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Biology subjects

Ng, A. S.

Publications and source records attributed to Ng, A. S..

4 recordsLinked to original sources

Bacteria-induced colitis in naked mole rats is alleviated by probiotic treatment: a new mammalian model for acute inflammatory disease

Enteropathogenic bacteria are a major cause of morbidity and mortality globally. Mouse models have been indispensable in advancing our understanding of infectious diseases caused by intestinal pathogens and in identifying physical, chemical and immunological barriers that limit these infections. However, there are significant differences between laboratory mice and human intestinal microbiota and immunobiology that underscore the need to develop other models that recapitulate the disease pathology and mucosal immune responses of human enteric diseases. Here we report how the pathogenic expansion of Citrobacter braakii in naked mole rats (NMRs) leads to colonic inflammation and epithelial injury that mimics pathological features of human hemorrhagic colitis. We observe mucosal erosions, ulcerations, depletion of goblet cells, extension of proliferative compartments to the surface of the glands, and active inflammation in the colonic lamina propria of infected NMRs. Without intervention, systemic inflammation associated with sepsis ensues in infected NMRs and results in high mortality. Interestingly, we demonstrate a strong therapeutic effect of probiotics comprising Lactobacillus, Bifidobacterium, Streptococcus salvarius subsp. thermophilus and Enterococcus faecium strains. Treatment with probiotics induces mucosal healing and restores intestinal homeostasis, including suppression of excessive proliferation of epithelial cells, replenishment of goblet cells and also has an anti-inflammatory effect. Taken together, we demonstrate that NMRs, beyond their use as an anti-ageing and disease-resistance model, can also be used to address disease mechanisms underlying infectious colitis, including disruptions in the mucosal barrier permeability, gut microbial ecology and in local and systemic immune regulation; and in testing functional probiotics strains as potential therapeutics.

pathology↗

GREMLIN1 disrupts intestinal epithelial-mesenchymal crosstalk to induce a wnt-dependent ectopic stem cell niche via stromal remodelling

In homeostasis, counterbalanced morphogen signalling gradients along the vertical axis of the intestinal mucosa regulate the fate and function of epithelial and stromal cell compartments. Here, we used a disease-positioned mouse, and human tissue, to explore the consequences of pathological Bone Morphogenetic Protein (BMP) signalling dysregulation on epithelial- mesenchymal interaction. Aberrant pan-epithelial expression of the secreted BMP antagonist GREM1, resulted in ectopic crypt formation with lineage tracing demonstrating the presence of Lgr5(-) stem/progenitor cells. Isolated epithelial cell Grem1 expression had no effect on individual cell fate, indicating an intercompartmental impact of mucosal-wide BMP antagonism. Treatment with a novel anti-Grem1 antibody abrogated the polyposis phenotype, and triangulation of specific pathway inhibitors defined a pathological sequence of events, with wnt-ligand dependent ectopic stem cell niches formed through stromal remodelling following BMP disruption. These data support an emerging co-evolutionary model of intestinal cell compartmentalisation based on bidirectional regulation of epithelial-mesenchymal cell fate and function. One Sentence SummaryPathological epithelial GREM1 expression induces therapeutically reversible ectopic stem cell niches through stromal remodelling

cancer biology↗

PRMT1 is a critical dependency in clear cell renal cell carcinoma through its role in post-transcriptional regulation of DNA damage response genes

Biallelic inactivation of the Von Hippel-Lindau (VHL) tumor suppressor gene occurs in almost all cases of clear cell renal cell carcinoma (ccRCC) and leads to disrupted oxygen sensing and the upregulation of hypoxia-related genetic programs. Although the loss of VHL appears to be a necessary oncogenic driver event in the majority of ccRCC instances, it is not always a sufficient one. Large genomics studies have revealed that co-deletions of VHL with genes involved in chromatin regulation are common and important co-drivers of tumorigenesis. Several conserved evolutionary subtypes have been described clinically and the majority implicate disruptions in epigenetic regulators. It is now clear that impairments in cellular epigenetic mechanisms are important co-drivers of disease and signal a potential vulnerability in the epigenetic network of ccRCC cells relative to their normal counterparts. Using a clinically relevant panel of ccRCC models, we herein sought to exploit this potential vulnerability by screening a library of small molecule inhibitors that target a spectrum of epigenetic regulators. We identified MS023, an inhibitor of type I protein arginine methyltransferases (PRMTs) as an agent with antitumor activity. Using orthogonal genetic technologies, we further validated PRMT1 as the specific critical dependency for cancer growth. Mechanistically, our transcriptomic and functional analyses suggest that MS023 treatment results in substantial impairments to cell cycle and DNA damage repair (DDR) pathways, while spawning an accumulation of DNA damage over time. Our PRMT1 specific proteomics analysis revealed an interactome rich in RNA binding proteins including the specific regulator of DDR mRNA metabolism: the BCLAF1/THRAP3 complex. Further investigation suggests that MS023 treatment may result in impairments to DDR specific mRNA activities including nucleocytoplasmic transport and RNA splicing. Together, our data supports PRMT1 as a compelling target in ccRCC and informs a potential mechanism-based strategy for translational development.

cancer biology↗

A spindle and thread-mechanism unblocks translation of N-terminally disordered proteins

Protein disorder is a major hurdle for structural biology. A prominent example is the tumour suppressor p53, whose low expression levels and poor conformational stability due to a high degree of disorder pose major challenges to the development of cancer therapeutics. Here, we address these issues by fusing p53 to an engineered spider silk domain termed NT*. The chimeric protein displays highly efficient translation in vitro and in E. coli and is fully active in human cancer cells. The transmission electron microscopy structure and native mass spectrometry reveal that the full-length p53 fusion protein adopts a compact conformation. Molecular dynamics simulations show that the disordered transactivation domain of p53 is wound around the NT* domain via a series of folding events, resulting in a globular structure. We find that expression of B-Raf, another partially disordered cancer target, is similarly enhanced by fusion to NT*. In summary, we demonstrate how inducing co-translational folding via a molecular "spindle and thread" mechanism can overcome poor translation efficiency of partially disordered proteins.

biochemistry↗