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. Author manuscript; available in PMC: 2015 May 14.
Published in final edited form as: Cell Host Microbe. 2014 May 14;15(5):578–586. doi: 10.1016/j.chom.2014.04.003

Table 1. Loss of Function Mutations in Y. pestis that Enabled Flea-borne Transmission.

Gene Gene IDa Mutation in Y. pestis Effect Occurrenceb
PDE2 (rtn) YPTB1308 y2909 frameshift (6A→7A) in ORF N-terminal truncation eliminates signal peptide sequence and phosphodiesterase activity; increased c-di-GMP levels all Y. pestis
PDE3c YPTB3308 y3389 a) point mutation (C→T) in promoter region (PDE3-pe' allele) decreased transcription (cf. Fig. S3B) some Y. pseudotuberculosis (e.g. YPIII) and Y. pestis Branch 0 strains Pestoides A (0.PE4b) and Microtus 91001 (0.PE4c)
b) PDE3-pe' mutation plus point mutation (nonsense) in ORF (PDE3-pe allele) N-terminal truncation eliminates transmembrane domain and phosphodiesterase activity; increased c-di-GMP levels all Y. pestis except Branch 0 strains Pestoides A (0.PE4b) and Microtus 91001 (0.PE4c)
c) deletion no PDE3 phosphodiesterase activity Y. pestis Branch 0 strains Pestoides F (0.PE2a) and Angola (0.PE3a)
rcsA YPTB2486 y1741 30-bp internal duplication in ORF* 10 amino acid tandem repeat insertion, eliminates RcsAB repression of hmsT diguanylate cyclase gene all Y. pestis except Branch 0 strain Pestoides A (0.PE4b)
a

Gene annotation numbers for Y. pseudotuberculosis IP32953 and Y. pestis KIM homologs

b

Cf. Figure 5;

c

See Figure S3A for PDE3 allele details

*

Two Branch 1 Y. pestis strains, 1.ANTa (Antiqua) and 1.ANTb (UG05), have a transposon (Tn) insertion in rcsA instead of an internal duplication.