Abstract

[This corrects the article DOI: 10.1371/journal.pgen.1006321.].

Highlights

  • The authors have verified that phenotypes of the following mutants are reported correctly in this publication: All the E712A containing double mutants (E712A/S1091A, E712A/S1091E, E712A/S1091C, E712A/K1092A, E712A/K1092D, E712A/K1093M) and the single substitution mutants T834P, S1091A, S1091E, S1091C, K1092A, K1092D, K1093M

  • Mutations in D716 (D716A/K) suppressed the S1091C and K1093M GOF phenotypes and conferred LOF phenotype (GalR) when combined with other S1091 alleles (D716A/S1091A, D716A/S1091E, D716K/S1091A, D716K/S1091E), the D716A/K or S1091A/E single substitutions did not confer strong transcription-related phenotypes (Fig 5D, S8F and S9A Figs). These allele-specific genetic interactions suggested that D716A/K and S1091A/E lost putatively redundant interactions that together conferred LOF phenotypes, and loss of D716 interaction(s) might suppress the putatively gain of interactions in GOF mutants S1091C and K1093M

  • K1092A/D single substitutions did not confer transcription-related phenotypes, but were able to suppress the E1307K GOF phenotypes (S8F and S9E Figs). This observed epistasis suggested that loss of potential interacting residues (E712 and K1092, respectively) relieved putative gain of interactions in the GOF mutants (K1093M and E1307K, respectively)

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Summary

OPEN ACCESS

Mutations in D716 (D716A/K) suppressed the S1091C and K1093M GOF phenotypes and conferred LOF phenotype (GalR) when combined with other S1091 alleles (D716A/S1091A, D716A/S1091E, D716K/S1091A, D716K/S1091E), the D716A/K or S1091A/E single substitutions did not confer strong transcription-related phenotypes (Fig 5D, S8F and S9A Figs) These allele-specific genetic interactions suggested that D716A/K and S1091A/E lost putatively redundant interactions that together conferred LOF phenotypes, and loss of D716 interaction(s) might suppress the putatively gain of interactions in GOF mutants S1091C and K1093M. K1092A/D single substitutions did not confer transcription-related phenotypes, but were able to suppress the E1307K GOF phenotypes (S8F and S9E Figs) This observed epistasis suggested that loss of potential interacting residues (E712 and K1092, respectively) relieved putative gain of interactions in the GOF mutants (K1093M and E1307K, respectively) (discussed above).

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