Abstract
Epigenetic modifications, including DNA methylation, stably alter gene expression without modifying genomic sequences. Recent evidence suggests that epigenetic regulation coupled with a long-term 'memory' effect plays a major role within bacterial persistence formation. Today, emerging high-resolution, single-molecule sequencing technologies allow an increased focus on DNA modifications as regulatory epigenetic marks, which presents a unique opportunity to identify possible epigenetic drivers of bacterial persistence.
Highlights
Concluding Remarks Our detailed understanding of the inner workings of the T6SS apparatus and the vital cellular epitopes targeted by effectors is due to productive efforts focused on the aggressor-side of the T6SS-mediated interbacterial interaction
Relatively little is known about the role of the T6SS in natural settings, including the identity of bacteria sharing overlapping niches that are targets of the T6SS, and the consequences of T6SS-mediated antagonism on bacterial coexistence within microbial communities
We propose that the investigation of specific or general (e.g., EPS or stress response) defense strategies that are utilized by bacteria to increase fitness in the face of T6SS attack will yield insight into these mysteries
Summary
Balanced cell division and death remains persistence acts as the perdebatable and challenges the traditional fect recipe for stress tolerance, granting viewpoint of 'true' dormancy [2]. protection against conditions otherwise harmful to normally growing cells, such as nutrient starvation, temperature shock, pH alteration, or antibiotic exposure. Bacterial persistence is commonly accepted as a fully reversible phenomenon [4], governed mainly by changes in regulation of gene expression rather than by genetic mutations [3,5,6]. It is, tempting to discuss whether bacterial persistence could be a consequence of epigenetically regulated mechanisms. The most studied epigenetic regulatory mechanism involves DNA methylation, orchestrated by addition of methyl groups to nucleotides within specific DNA sequences. Overall, this process is implicated in regulating multiple cellular processes, including timing of chromosome replication, DNA mismatch repair, and host defense [7]. The best-known example involves regulation of bacterial phase variation [7]
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