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Volume 23, Number 7—July 2017
Dispatch

Locally Acquired mcr-1 in Escherichia coli, Australia, 2011 and 2013

Justin A. Ellem, Andrew N. Ginn, Sharon C.-A. Chen, John Ferguson, Sally R. Partridge, and Jonathan R. IredellComments to Author 
Author affiliations: Westmead Hospital, Westmead, New South Wales, Australia (J.A. Ellem, A.N. Ginn, S.C.-A. Chen, S.R. Partridge, J.R Iredell); New South Wales Health Pathology, Westmead (J.A. Ellem, A.N. Ginn, S.C.-A. Chen, J.R. Iredell); The University of Sydney, Sydney, New South Wales, Australia (A.N. Ginn, S.C.-A. Chen, S.R. Partridge, J.R. Iredell); The Westmead Institute for Medical Research, Westmead (A.N. Ginn, S.R. Partridge, J.R. Iredell); John Hunter Hospital, Newcastle, New South Wales, Australia (J. Ferguson); Pathology North, Newcastle (J. Ferguson); University of Newcastle, Newcastle (J. Ferguson)

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Figure

Differences in promoter and ribosome binding site regions of mcr-1 in plasmids from Escherichia coli in Australia (indicated by arrows) and in other sequences available from GenBank. The sequences end with the ATG start codon of mcr-1 and a second ATG codon that follows it. The −35 and −10 regions of the proposed promoter (11) are indicated by arrows. The numbers to the right indicate how many times each variant has been seen among available sequences.

Figure. Differences in promoter and ribosome binding site regions of mcr-1 in plasmids from Escherichia coli in Australia (indicated by arrows) and in other sequences available from GenBank. The sequences end with the ATG start codon of mcr-1 and a second ATG codon that follows it. The −35 and −10 regions of the proposed promoter (11) are indicated by arrows. The numbers to the right indicate how many times each variant has been seen among available sequences.

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