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Buddle, J. E.

Publications and source records attributed to Buddle, J. E..

3 recordsLinked to original sources

Protein architectures of the bacterial spore envelope - common principles of assembly

Bacterial spores are among the most durable of cell forms, protected by robust envelopes of layered protein assemblies. Remarkably, these envelopes often share similar architectures across distantly related bacteria despite extensive divergence in their molecular components. How evolution has converged on such similar highly ordered and resilient cellular structures is relatively unexplored. Here, we combine targeted mutagenesis, cryo-electron microscopy, atomic force microscopy and structure prediction to determine the organisation and assembly of the outer spore envelope of Clostridium sporogenes, a genetically tractable surrogate for Group I Clostridium botulinum. We reveal a hierarchy of protein structures, including a semi-permeable two-dimensional crystalline exosporium; CsxA forms the exosporium scaffold with an outer "hairy nap" partially composed of BclA. We observe a previously uncharacterised multilayered three-dimensional crystalline parasporal assembly within the interspace between exosporium and coat (CsxC). These distinct structures are built from related cysteine-rich SPOCS (SpoVID-CotE-SipL)-domain proteins that self-assemble into highly ordered lattices. Such crystalline organisation, combined with high symmetry, can provide a template for local enhancement of cysteine concentration, favouring cooperative disulphide cross-linking and the formation of exceptionally stable supramolecular structures. Unexpectedly, the three-dimensional CsxC structure grows through screw dislocations, a mechanism familiar from inorganic and synthetic crystal growth but rarely demonstrated in native biological assemblies, with the exception of some biomineralisation processes. Our observations now suggest that this classical crystal-growth mechanism can be exploited in both mineralised and proteinaceous biological materials. Related SPOCS-domain proteins are implicated in spore-envelope assembly across diverse Clostridia, where they have diversified to act as both structural components and morphogenetic organisers. Remarkably, distantly related Bacilli construct similarly highly symmetric crystalline, cysteine-rich and disulphide-stabilised spore layers using proteins with very different protein folds. Thus, crystallisation and cooperative disulphide formation appear to represent a convergent physicochemical strategy for building diverse self-assembling proteins into exceptionally robust cellular assemblies. Together these findings provide the first molecular framework for understanding the organisation and assembly of the Clostridium spore envelope and reveal previously unrecognised principles governing the evolution of protective proteinaceous structures across the Bacillota (Firmicutes).

microbiology↗

A novel two-component system controls vancomycin resistance in epidemic Clostridioides difficile

The glycopeptide antibiotic vancomycin is the frontline treatment for C. difficile infection in the UK. There have been only sporadic reports of resistance in the clinic but testing is rare so the true resistance landscape is unclear. We have previously shown that resistance can emerge rapidly in vitro via distinct but complementary pathways. Strain Bc2, characterised here, is an experimentally evolved derivative of C. difficile strain R20291 that displays a 16-fold increase in vancomycin MIC over its parent. Bc2 has point mutations in dacS, bclA3, CDR20291_0794, CDR20291_1871 and CDR20291_3124 (vnrS). By genetically engineering a wild-type vancomycin susceptible strain, we demonstrated that a combination of just two mutations, dacSc.798A>T and vnrSc.692G>T, both of which encode two-component system histidine kinases, was sufficient to recapitulate Bc2 resistance. We have previously shown that mutations in dacS can confer low level resistance via increases in the expression of a D,D-carboxypeptidase DacJ. dacSc.798A>T also led to increased transcription of dacJ and led to a modest increase in vancomycin MIC. Surprisingly vnrSc.692G>T led to overexpression of the vanG cluster, which encodes all of the enzymes needed for resistance via substitution of the terminal D-Ala on peptidoglycan lipid II precursors with D-Ser. Genomic analysis of a large collection of European C. difficile strains showed that a three gene cluster, which includes vnrS, vnrR (encoding the cognate response regulator) and an adjacent gene CDR20291_3123, is unique to the phylogenetic branch that contains strains belonging to epidemic ribotypes 027 and 176. Transcriptomic analysis of the wider VnrS regulon also revealed an additional previously unknown role in regulating the expression of the flagellum, an important virulence factor in C. difficile. Analysis of the response to vancomycin exposure also revealed that dacJ is one of a small set of genes that are upregulated shortly after antibiotic stress, even in the absence of mutations that typically lead to its overexpression. Together these data reveal a new synergistic route, needing only two point mutations, by which epidemic lineages of C. difficile can attain vancomycin resistance. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=147 HEIGHT=200 SRC="FIGDIR/small/671617v1_ufig1.gif" ALT="Figure 1"> View larger version (31K): org.highwire.dtl.DTLVardef@bba369org.highwire.dtl.DTLVardef@e562acorg.highwire.dtl.DTLVardef@1b112deorg.highwire.dtl.DTLVardef@4dcf8a_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗

Multiple evolutionary pathways lead to vancomycin resistance in Clostridioides difficile

Clostridioides difficile is an important human pathogen, for which there are very limited treatment options, primarily the glycopeptide antibiotic vancomycin. In recent years vancomycin resistance has emerged as a serious problem in several Gram positive pathogens, but high level resistance has yet to be reported for C. difficile, although it is not known if this is due to constraints upon resistance evolution in this species. Here we show that resistance to vancomycin can evolve rapidly under ramping selection but is accompanied by severe fitness costs and pleiotropic trade-offs, including sporulation defects that would be expected to severely impact transmission. We identified two distinct pathways to resistance, both of which are predicted to result in changes to the muropeptide terminal D-Ala-D-Ala that is the primary target of vancomycin. One of these pathways involves a previously uncharacterised D,D-carboxypeptidase, expression of which is controlled by a dedicated two-component signal transduction system. Our findings suggest that while C. difficile is capable of evolving high-level vancomycin resistance, this outcome may be limited clinically due to pleiotropic effects on key pathogenicity trains. Moreover, our data provide a mutational roadmap to inform genomic surveillance.

microbiology↗