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. 2016 Dec 15;11(12):e0168112. doi: 10.1371/journal.pone.0168112

Fig 4. Complementation of the alpha-amylase synthesised by the HtrB, HtrA1 and HtrA2 deficient strains by propagation in multicopy of their respective genes.

Fig 4

(A) Extracellular alpha-amylase present in the supernatants of the HtrB-deficient strain transformed with pFD666 derivative plasmids containing htrB, htrA1 and htrA2 (pFDB, pFDA1 and pFDA2, respectively) (B) HtrA1-deficient strain transformed with pFDB, pFDA1 and pFDA2 (C), HtrA2-deficient strain transformed with pFDB, pFDA1 and pFDA2 (D) and S. lividans TK21 transformed with pFDB, pFDA1 and pFDA2 were analysed at different times of growth (16, 24, 36, 48 and 60 h) by Western blotting assays using antibodies raised against AmlB. The amount of protein loaded onto the gels was corrected by the dried weight of the bacterial cultures. Molecular size markers are indicated on the side of each panel. The arrows indicate the relative mobility of the mature AmlB.