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Rochette, A.

Publications and source records attributed to Rochette, A..

2 recordsLinked to original sources

The fidelity of mRNA translation as a novel regulatory layer for brain development

Although the fidelity of mRNA translation is essential for maintaining proteome integrity, whether translation error rates vary across cell types and developmental stages in vivo remains largely unexplored. Here, we generate a gain-of-activity dual-luciferase knock-in reporter mouse that enables quantitative monitoring of translation errors in vivo. Using this system, we systematically characterize the spatiotemporal dynamics of translation fidelity across mammalian development. Mature organs exhibit lower error rates than pluripotent embryonic stem cells. Translation fidelity diverges sharply among organs, becoming progressively established during embryonic development, with brain and muscle displaying the highest accuracy. To determine functional significance, we experimentally increased translation errors during cerebral organoid formation and in vitro neuronal differentiation. Elevated error rates reduced neuronal output by impairing neuronal maturation without altering neural progenitor populations. Consistently, differentiated neurons display uniformly elevated fidelity across multiple classes of translation errors, including stop codon readthrough, amino acid misincorporation, and ribosomal frameshifting. These findings demonstrate that translation fidelity is not a fixed intrinsic property of the translation machinery but is developmentally regulated and required for efficient neuronal differentiation. Together, our results identify translation fidelity as a developmentally tuned, tissue-specific dimension of gene expression in vivo.

developmental biology↗

Direct reprogramming of the intestinal epithelium by parasitic helminths subverts type 2 immunity

Enteric helminths form intimate physical connections with the intestinal epithelium, yet their ability to directly alter epithelial stem cell fate has not been resolved. Here we demonstrate that infection of mice with the symbiotic parasite Heligmosomoides polygyrus bakeri (Hbp), reprograms the intestinal epithelium into a fetal-like state marked by the emergence of Clusterin-expressing revival stem cells (revSCs). Organoid-based studies using parasite-derived excretory/secretory products reveal that Hpb-mediated revSC generation occurs independent of host-derived immune signals and inhibits type 2 cytokine-driven differentiation of secretory epithelial lineages that promote their expulsion. Reciprocally, type 2 cytokine signals limit revSC differentiation and, consequently, Hpb fitness indicating that helminths compete with their host for control of the intestinal stem cell niche to promote continuation of their life cycle.

immunology↗