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Biology subjects

Betjes, M. A.

Publications and source records attributed to Betjes, M. A..

4 recordsLinked to original sources

NuclearIDTracker resolves intestinal cell identity and lineage dynamics through nuclear phenotypic signatures

Organoid models have transformed our understanding of intestinal renewal. Fluorescent imaging has been extensively used to identify key cell types and their differentiation pathways, but immunofluorescence provides only static readouts, whereas live imaging requires fluorescent-reporter engineering and is constrained by limited multiplexing and spectral overlap. Here, we introduce NuclearIDTracker, an explainable machine-learning framework that infers cell identity directly from 3D nuclear segmentations. Using a single nuclear marker, NuclearIDTracker accurately classifies intestinal cell types and integrates with single-cell tracking to resolve lineages and reconstruct dynamic state transitions during organoid development. We show that TA-like cells, rather than stem cells, drive early crypt formation and generate enterocyte and Paneth lineages, as well as the stem-cell population, which emerges only later and subsequently replenishes the TA-like compartment. Following stem-cell ablation, crypt regeneration was not driven by a single discrete cell type. Instead, multiple epithelial populations converged on a proliferative regenerative state with a nuclear phenotypic signature that resembled, but remained distinct from, that of homeostatic TA-like cells, and a YAP/TAZ-associated fetal-like transcriptional signature. Thus, nuclear phenotypic signatures resolve cell identity and reveal coordinated epithelial plasticity during crypt regeneration. NuclearIDTracker establishes a non-perturbative tool to quantify cell identity and state dynamics at single-cell resolution, revealing previously inaccessible biological dynamics and expanding the toolkit for studying epithelial homeostasis, regeneration, and disease.

cell biology↗

Mature tuft cell phenotypes are sequentially expressed along the intestinal crypt-villus axis following cytokine-induced tuft cell hyperplasia

Intestinal tuft cells are epithelial sentinels that trigger host defense upon detection of parasite-derived compounds. While representing interesting targets for immunomodulatory therapies in inflammation-driven intestinal diseases, their detailed functioning is poorly understood. Although two distinct intestinal tuft cell types have been described, we reveal common intermediary transcriptomes among tuft cells in mouse and human. Tuft cell-specific reporter knock-ins in organoids show that the two tuft types are sequentially expressed transcriptomic states that represent different maturation stages. Moreover, cytokines interleukin-4 and interleukin-13 only induce lineage specification to Nrep+ tuft-1 cells, while BMP and cholinergic signalling advance differentiation towards immune-related ChAT+ tuft-2 phenotypes. Functionally, both tuft cell states have chemosensory capacity and respond to stimuli like succinate, but reaction probability increases during tuft cell maturation. Our tuft type-specific reporters and optimized differentiation strategy in organoids provide an experimental platform to study the functioning of tuft cells and their unique chemosensory properties.

cell biology↗

Cell tracking with accurate error prediction

Cell tracking is an indispensable tool for studying development by time-lapse imaging. However, existing cell trackers cannot assign confidence to predicted tracks, which prohibits fully automated analysis without manual curation. We present a fundamental advance: an algorithm that combines neural networks with statistical physics to determine cell tracks with error probabilities for each step in the track. From these we can obtain error probabilities for any tracking feature, from cell cycles to lineage trees, that function like p-values in data interpretation. Our method greatly speeds up tracking analysis by limiting manual curation to rare low-confidence tracking steps. Importantly, it also enables fully-automated analysis by retaining only high-confidence track segments, which we demonstrate by analyzing cell cycles and differentiation events at scale, for thousands of cells in multiple intestinal organoids. Our approach brings cell dynamics-based organoid screening within reach, and enables transparent reporting of cell tracking results and associated scientific claims.

bioinformatics↗

Dormancy as a spectrum measuring spore’s proximity to death and to replicative life

Dormancy is colloquially considered as extending lifespan by being still. Starved yeasts form dormant spores that wake-up (germinate) when nutrients reappear but cannot germinate (die) after some time. What sets their lifespans and how they age are open questions because what processes occur - and by how much - within each dormant spore remains unclear. With single-cell-level measurements, we discovered how dormant yeast spores age and die: spores have a quantifiable gene-expressing ability during dormancy that decreases over days to months until it vanishes, causing death. Specifically, each spore has a different probability of germinating that decreases because its ability to - without nutrients - express genes decreases, as revealed by a synthetic circuit that forces GFP expression during dormancy. Decreasing amounts of molecules required for gene expression - including RNA polymerases - decreases gene-expressing ability which then decreases chances of germinating. Spores gradually lose these molecules because they are produced too slowly compared to their degradations, causing gene-expressing ability to eventually vanish and, thus, death. Our work provides a systems-level view of dormancy-to-death transition. Short summaryThis study identifies systems-level quantities that decay during dormancy in Saccharomyces cerevisiae spores and thereby reveals the meaning of ageing for dormant yeast spores and shows that they die when their gene-expressing ability is irreversibly lost. HighlightsO_LIFor a given glucose concentration, a dormant yeast spore has a well-defined probability of germinating ("germination ability"). C_LIO_LIA spores germination ability positively correlates with its RNAP I-III levels and the gene-expression (GFP) level it can realize when the expression is forced without nutrients. C_LIO_LIAgeing during dormancy means gradual decreases in germination ability, RNAP levels, and GFP-level realizable when expression is forced. C_LIO_LISpores die after sufficiently losing gene-expressing ability and drugs that inhibit gene expression during dormancy shorten spores lifespans (e.g., from months to a day). C_LI

systems biology↗