Biology subjects

Bulteau, R.

Publications and source records attributed to Bulteau, R..

5 recordsLinked to original sources

bioRxiv2026

A nuclear role for the contractile protein troponin I/UNC-27 in regulating muscle aging in C. elegans

Muscle ageing is characterized by evolutionarily conserved subcellular alterations across diverse organisms. In Caenorhabditis elegans, the decline in sarcomeric gene expression is among the earliest detectable ageing-associated changes, emerging at the onset of adulthood. To identify causal regulators of muscle ageing in an unbiased manner, we developed a genetic screening strategy that enables visual monitoring of muscle ageing at both cellular and organismal scales. Using this approach, we identified a mutation that delays the age-associated loss of sarcomeric transcripts. Unexpectedly, the mutation maps to the troponin I gene unc-27, which encodes a conserved regulator of muscle contraction not previously implicated in gene regulation. The mutation alters a single amino acid within a predicted nuclear localization signal (NLS). We found that multiple NLS motifs mediate the active transport of UNC-27 into muscle nuclei from early adulthood onward. Disruption of UNC-27 nuclear localization preserves sarcomeric gene expression during ageing and delays early hallmarks of muscle decline, including proteostatic imbalance and mitochondrial fragmentation. Transcriptomic analyses further revealed that nuclear UNC-27 selectively regulates the expression of genes encoding structural components of the muscle apparatus in adult animals. These results support the existence of a homeostatic sarcomere surveillance pathway, in which a structural protein unexpectedly acquires a transcriptional regulatory role in response to age-associated physiological state. The conservation of NLS motifs in mammalian UNC-27 orthologues suggests that this mechanism may be evolutionarily conserved, with potential relevance to human muscle physiology and disease.

cell biology↗

bioRxiv2025

Atomic Force Microscopy reveals differences in mechanical properties linked to cortical structure in mouse and human oocytes

Cell mechanical properties regulate biological processes such as oocyte development. Cortical tension is regulated via actomyosin cortex remodeling to ensure optimal oocyte quality. However, the evolution of other mechanical parameters and their relationship with cortex structure remain poorly understood in mammalian oocytes. In this work, we propose a methodology combining multiple mechanical parameters measured through Atomic Force Microscopy to investigate the relationship between oocyte mechanical properties and cortex organization. By studying mouse oocytes at various stages of development, along with engineered ones with specific cortex organization, we demonstrate that a thin actin cortex corresponds to stiff oocytes while a thick one is associated with softer oocytes. We further reveal that maternal age, a critical factor for fertility, affects mouse oocytes mechanics correlating with alterations in their cortex structure. Finally, we show that the evolution of mechanical properties differs between human and mouse oocyte development, highlighting species-specific differences in cortex organization.

biophysics↗

bioRxiv2025

Non-invasive characterization of oocyte deformability in micro-constrictions

Oocytes naturally present mechanical defects that hinder their development after fertilization. Thus, in the context of assisted reproduction, oocyte selection based on their mechanical properties has great potential to improve the quality of the resulting embryos and the success rate of these procedures. However, the use of mechanical properties as a quantifiable selective criterion requires robust and non-destructive measurement tools. This study developed a constriction-based microfluidic device that monitors the deformation of mouse oocytes under controlled pressure. The device can distinguish mechanically aberrant oocyte groups from healthy control ones. Based on a mathematical model, we propose that deformability measurements infer both oocyte tension and elasticity, elasticity being the most discriminating factor in our geometry. Despite force transmission during oocyte deformation, no long-term damage was observed. This non-invasive characterization of mouse oocyte deformability in micro-constrictions allows for a significant advance in assessing the mechanical properties of mammalian oocytes and has potential application as a quantifiable selective criterion in medically assisted reproduction. TeaserA measurement method for translating advances in oocyte mechanics into selection criteria for improving medically assisted reproduction.

developmental biology↗

bioRxiv2022

Carm1 regulates the speed of C/EBPa-induced transdifferentiation by a cofactor stealing mechanism

Cell fate decisions are driven by lineage-restricted transcription factors but how they are regulated is incompletely understood. The C/EBP-induced B cell to macrophage transdifferentiation (BMT) is a powerful system to address this question. Here we describe that C/EBP with a single arginine mutation (C/EBPR35A) induces a dramatically accelerated BMT in mouse and human cells. Changes in the expression of lineage-restricted genes occur as early as within 1 hour compared to 18 hours with the wild type. Mechanistically C/EBPR35A exhibits an increased affinity for PU.1, a bi-lineage transcription factor required for C/EBP-induced BMT. The complex induces more rapid chromatin accessibility changes and an enhanced relocation (stealing) of PU.1 from B cell to myeloid gene regulatory elements. Arginine 35 is methylated by Carm1 and inhibition of the enzyme accelerates BMT, similar to the mutant. Our data suggest that the relative proportions of methylated and unmethylated C/EBP in a bipotent progenitor can determine the velocity of cell fate choice and lineage directionality.

cell biology↗

bioRxiv2021

Real Age Prediction from the Transcriptome with RAPToR

Transcriptomic data is often affected by uncontrolled variation among samples that can obscure and confound the effects of interest. This is frequently due to unintended differences in developmental stages between samples. The transcriptome itself can be used to estimate developmental progression, but existing methods require many samples and do not estimate a real developmental time. Here we present RAPToR, a simple and precise computational method that estimates the real age of a sample from its transcriptome, exploiting existing time-series data as reference. RAPToR works with whole animal, dissected tissue and single-cell data, for the most common animal models, humans and even for nonmodel organisms lacking reference data. We show RAPToR estimated age improves differential expression analysis by recovering the signal of interest when confounded with age. RAPToR will be especially useful in large scale single organism profiling because it eliminates the need for accurate staging or synchronization before profiling.

bioinformatics↗