Epigenetic and Epitranscriptomic Determinants of Host-Microbe Interactions

A special issue of Epigenomes (ISSN 2075-4655).

Deadline for manuscript submissions: closed (31 January 2024) | Viewed by 4185

Special Issue Editors


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Guest Editor
Department of Pathology and Cancer Center, College of Medicine, Howard University, Washington, DC 20059, USA
Interests: epigenetics; cancer; histone; PTMs; adenocarcinoma

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Guest Editor
Advanced Diagnostic Research Center, MSMF, Narayana Health City, Bommasandra, Bangalore 560099, India
Interests: genetics; cell culture; biotherapeutics; tumor immunology

Special Issue Information

Dear Colleagues,

Humans interact with a myriad of microorganisms from environmental exposures and the microbiome. Many of these microbes are essential to human health, such as the heterogeneous gastrointestinal microbiome responsible for the digestion of nutrients, immune surveillance, and critical metabolites, while others pose threats as primary or opportunistic pathogens. While the molecular mechanisms of microbial pathogenesis have been studied for more than a century, we are only now beginning to appreciate how the diversity of bacteria, archaea, viruses, and fungi in the microbiome, which varies significantly among individuals due to diet, lifestyle and host genetics, determines human health and disease. Growing evidence links microbiome dysbiosis to various diseases, including cancer, due to a complex metabolic interplay between the microbes and the human host. For example, it is well established that normally commensal microbes can become pathogenic due to ill-defined mechanisms of immune dysfunction and microbiome imbalances. Similarly, host pathologies such as inflammatory bowel disease are known to alter the gut microbiome but with unknown causes and consequences.

All microbes and their human hosts share two features of molecular genetics with surprisingly strong links to health and disease: epigenetic and epitranscriptomic regulation of gene expression. While the Central Dogma defines the “what” of biology—that genes are transcribed into messenger RNAs that are translated into proteins—it says nothing about the “when” or “how much” of expressing 4000–5000 genes in bacteria or >20,000 genes in humans. Convergent technologies have revealed information-rich scheduling systems for gene expression involving the dozens of chemical modifications of DNA, RNA, and histone proteins in every cell—the epigenome and epitranscriptome. Many of the epigenome and epitranscriptome components have been known for more than 50 years, but their functions have only recently emerged. DNA modifications, such as 5-methyl-2’-deoxycytidine in humans, are now known to regulate gene expression at the transcription level, with microbes possessing a much larger diversity of DNA modifications also involved in antimicrobial defense. Epigenetic control of gene expression in eukaryotes is regulated in parallel by dozens of histone protein secondary modifications. Analogously, the epitranscriptome comprises >170 chemical modifications of all forms of RNA in all organisms, with roughly 50 RNA modifications in every organism functioning in part to regulate gene expression at the translation level.

This Special Issue of Epigenomes presents the most up-to-date overview of the role of epigenomes and epitranscriptomes in the interplay between microbes and humans in healthy homeostasis and disease. Among the many topics covered here, the articles address discoveries of epigenetic marks in bacteriophage and bacteria, comparative genomics of epigenome and epitranscriptome machinery, breakthroughs in understanding the epitranscriptome-linked metabolic interdependencies of microbes and humans, and convergent analytical and informatic technologies for discovering, quantifying and mapping DNA and RNA modifications. Through a collection of research articles, reviews, and perspectives, readers will gain insights into the latest advancements in the emerging field of epigenetic and epitransciptomic determinants of host–microbe interactions.

Dr. Mudasir Rashid
Dr. Manjula Das
Guest Editors

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Keywords

  • microbiome
  • bacteria
  • viruses
  • fungi
  • archaea
  • bacteriophage
  • epigenetics
  • epitranscriptomics
  • metabolism
  • DNA methylation
  • histone modifications
  • non-coding RNA
  • RNA modifications
  • host–pathogen interactions
  • microbiology
  • innate immunity
  • inflammation
  • restriction modification

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Published Papers (2 papers)

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Research

18 pages, 9336 KiB  
Article
Deciphering the Diversity in Bacterial Transporters That Salvage Queuosine Precursors
by Samia Quaiyum, Yifeng Yuan, Paul J. Kuipers, Maria Martinelli, Marshall Jaroch and Valérie de Crécy-Lagard
Epigenomes 2024, 8(2), 16; https://doi.org/10.3390/epigenomes8020016 - 25 Apr 2024
Cited by 2 | Viewed by 1531
Abstract
Queuosine (Q) is a modification of the wobble base of tRNA harboring GUN anticodons with roles in decoding accuracy and efficiency. Its synthesis is complex with multiple enzymatic steps, and several pathway intermediates can be salvaged. The only two transporter families known to [...] Read more.
Queuosine (Q) is a modification of the wobble base of tRNA harboring GUN anticodons with roles in decoding accuracy and efficiency. Its synthesis is complex with multiple enzymatic steps, and several pathway intermediates can be salvaged. The only two transporter families known to salvage Q precursors are QPTR/COG1738 and QrtT/QueT. Analyses of the distribution of known Q synthesis and salvage genes in human gut and oral microbiota genomes have suggested that more transporter families remain to be found and that Q precursor exchanges must occur within the structured microenvironments of the mammalian host. Using physical clustering and fusion-based association with Q salvage genes, candidate genes for missing transporters were identified and five were tested experimentally by complementation assays in Escherichia coli. Three genes encoding transporters from three different Pfam families, a ureide permease (PF07168) from Acidobacteriota bacterium, a hemolysin III family protein (PF03006) from Bifidobacterium breve, and a Major Facilitator Superfamily protein (PF07690) from Bartonella henselae, were found to allow the transport of both preQ0 and preQ1 in this heterologous system. This work suggests that many transporter families can evolve to transport Q precursors, reinforcing the concept of transporter plasticity. Full article
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15 pages, 994 KiB  
Article
Comparison of Yersinia enterocolitica DNA Methylation at Ambient and Host Temperatures
by Dustin J. Van Hofwegen, Carolyn J. Hovde and Scott A. Minnich
Epigenomes 2023, 7(4), 30; https://doi.org/10.3390/epigenomes7040030 - 30 Nov 2023
Cited by 1 | Viewed by 2010
Abstract
Pathogenic bacteria recognize environmental cues to vary gene expression for host adaptation. Moving from ambient to host temperature, Yersinia enterocolitica responds by immediately repressing flagella synthesis and inducing the virulence plasmid (pYV)-encoded type III secretion system. In contrast, shifting from host to ambient temperature [...] Read more.
Pathogenic bacteria recognize environmental cues to vary gene expression for host adaptation. Moving from ambient to host temperature, Yersinia enterocolitica responds by immediately repressing flagella synthesis and inducing the virulence plasmid (pYV)-encoded type III secretion system. In contrast, shifting from host to ambient temperature requires 2.5 generations to restore motility, suggesting a link to the cell cycle. We hypothesized that differential DNA methylation contributes to temperature-regulated gene expression. We tested this hypothesis by comparing single-molecule real-time (SMRT) sequencing of Y. enterocolitica DNA from cells growing exponentially at 22 °C and 37 °C. The inter-pulse duration ratio rather than the traditional QV scoring was the kinetic metric to compare DNA from cells grown at each temperature. All 565 YenI restriction sites were fully methylated at both temperatures. Among the 27,118 DNA adenine methylase (Dam) sites, 42 had differential methylation patterns, while 17 remained unmethylated regardless of the temperature. A subset of the differentially methylated Dam sites localized to promoter regions of predicted regulatory genes including LysR-type and PadR-like transcriptional regulators and a cyclic-di-GMP phosphodiesterase. The unmethylated Dam sites localized with a bias to the replication terminus, suggesting they were protected from Dam methylase. No cytosine methylation was detected at Dcm sites. Full article
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