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Shown are vectorized false-coloured images of L-form-like Enterococcus faecalis cells that are in the process of escaping the cell wall sacculus. Wohlfarth et al. report that L-form escape is triggered by the phage-derived endolysin Ply007, which functions as a peptidoglycan hydrolase. In Gram-positive bacteria, L-form conversion enables transient escape from further phage infection.
The extent and diversity of exposures to microbial stimuli have a crucial role in regulating the capacity of a host to mount an immune response to a challenge, such as vaccination, making exposure history an important factor to optimize in rodent models.
Phage-encoded endolysins released from neighbouring infected bacterial cells can confer a temporary resistance to phage infection by mediating the reversible loss of the cell wall.
Mycobacterium abscessus requires high levels of biotin biosynthesis during infection, because this vitamin enables key adaptations to the alkaline lung airway environment through fatty acid remodelling that increases fluidity of the cell envelope.
A combined quantitative and isotope-tracking proteomics approach illuminates how scarce nitrogen is allocated to protein biosynthesis by members of an ocean-surface microbial community. We identify taxon-specific substrate preferences and a distinct subset of functions — particularly infrastructure for protein production, folding and turnover — that constitute the bulk of community nitrogen demand.
Human cytomegalovirus (HCMV) has two modes of infection: productive and latent. Tracking HCMV infection with single-cell transcriptomics revealed that infection outcome (productive or latent) is based on viral gene expression levels at early stages of infection. Moreover, intrinsic levels of interferon-stimulated genes affect viral gene expression and the outcome of infection.
Phage-encoded endolysins released from lysed bacteria trigger neighbouring cells to convert into cell wall-deficient L-forms that are resistant to subsequent phage infection.
Deployment of some CRISPR-Cas systems stunts host growth by degrading all transcripts, but Listeria seeligeri reverses dormancy using restriction-modification-based phage DNA targeting.
Application of reprogrammed bacteriophage to functional metagenomics in clinically relevant bacterial strains improves identification of antibiotic resistance genes, including those against recently developed or approved antibiotics.
Systems genetics reveals interactions between host and microbial phenotypes in the murine gut, including a role for Akkermansia muciniphila in the production of immunomodulatory ornithine lipids.
Stable isotope-labelled amino acid incorporation into proteins reveals that genetically homogeneous yeast colonies contain metabolically distinct subpopulations that cross-feed each other and are phenotypically diverse.
Temporal single-cell RNA sequencing analysis of viral and host transcriptional responses during human cytomegalovirus infection of macrophages and monocytes reveals molecular features influencing distinct infection courses and suggests additional latency reservoirs.
Biotin biosynthesis enables fatty acid remodelling and increased cell envelope fluidity, which counter alkaline pH in the lung and promote Mycobacterium abscessus growth during infection.
Tracking labelled nitrogen atoms from multiple substrates into individual peptides within complex microbial communities shows which cellular functions constitute the bulk of proteomic N demand and the metabolic basis of N limitation.
Single-cell imaging, metabolomics and modelling quantify metabolic exchanges between cyanobacteria and heterotrophic bacteria, showing transient nutritional exchanges facilitated by chemotaxis of the heterotroph.
Eighty-nine percent of the Trypanosomabrucei proteome is mapped using fluorescence microscopy and cell lines expressing endogenously tagged proteins, and presented in a resource for the community named TrypTag.org.
A resource of >3,700 Ser/Thr protein kinase-substrate interactions and their transcriptional effects establishes O-phosphorylation as a dominant signalling mechanism in Mycobacterium tuberculosis.