<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zhou K</submitter><funding>National Natural Science Foundation of China</funding><pagination>2464</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10147710</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(1)</volume><pubmed_abstract>Adaptation to selective pressures is crucial for clinically important pathogens to establish epidemics, but the underlying evolutionary drivers remain poorly understood. The current epidemic of carbapenem-resistant Klebsiella pneumoniae (CRKP) poses a significant threat to public health. In this study we analyzed the genome sequences of 794 CRKP bloodstream isolates collected in 40 hospitals in China between 2014 and 2019. We uncovered a subclonal replacement in the predominant clone ST11, where the previously prevalent subclone OL101:KL47 was replaced by O2v1:KL64 over time in a stepwise manner. O2v1:KL64 carried a higher load of mobile genetic elements, and a point mutation exclusively detected in the recC of O2v1:KL64 significantly promotes recombination proficiency. The epidemic succes</pubmed_abstract><journal>Nature communications</journal><pubmed_title>A point mutation in recC associated with subclonal replacement of carbapenem-resistant Klebsiella pneumoniae ST11 in China.</pubmed_title><pmcid>PMC10147710</pmcid><funding_grant_id>81902030</funding_grant_id><funding_grant_id>82172330</funding_grant_id><funding_grant_id>81971984</funding_grant_id><pubmed_authors>Hu S</pubmed_authors><pubmed_authors>Shen J</pubmed_authors><pubmed_authors>Dong Y</pubmed_authors><pubmed_authors>Quan B</pubmed_authors><pubmed_authors>Shen P</pubmed_authors><pubmed_authors>Man S</pubmed_authors><pubmed_authors>Zhang L</pubmed_authors><pubmed_authors>Luan L</pubmed_authors><pubmed_authors>Wang J</pubmed_authors><pubmed_authors>Wang L</pubmed_authors><pubmed_authors>Sun L</pubmed_authors><pubmed_authors>Wan C</pubmed_authors><pubmed_authors>Guo L</pubmed_authors><pubmed_authors>Gu B</pubmed_authors><pubmed_authors>Lam MMC</pubmed_authors><pubmed_authors>Dong H</pubmed_authors><pubmed_authors>Wang S</pubmed_authors><pubmed_authors>Liang J</pubmed_authors><pubmed_authors>Liang K</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Kang J</pubmed_authors><pubmed_authors>Zhang B</pubmed_authors><pubmed_authors>Liao Z</pubmed_authors><pubmed_authors>Liao Y</pubmed_authors><pubmed_authors>Xia X</pubmed_authors><pubmed_authors>Xu R</pubmed_authors><pubmed_authors>Qiao D</pubmed_authors><pubmed_authors>Chen F</pubmed_authors><pubmed_authors>Xu H</pubmed_authors><pubmed_authors>Jin Y</pubmed_authors><pubmed_authors>Yang Z</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Li Z</pubmed_authors><pubmed_authors>Hu H</pubmed_authors><pubmed_authors>Du F</pubmed_authors><pubmed_authors>Xu T</pubmed_authors><pubmed_authors>Lin H</pubmed_authors><pubmed_authors>BRICS Working Group</pubmed_authors><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>Ding H</pubmed_authors><pubmed_authors>Ma L</pubmed_authors><pubmed_authors>Cao J</pubmed_authors><pubmed_authors>Wyres KL</pubmed_authors><pubmed_authors>Mao H</pubmed_authors><pubmed_authors>Liu Q</pubmed_authors><pubmed_authors>Dai Y</pubmed_authors><pubmed_authors>Liu Y</pubmed_authors><pubmed_authors>Qi X</pubmed_authors><pubmed_authors>Wei S</pubmed_authors><pubmed_authors>Liao G</pubmed_authors><pubmed_authors>Zheng L</pubmed_authors><pubmed_authors>Li A</pubmed_authors><pubmed_authors>Zhou K</pubmed_authors><pubmed_authors>Xue CX</pubmed_authors><pubmed_authors>Xiao Y</pubmed_authors><pubmed_authors>Zhou Y</pubmed_authors><pubmed_authors>Yan X</pubmed_authors><pubmed_authors>Huang Y</pubmed_authors><pubmed_authors>Zhu L</pubmed_authors><pubmed_authors>Holt KE</pubmed_authors><pubmed_authors>Zhu W</pubmed_authors><pubmed_authors>Liu D</pubmed_authors></additional><is_claimable>false</is_claimable><name>A point mutation in recC associated with subclonal replacement of carbapenem-resistant Klebsiella pneumoniae ST11 in China.</name><description>Adaptation to selective pressures is crucial for clinically important pathogens to establish epidemics, but the underlying evolutionary drivers remain poorly understood. The current epidemic of carbapenem-resistant Klebsiella pneumoniae (CRKP) poses a significant threat to public health. In this study we analyzed the genome sequences of 794 CRKP bloodstream isolates collected in 40 hospitals in China between 2014 and 2019. We uncovered a subclonal replacement in the predominant clone ST11, where the previously prevalent subclone OL101:KL47 was replaced by O2v1:KL64 over time in a stepwise manner. O2v1:KL64 carried a higher load of mobile genetic elements, and a point mutation exclusively detected in the recC of O2v1:KL64 significantly promotes recombination proficiency. The epidemic succes</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Apr</publication><modification>2026-04-30T12:32:32.82Z</modification><creation>2024-11-12T07:05:48.483Z</creation></dates><accession>S-EPMC10147710</accession><cross_references><pubmed>37117217</pubmed><doi>10.1038/s41467-023-38061-z</doi></cross_references></HashMap>