. Author manuscript; available in PMC: 2013 Jun 8.

Published in final edited form as: J Mol Biol. 2012 Mar 28;419(0):139–157. doi: 10.1016/j.jmb.2012.03.019

Table 1.

Epistatic interactions between alanine substitutions of σ⁷⁰ R4 and alanine substitutions of the class II PC surface of Rob and SoxS at the fumC and micF promoters

σ⁷⁰ R4 substitution	Epistasis between alanine substitutions of σ⁷⁰ R4 and alanine substitutions of the class II PC surface of Rob and SoxS at two promoters
	fumC promoter		micF promoter
	Rob	SoxS	Rob	SoxS
K593A	None	D75A, M78A	N.A.	M78A, D79A
R596A	N.A.	None	N.A.	None
R599A	D75A	D75A	N.A.	None
R603A	N.A.	None	D75A	D75A, D79A

All amino acids of σ⁷⁰ R4 that confer a defect in Rob-dependent transcription activation (Fig. 1) or SoxS-dependent transcription activation¹² of the fumC and/or micF promoters when substituted with alanine are listed even if no interacting partners have been identified. The alanine substitutions within the class II PC surface of Rob (Figs. 5 and 6) and SoxS¹² that are epistatic partners of the listed alanine substitutions of σ⁷⁰ R4 are shown according to the promoter at which the epistasis was observed. N.A., not applicable because this substitution of σ⁷⁰ R4 has no effect on the activity of the activator; none, no epistasis occurs between these combinations of the activator and the σ⁷⁰ R4 substitutions.