It was founded in 1987.
Abstract Staphylococcal cassette chromosome (SCC) elements are mobile genetic elements that integrate at the rlmH gene and are predominantly responsible for methicillin resistance in staphylococci. Although SCC mec typing tools exist, none can extract the element sequence itself or explicitly classify SCC elements that lack methicillin resistance genes. Here we present SCC mec Extractor, a lightweight Python toolkit that identifies SCC element boundaries through degenerate attachment site ( att ) pattern matching, extracts complete elements from whole-genome assemblies and characterises their mec and ccr gene content. Benchmarking on 7,297 genomes spanning 70 species across Staphylococcus and Mammaliicoccus demonstrated 100% typing concordance with the sccmec tool 1 on 1,454 S. aureus genomes. The tool extracted 1,562 SCC elements, from 1,454 S. aureus , 5,295 non- aureus Staphylococcus and 548 Mammaliicoccus genomes, achieving effective extraction rates (excluding assembly-limited genomes and those lacking valid ccr pairs) of 87.3% for S. aureus , 58.8% for non- aureus Staphylococcus , and 61.9% for Mammaliicoccus . Notably, 616 of the 1,562 extracted elements (39.4%) were non- mec SCC elements lacking methicillin resistance genes, a class of mobile element often overlooked. Non- mec SCC prevalence increased from 12.2% in S. aureus to 55.6% in non- aureus Staphylococcus and 76.0% in Mammaliicoccus , revealing a substantial reservoir of SCC diversity beyond methicillin resistance. SCC mec Extractor is freely available via PyPI, Docker and Singularity under an MIT licence. Impact Statement Staphylococcal cassette chromosome (SCC) elements are mobile genetic elements responsible for methicillin resistance in staphylococci and are central to methicillin resistant Staphylococcus aureus (MRSA) epidemiology. Existing tools focus on typing SCC mec from assemblies but cannot extract the element itself, limiting our ability to comprehensively monitor and examine these elements. SCC mec Extractor is a lightweight, portable tool that detects the attachment sites, required by SCC elements to integrate into the genome, extracts the SCC element, both mec gene carrying and not, and characterises their gene content. Applied across 7,297 genomes spanning two genera, we demonstrate that non- mec SCC elements are the dominant SCC class outside S. aureus , a finding enabled by systematic extraction and classification of SCC elements regardless of mec gene content. SCC mec Extractor provides the research community with an accessible, confidence-first approach (based on biology) to SCC element analysis across all staphylococci and mammaliicocci species. Data Summary The code for this pipeline is available at: https://github.com/AlisonMacFadyen/SCCmecExtractor , with a Docker image available at: https://hub.docker.com/repository/docker/alisonmacfadyen/sccmecextractor and PyPi package at: https://pypi.org/project/sccmecextractor/ . All reference databases are bundled with the tool. Benchmarking genome accessions: 1,454 S. aureus , 5,295 non-aureus Staphylococcus , and 548 Mammaliicoccus genomes from NCBI. A complete list of genome accessions is provided as supplementary data (Supplementary Table S1). Extracted SCC elements can be obtained from Zenodo: 10.5281/zenodo.19355206
Abstract To cause rice blast disease, the filamentous fungus Magnaporthe oryzae develops a specialised infection cell called an appressorium, which generates enormous turgor to breach the rice leaf cuticle. Although key regulators of appressorium development have been identified, it is not known how they drive the extensive transcriptional reprogramming required for infection-related morphogenesis. Here, we show that the Pmk1 MAP kinase orchestrates plant infection by regulating a transcriptional network controlled by the Mst12 and Bip1 transcription factors. Bip1 is regulated both by Pmk1-dependent phosphorylation and at the transcriptional level, while Mst12 binds to a cis -acting element upstream of BIP1 essential for pathogenesis. Bip1 and Mst12 are both necessary for regulating a set of Pmk1-dependent appressorium-specific genes, including transcriptional regulators, cell wall-degrading enzymes, and effector proteins. In addition, Mst12 specifically regulates functions required for appressorium-mediated penetration, while Bip1 controls a distinct sub-set of effector genes deployed during invasion of plant tissue. When considered together, these findings define a Pmk1-dependent transcriptional network required for plant infection by the blast fungus.
Plant nucleotide–binding leucine–rich repeat (NLR) immune receptors typically confer resistance through recognition of specific pathogen effectors. The Arabidopsis NLR WRR4A defies this paradigm by recognizing multiple sequence-divergent effectors from Albugo candida, conferring resistance to multiple pathogen races. Despite minimal sequence similarity, these effectors share a conserved N–terminal ferredoxin–like fold. Through cryo–EM structure determination of two WRR4A resistosomes bound to sequence–distinct effectors, combined with AlphaFold modelling, we reveal a shape–based recognition mechanism: WRR4A engages structurally conserved backbone features of the effectors in a mostly side chain-independent manner, enabling recognition of diverse effectors with similar three–dimensional architectures. These insights guided successful engineering of WRR4A to acquire novel recognition specificity. In addition, analysis of the monomeric WRR4A resting state reveals a distinct domain architecture characteristic of C–JID—containing TIR–NLRs and informs their activation mechanism. This work provides insights into NLR–mediated broad-spectrum recognition and the potential for structure–informed engineering of improved crop resistance. ### Competing Interest Statement The authors have declared no competing interest. BBSRC, BB/P021646/1, BB/S018832/1, BB/W017423/1 Gatsby Charitable Foundation UKRI Biotechnology and Biological Sciences Research Council Norwich Research Park Biosciences Doctoral Training Partnership, BB/T008717/1 Wellcome Trust, 202679/Z/16/Z, 206166/Z/17/Z EMBO Postdoctoral Fellowship, EMBO ALTF88-2021
Microbial homeostasis is crucial for host health and ecosystem function, yet the molecular and ecological mechanisms underlying community assembly and stability remain elusive. Here, we uncover a conserved yeast-oomycete metabolic mutualism that promotes their coexistence in the leaf microbiome. Using a continental-scale microbiome survey, we identified a mutualistic interaction between two eukaryotic hub microbes: the yeast Dioszegia hungarica and the obligate oomycete Albugo laibachii. We show that Dioszegia facilitates Albugo colonization by supplying thiamine via a dedicated membrane permease, alleviating Albugo’s auxotrophy. Genomic and transcriptomic analyses reveal that natural selection has acted on thiamine production in D. hungarica, shaping this mutualistic interaction. In planta assays further demonstrate that cross-feeding enhances Albugo colonization and promotes Dioszegia persistence. Our study illustrates how the evolution of nutrient cross-feeding mediates microbial coexistence and microbiome stability. Targeting microbial nutrient flows offers new strategies for engineering microbiomes and enhancing plant resilience in natural and agricultural systems.
