Biology subjects

Kent, R.

Publications and source records attributed to Kent, R..

4 recordsLinked to original sources

bioRxiv2026

The Spontaneous Evolution of Biology

We have demonstrated the potential of amino acids to polymerise into peptides, proteins, and form cell-like structures in the absence of cellular machinery, including nucleic acids, lipids or sugars. Not only has cell-free protein replication been observed, but evidence of protein templating strongly suggests protein mediated replication. We believe this is the first experimental demonstration of the link between the Miller-Urey experiment which produced amino acids from elemental starting material, and cell-like structures. Life, by definition, is the condition that distinguishes animals and plants from inorganic matter, including the capacity for growth, reproduction, functional activity, and continual change preceding death. Here we have characterised peptides which form reproducibly, into structures with longevity and which subsequently catalyse the polymerisation of free amino acids into copies of themselves. The proteomic analysis of these samples over time also enables evolution of peptide sequences to be seen and quantified. This evolution of both complex structure and functionally active proteins may potentially demonstrate a credible path to the beginnings of life, which we call the Spontaneous Evolution of Biology (SEB) Theory. One Sentence SummaryWe have shown how peptides and proteins can be made from amino acids in an aqueous media without cells, lipids or nucleic acids, duplicating themselves and forming complex structures which resemble cells.

biochemistry↗

bioRxiv2025

Perivascular matrix densification dysregulates angiogenesis and activates pro-inflammatory endothelial cells

Fibrosis is central to numerous fatal conditions including solid cancers, pulmonary fibrosis, cirrhosis and post-infarct cardiac fibrosis amongst many others, thereby collectively contributing to 45% of all deaths in developed nations. The potential for fibrosis across most organ systems may stem from its connections to wound healing and the ubiquitous presence of vascular endothelium. Endothelial cells (ECs) and angiogenesis, cells and associated biological program central to wound healing, have been heavily implicated in many organ-specific fibroses, but the relationship between angiogenesis and fibrogenesis remains debated and little has been established in terms of how the EC phenotype governs tissue healing vs. fibrosis. Here, we examine a murine lung injury model enabling EC lineage tracing and observe the invasion of aberrant ECs from the bronchial microvasculature following lung injury along with concurrent densification of matrix fibers surrounding these vessels. To investigate the underlying mechanisms governing their appearance, we established a microphysiological system (MPS) of arteriole/venule-scale microvessels embedded within a tunable stromal mimetic matrix and find that heightened extracellular matrix fiber density activates ECs, drives endothelial to mesenchymal transition, and promotes aberrant tip EC (ATEC) invasion into the matrix. ATECs remain adherent to fibrotic matrix and possess a pro-inflammatory phenotype that secretes TGF-{beta}2. Notably, our studies establish that the formation of ATECs is gated by destabilization of endothelial adherens junction upon EC adhesion to fibrous matrix, and associated regulation of TGF-{beta} signaling that is mediated by a novel VE-cadherin - TGF-{beta}R2 axis. The current lack of effective anti-fibrotic therapies suggests potential critical involvement of other cell types such as ECs, and our findings suggest new contributions of ECs to fibrotic progression that may better inform future targets for novel anti-fibrotic therapeutics.

bioengineering↗

bioRxiv2021

Sulfite preservatives effects on the mouth microbiome: changes in viability, diversity and composition of microbiota

Processed foods make up about 70 percent of the American diet. Sulfites and other food preservatives are added to these foods largely to limit bacterial contamination. The mouth microbiota and its associated enzymes are the first to encounter food and therefore likely to be the most affected. Eight saliva samples from ten individuals were exposed to two sulfite preservatives, sodium sulfite and sodium bisulfite. One sample set was evaluated for bacteria composition utilizing 16s rRNA sequencing, and the number of viable cells in all sample sets was determined utilizing ATP assays at 10 and 40-minute exposure times. All untreated samples were analyzed for baseline lysozyme activity, and possible correlations between the number of viable cells and lysozyme activity. Sequencing results indicated significant increases in alpha diversity with sodium bisulfite exposure and changes in relative abundance of 3 amplicon sequence variants (ASV). Sodium sulfite treated samples showed a significant decrease in the Firmicutes/Bacteroidetes ratio, a marginally significant change in alpha diversity, and a significant change in the relative abundance for Proteobacteria, Firmicutes, Bacteroidetes, and for 6 ASVs. Beta diversity didnt show any separation between groups, however, all but one sample set was observed to be moving in the same direction under sodium sulfite treatment in a principal component analysis. ATP assays indicated a significant and consistent average decrease in activity ranging from 24 - 46% at both exposure times with both sulfites. Average initial rates of lysozyme activity between all individuals ranged from +/- 76% compared to individual variations of +/- 10 - 34%. No consistent, significant correlation was found between ATP and lysozyme activity in any sample sets. ConclusionsSulfite preservatives, at concentrations regarded as safe by the FDA, alter the relative abundance and richness of the microbiota found in saliva, and decrease the number of viable cells, within 10 minutes of exposure.

microbiology↗

bioRxiv2019

Differential requirements of cyclase associated protein (CAP) for actin turnover during the lytic cycle of Toxoplasma gondii

Toxoplasma gondii contains a limited subset of actin binding proteins. Here we show that ablation of the putative actin regulator cyclase-associated protein (TgCAP) leads to significant defects in some but not all actin dependent processes, including a defect in cell-cell communication, but surprisingly not synchronicity of division. Two CAP isoforms originate from alternative translational start sites and are beneficial for parasite fitness while a single isoform is sufficient for virulence in mice. Examination of the mutant parasites by 3D electron microscopy reveals that loss of CAP results in a defect to form a normal residual body, but all parasites remain connected within the vacuole. This dissociates synchronicity of division and parasite rosetting and reveals that establishment and maintenance of the residual body may be more complex than previously thought. These results highlight the different spatial requirements for actin turnover in Toxoplasma, controlled by a reduced subset of actin binding proteins.

microbiology↗