Journal of Microbiology

Journal Article

Identification and Characterization of HEPN‑MNT Type II TA System from Methanothermobacter thermautotrophicus ΔH: Wonho Choi , Anoth Maharjan , Hae Gang Im , Ji-Young Park , Jong-Tae Park , Jung-Ho Park; J. Microbiol. 2023;61(4):411-421. Published online April 18, 2023; DOI: https://doi.org/10.1007/s12275-023-00041-9

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Toxin-antitoxin (TA) systems are widespread in bacteria and archaea plasmids and genomes to regulate DNA replication, gene transcr!ption, or protein translation. Higher eukaryotic and prokaryotic nucleotide-binding (HEPN) and minimal nucleotidyltransferase (MNT) domains are prevalent in prokaryotic genomes and constitute TA pairs. However, three gene pairs (MTH304/305, 408/409, and 463/464) of Methanothermobacter thermautotropicus ΔH HEPN-MNT family have not been studied as TA systems. Among these candidates, our study characterizes the MTH463/MTH464 TA system. MTH463 expression inhibited Escherichia coli growth, whereas MTH464 did not and blocked MTH463 instead. Using site-directed MTH463 mutagenesis, we determined that amino acids R99G, H104A, and Y106A from the R[ɸX]4-6H motif are involved with MTH463 cell toxicity. Furthermore, we established that purified MTH463 could degrade MS2 phage RNA, whereas purified MTH464 neutralized MTH463 activity in vitro. Our results indicate that the endonuclease toxin MTH463 (encoding a HEPN domain) and its cognate antitoxin MTH464 (encoding the MNT domain) may act as a type II TA system in M. thermautotropicus ΔH. This study provides initial and essential information studying TA system functions, primarily archaea HEPN-MNT family.

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Extensive Genomic Rearrangement of Catalase-Less Cyanobloom-Forming Microcystis aeruginosa in Freshwater Ecosystems
Minkyung Kim, Jaejoon Jung, Wonjae Kim, Yerim Park, Che Ok Jeon, Woojun Park
Journal of Microbiology.2024; 62(11): 933. CrossRef

Research Support, Non-U.S. Gov't

Innate signaling mechanisms controlling Mycobacterium chelonae-mediated CCL2 and CCL5 expression in macrophages: Yi Sak Kim , Ji Hye Kim , Minjeong Woo , Tae-sung Kim Kim , Kyung Mok Sohn , Young-Ha Lee , Eun-Kyeong Jo , Jae-Min Yuk; J. Microbiol. 2015;53(12):864-874. Published online December 2, 2015; DOI: https://doi.org/10.1007/s12275-015-5348-1

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Abstract

Mycobacterium chelonae (Mch) is an atypical rapidly growing mycobacterium (RGM) that belongs to the M. chelonae complex, which can cause a variety of human infections. During this type of mycobacterial infection, macrophagederived chemokines play an important role in the mediation of intracellular communication and immune surveillance by which they orchestrate cellular immunity. However, the intracellular signaling pathways involved in the macrophage- induced chemokine production during Mch infections remain unknown. Thus, the present study aimed to determine the molecular mechanisms by which Mch activates the gene expressions of chemokine (C-C motif) ligand 2 (CCL2) and CCL5 in murine bone marrow-derived macrophages (BMDMs) and in vivo mouse model. Toll-like receptor 2 (TLR2)-deficient mice showed increased bacterial burden in spleen and lung and decreased protein expression of CCL2 and CCL5 in serum. Additionally, Mch infection triggered the mRNA and protein expression of CCL2 and CCL5 in BMDMs via TLR2 and myeloid differentiation primary response gene 88 (MyD88) signaling and that it rapidly activated nuclear factor (NF)-κB signaling, which is required for the Mch-induced expressions of CCL2 and CCL5 in BMDMs. Moreover, while the innate receptor Dectin-1 was only partly involved in the Mch-induced expression of the CCL2 and CCL5 chemokines in BMDMs, the generation of intracellular reactive oxygen species (ROS) was an important contributor to these processes. Taken together, the present data indicate that the TLR2, MyD88, and NF-κB pathways, Dectin-1 signaling, and intracellular ROS generation contribute to the Mch-mediated expression of chemokine genes in BMDMs.

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The Rise of Non-Tuberculosis Mycobacterial Lung Disease
Champa N. Ratnatunga, Viviana P. Lutzky, Andreas Kupz, Denise L. Doolan, David W. Reid, Matthew Field, Scott C. Bell, Rachel M. Thomson, John J. Miles
Frontiers in Immunology.2020;[Epub] CrossRef
A Comparative Analysis of Edwardsiella tarda-Induced Transcriptome Profiles in RAW264.7 Cells Reveals New Insights into the Strategy of Bacterial Immune Evasion
Huili Li, Boguang Sun, Xianhui Ning, Shuai Jiang, Li Sun
International Journal of Molecular Sciences.2019; 20(22): 5724. CrossRef
Abnormal Microglia and Enhanced Inflammation-Related Gene Transcription in Mice with Conditional Deletion ofCtcfinCamk2a-Cre-Expressing Neurons
Bryan E. McGill, Ruteja A. Barve, Susan E. Maloney, Amy Strickland, Nicholas Rensing, Peter L. Wang, Michael Wong, Richard Head, David F. Wozniak, Jeffrey Milbrandt
The Journal of Neuroscience.2018; 38(1): 200. CrossRef

Expression of Chemokine and Tumor Necrosis Factor Alpha Genes in Murine Peritoneal Macrophages Infected with Orientia tsutsugamushi: Young-Sang Koh; J. Microbiol. 2001;39(3):186-194.

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Abstract: Scrub typhus, caused by Orientia tsutsugamushi infection, is clinically and histopathologically characterized by local as well as systemic inflammatory reactions, indicating that orientiae induce mechanisms that amplify the inflammatory response. To reveal underlying mechanisms of chemoattraction and activation of responding leukocytes, expression of chemokine and tumor necrosis factor alpha (TNF-[alpha]) genes in murine peritoneal macrophages after infection with the obligate intracellular bacterium O. tsutsugamushi was investigated. The genes that were upregulated included macrophage inflammatory proteins 1[alpha]/[beta] (MIP-1[alpha]/[beta]), MIP-2, monocyte chemoattractant protein 1 (MCP-1), RANTES (regulated upon activation, normal T-cell expressed and secreted), gamma-interferon-inducible protein 10 (IP-10), and TNF-[alpha]. Peak expression of these chemokines and TNF-[alpha] was observed between 1 and 3 h after infection. These responses returned to or approached baseline preinfection levels 6 h after challenge. Semiquantitative reverse transcription (RT)-PCR analysis revealed dramatic increases during infection in the steady-state levels of mRNA coding for the inhibitory subunit of NF-[kappa]B (I[kappa]B[alpha]), whose transcription is enhanced by binding of NF-[kappa]B within the I[kappa]B[alpha] promoter region. Thus, O. tsutsugamushi appears to be a strong inducer of chemokines and TNF-[alpha] which may significantly contribute to inflammation and tissue damage observed in scrub typhus by attracting and activating phagocytic leukocytes.

Chemokine Gene Expression in Mice during Orientia tsutsugamushi Infection: Young-Sang Koh; J. Microbiol. 2003;41(3):266-270.

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Abstract: Orientia tsutsugamushi, an obligate intracellular bacterium, is the causative agent of scrub typhus which is histopathologically characterized by inflammatory manifestations. To understand the pathogenesis of scrub typhus, chemokine gene expression in mice after infection with O. tsutsugamushi was investigated. The mRNAs that were upregulated included macrophage inflammatory proteins 1[alpha]/[beta] (MIP-1[alpha]/[beta]), MIP-2, monocyte chemoattractant protein 1, RANTES (regulated upon activation, normal T-cell expressed and secreted), and gamma-interferon-inducible protein 10. Peak expression of these chemokines was observed six days after infection. These responses returned to or approached baseline preinfection levels by eight days after infection. Chemokine profiles in infected mice were well correlated with the kinetics of inflammatory cell infiltration. Thus, O. tsutsugamushi appears to be a strong inducer of chemokines which may significantly contribute to the inflammation observed in scrub typhus by attracting and activating phagocytic leukocytes.

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