Evaluating EcxR for Its Possible Role in Ehrlichia chaffeensis Gene Regulation

, a tick-transmitted intraphagosomal bacterium, is the causative agent of human monocytic ehrlichiosis. The pathogen also infects several other vertebrate hosts. has a biphasic developmental cycle during its growth in vertebrate monocytes/macrophages and invertebrate tick cells. Host- and vector-spe...

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Veröffentlicht in:International journal of molecular sciences 2022-10, Vol.23 (21), p.12719
Hauptverfasser: Liu, Huitao, Knox, Cheyenne A, Jakkula, Laxmi U M R, Wang, Ying, Peddireddi, Lalitha, Ganta, Roman R
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Sprache:eng
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Zusammenfassung:, a tick-transmitted intraphagosomal bacterium, is the causative agent of human monocytic ehrlichiosis. The pathogen also infects several other vertebrate hosts. has a biphasic developmental cycle during its growth in vertebrate monocytes/macrophages and invertebrate tick cells. Host- and vector-specific differences in the gene expression from many genes of are well documented. It is unclear how the organism regulates gene expression during its developmental cycle and for its adaptation to vertebrate and tick host cell environments. We previously mapped promoters of several genes which are recognized by its only two sigma factors: σ and σ . In the current study, we investigated in assessing five predicted transcription regulators; EcxR, CtrA, MerR, HU and Tr1 for their possible roles in regulating the pathogen gene expression. Promoter segments of three genes each transcribed with the RNA polymerase containing σ (HU, P28-Omp14 and P28-Omp19) and σ (ClpB, DnaK and GroES/L) were evaluated by employing multiple independent molecular methods. We report that EcxR binds to all six promoters tested. Promoter-specific binding of EcxR to several gene promoters results in varying levels of gene expression enhancement. This is the first detailed molecular characterization of transcription regulators where we identified EcxR as a gene regulator having multiple promoter-specific interactions.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms232112719