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McMillan, P. J.

Publications and source records attributed to McMillan, P. J..

3 recordsLinked to original sources

The Spatial Architecture of Human Subgingival Biofilms

Human microbiome studies have transformed understanding of disease-associated microbial communities, yet most approaches collapse polymicrobial biofilms into compositional profiles and lose the spatial relationships through which microorganisms interact in vivo. Periodontitis provides a clinically important model to investigate microbial spatial organisation because the disease is associated with deep, anaerobic periodontal pockets colonized by dense polymicrobial biofilms. Here, using multiplex fluorescence in situ hybridization with spectral and confocal microscopy of subgingival plaque across 174 sites from 36 individuals with periodontitis, we define taxon-resolved spatial architectures of the human subgingival plaque microbiome. We show that subgingival plaque is organized into recurrent multicellular assemblages of microbial consortia rather than unstructured layers of biomass, including assemblages defined as test-tube-brushes, corncobs and additional polymicrobial architectures with distinct taxonomic patterning. Test-tube brushes were enriched in severe periodontal niches, and their detection and burden increased with pocket depth, with distinct patterns observed in smoking-associated disease sites. In a longitudinal treatment subset, sites containing test-tube brushes before therapy lacked detectable test-tube brushes after treatment and instead showed corncobs concomitant with reduced pocket depth and resolution of disease. In addition to canonical oral biofilm structures, we identify previously undescribed polymicrobial assemblages whose occurrence is patterned by pocket depth and anatomical tooth site. These findings show that disease-associated human biofilms are organized into reproducible spatial states and suggest that microbial architecture provides an additional axis for interpreting microbiome-associated disease.

microbiology↗

SMAD4 loss drives chromosomal instability during tumourigenesis via translational reprogramming

Chromosomal instability (CIN), arising from errors in chromosome segregation during cell division, is a hallmark of cancer. Whilst CIN can result from several mitotic defects, the mechanisms that initiate CIN to drive tumourigenesis remain incompletely understood. Here, we show that loss of SMAD4 reprograms translation to induce CIN, resulting in tumour formation. Multi-omics analysis of tumourigenesis models driven by loss of SMAD4 complemented by functional studies demonstrate that loss of SMAD4 in pre-neoplastic cells leads to dysfunctional mitosis and an altered global translation landscape. We show that CDK11B is translationally downregulated in SMAD4-\- cells, and re-expression of the mitosis-specific isoform of this protein (CDK11B-p58) rescues the mitotic defects. Analysis of patient tumours reveals a strong correlation between markers of CIN and SMAD4 status, indicating the clinical relevance of this phenotype. Collectively, we reveal a previously unrecognised role for SMAD4 as a gatekeeper for CIN-mediated tumourigenesis via regulation of translation.

cancer biology↗

Viral hijacking of the nucleolar DNA-damage response machinery: a novel mechanism to regulate host cell biology

Recent landmark studies indicate that nucleoli play critical roles in the DNA-damage response (DDR) via interaction of DDR machinery including NBS1 with nucleolar Treacle protein, a key mediator of ribosomal RNA (rRNA) transcription and processing, implicated in Treacher-Collins syndrome. Here, using proteomics, confocal/super-resolution imaging, and infection under BSL-4 containment, we present the first report that this nucleolar DDR pathway is targeted by infectious pathogens. We find that Treacle has antiviral activity, but that matrix protein of Henipaviruses and P3 protein of rabies virus, highly pathogenic viruses of the order Mononegavirales, interact with Treacle and inhibit its function, thereby silencing rRNA biogenesis, consistent with mimicking NBS1-Treacle interaction during a DDR. These data identify a novel mechanism for viral modulation of host cells by appropriating the nucleolar DDR; this appears to have developed independently in different viruses, and represents, to our knowledge, the first direct intra-nucleolar function for proteins of any mononegavirus.

microbiology↗