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. 2005 Jun;187(12):4042–4049. doi: 10.1128/JB.187.12.4042-4049.2005

FIG. 4.

FIG. 4.

(A) Complementation of spx with wild-type and CXXC mutant alleles of spx. Cells were grown in TSS media containing either sulfate or methionine as sole sulfur sources in the absence (lanes 1 to 3 and 7 to 9) and the presence (lanes 4 to 6 and 10 to 12) of IPTG. Samples were collected as described in the legend to Fig. 3. β-Galactosidase activity was expressed in Miller units. Experiments were performed in triplicate. Lanes 1, 4, 7 and 10, ORB4807 (ytmI-lacZ spx amyE::Pspank-hy-spx); lanes 2, 5, 8, and 11, ORB4863 [ytmI-lacZ spx amyE::Pspank-hy-spx(C10A)]; lanes 3, 6, 9, and 12, ORB4864 [ytmI-lacZ spx amyE::Pspank-hy-spx(C13A)]. (B) The ytmI-lacZ fusion is still controlled by Spx when ytlI is constitutively expressed. Strains containing ytmI-lacZ and Pspank-hy-ytlI with or without an spx mutation were grown in TSS containing either sulfate, cysteine, or methionine as the sole sulfur source. The absence (−) and the presence (+) of IPTG is indicated. Lanes 1, 3, 5, 7, 9, and 11, ORB4979 (ytmI-lacZ amyE::Pspac-ytlI ytlI::aphA3); lanes 2, 4, 6, 8, 10 and 12, ORB4983 (ytmI-lacZ amyE::Pspac-ytlI ytlI::aphA3 spx::spc).