis of the aqueous-methanol extracts of WT apnC (top) and KO apnC, deficient in AP synthesis (bottom). Peaks 1 and 2 represent aeruginosides 126A (m/z 691; 9.07 min) and 126B (m/z 715; 10.56 min); peak 3, microviridin K (m/z 1,771; 16.09 min); peaks 4 and 5, AP 908 (m/z 909; 18.29 min) and AP 915 (m/z 916; 22.67 min); and peaks 6 and 7, MC-RR (m/z 1,024; 26.61 min) and MC-LR (m/z 981; 33.83 min), respectively.