François Gerbe

Institut de Génomique Fonctionnelle

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Philippe Jay

Institut de Génomique Fonctionnelle

Pierre Cesses

Inserm

Alicia Giordano

Institut de Génomique Fonctionnelle

Marco Bruschi

Institut Gustave Roussy

Laure Garnier

University of Geneva

Elouan Cleroux

Université de Strasbourg

Thomas Kergrohen

Inserm

Anaïs F. Bardet

Centre National de la Recherche Scientifique

Stanislas Quesada

Institut de Recherche en Cancérologie de Montpellier

Michael Weber

Medical University of Vienna

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Centre National de la Recherche Scientifique

108

Inserm

Université de Montpellier

Institut de Génomique Fonctionnelle

Institut de Génétique Moléculaire de Montpellier

La Ligue Contre le Cancer

University of Glasgow

Centre National pour la Recherche Scientifique et Technique (CNRST)

Wellcome Centre for Molecular Parasitology

University of Edinburgh

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The intestinal epithelium tuft cells: specification and function

Cellular and Molecular Life Sciences (2012)

François Gerbe Catherine Legraverend Philippe Jay

The intestinal epithelium, composed of at least seven differentiated cell types, represents an extraordinary model to understand the details of multi-lineage differentiation, a question that is highly relevant in developmental biology as well as for clinical applications. This review focuses on intestinal epithelial tuft cells that have been acknowledged as a separate entity for more than 60 years but whose function remains a mystery. We discuss what is currently known about the molecular basis of tuft cell fate and differentiation and why elucidating tuft cell function has been so difficult. Finally, we summarize the current hypotheses on their potential involvement in diseases of the gastro-intestinal tract.

Tuft

Intestinal epithelium

Lineage (genetic)

Cell lineage

10.1007/s00018-012-0984-7

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Citations (241)

Table S1 : RNA-seq data from Lgr5-GFP+ cells from Loss of Apc Rapidly Impairs DNA Methylation Programs and Cell Fate Decisions in Lgr5+ Intestinal Stem Cells

Marco Bruschi Laure Garnier Elouan Cleroux Alicia Giordano Michael Dumas

This file contains all RNAseq results for gene expression comparisons between FACS sorted ApcWT-, ApcHET-, and ApcKO-Lgr5-GFP profiles.

LGR5

10.1158/0008-5472.22423848.v1

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Table S3 : GSEA on KEGG collection results from Loss of Apc Rapidly Impairs DNA Methylation Programs and Cell Fate Decisions in Lgr5+ Intestinal Stem Cells

Marco Bruschi Laure Garnier Elouan Cleroux Alicia Giordano Michael Dumas

This file contains GSEA results from ApcWT- and ApcKO-Lgr5 cells for collections of signatures related to KEGG functional pathways.

LGR5

Table (database)

KEGG

10.1158/0008-5472.22423842.v1

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Tuft cell-derived acetylcholine is an effector of type 2 immunity and directly targets helminth parasites in the gut lumen

bioRxiv (Cold Spring Harbor Laboratory) (2023)

Marième Ndjim Fabien Herbert Imène Gasmi Charlène Joséphine Sylvain Henri

SUMMARY Upon parasitic helminth infection, activated intestinal tuft cells secrete IL-25, which initiates a type 2 immune response during which lamina propria ILC2s produce IL-13. This causes epithelial remodelling, including tuft cell hyperplasia with an unknown function. We describe a novel cholinergic effector function of tuft cells, which we show are the only epithelial cells expressing Choline Acetyltransferase (ChAT). During parasite infections, mice with epithelial-specific deletion of ChAT have increased worm burden and faecal egg counts although they are able to mount a comparable type 2 immune response. Mechanistically, IL-13-amplified tuft cells release acetylcholine (ACh) into the gut lumen. We demonstrate a direct effect of ACh on worms, reducing their viability and fecundity via helminth muscarinic ACh receptors, with effects promoted by inhibition of acetylcholinesterase, an helminth-secreted enzyme. Thus, tuft cells are sentinels in naive mice, and their amplification upon helminth infections serves an additional type 2 immune response effector function.

10.1101/2023.12.08.570757

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CDK8 and CDK19 act redundantly to control the CFTR pathway in the intestinal epithelium

Susana Prieto Geronimo Dubra Alain Camasses Ana Bella Aznar Christina Begon-Pescia

Intestinal epithelium

10.15252/embr.202154261

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Citations (2)

Supplementary Figure Legends from Cell-Cycle Regulation Accounts for Variability in Ki-67 Expression Levels

Michal Sobecki Karim Mrouj Jacques Colinge François Gerbe Philippe Jay

Detailed legends for Supplementary Figures S1-S6.

Expression (computer science)

10.1158/0008-5472.22413951.v1

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Table S5 : lists of differentially methylated regions in Lgr5-GFP+ cells from Loss of Apc Rapidly Impairs DNA Methylation Programs and Cell Fate Decisions in Lgr5+ Intestinal Stem Cells

Marco Bruschi Laure Garnier Elouan Cleroux Alicia Giordano Michael Dumas

This file contains the lists of DMR found by RRBS in FACS-sorted ApcHET- and ApcKO-Lgr5-GFP cells.

LGR5

10.1158/0008-5472.22423836

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Tuft Cells: Detectors, Amplifiers, Effectors and Targets in Parasite Infection

Cells (2023)

Marta Campillo Poveda Collette Britton Eileen Devaney Tom N. McNeilly François Gerbe

Tuft cells have recently emerged as the focus of intense interest following the discovery of their chemosensory role in the intestinal tract, and their ability to activate Type 2 immune responses to helminth parasites. Moreover, they populate a wide range of mucosal tissues and are intimately connected to immune and neuronal cells, either directly or through the release of pharmacologically active mediators. They are now recognised to fulfil both homeostatic roles, in metabolism and tissue integrity, as well as acting as the first sensors of parasite infection, immunity to which is lost in their absence. In this review we focus primarily on the importance of tuft cells in the intestinal niche, but also link to their more generalised physiological role and discuss their potential as targets for the treatment of gastrointestinal disorders.

Tuft

10.3390/cells12202477

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Caractérisation de gènes impliqués dans la formation de l'endoderme primitif lors de l'embryogenèse précoce de la souris

François Gerbe

De nombreux travaux menes sur l'embryon de souris ont permis de caracteriser morphologiquement les 1eres etapes de developpement des mammiferes. En revanche, les mecanismes moleculaires regissant le deroulement de ces etapes sont encore peu connus a ce jour. Dans l'equipe, notre but est de comprendre ces mecanismes en se focalisant sur la formation de l'endoderme primitif (EPr), le 2eme type cellulaire a se differencier au cours de l'embryogenese. L'EPr est un tissu extra-embryonnaire qui se forme avant l'implantation dans l'uterus maternel. Bien que ne contribuant pas a la formation de l'embryon lui-meme, ce tissu reste neanmoins necessaire a sa survie et a son developpement correct. Afin d'identifier de nouveaux genes impliques dans la formation de l'EPr, j'ai analyse un microarray realise sur les 1ers stades de l'embryogenese. Cette analyse a permis de definir de nouveaux genes precoces, potentiellement specifiques de l'EPR. En utilisant les techniques de RT-PCR et de localisation in situ, j'ai analyse 2 des genes selectionnes : Lrp2 et Dkkl. L'etude approfondie du profil d'expression du recepteur LRP2 entre E2. 5 et E4. 5 a permis l'elaboration d'un modele de differenciation epitheliale. Parallelement a ces travaux, j'ai developpe une nouvelle technique pour realiser des analyses fonctionnelles in vivo. Cette methode d'electroporation in vivo combine les techniques d'electroporation, d'interference ARN et de culture d'embryons et ouvre de nombreuses perspectives pour les travaux sur l'embryogenese precoce.

Source

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Cell-Cycle Regulation Accounts for Variability in Ki-67 Expression Levels

Cancer Research (2017)

Michal Sobecki Karim Mrouj Jacques Colinge François Gerbe Philippe Jay

The cell proliferation antigen Ki-67 is widely used in cancer histopathology, but estimations of Ki-67 expression levels are inconsistent and understanding of its regulation is limited. Here we show that cell-cycle regulation underlies variable Ki-67 expression in all situations analyzed, including nontransformed human cells, normal mouse intestinal epithelia and adenomas, human cancer cell lines with or without drug treatments, and human breast and colon cancers. In normal cells, Ki-67 was a late marker of cell-cycle entry; Ki-67 mRNA oscillated with highest levels in G2 while protein levels increased throughout the cell cycle, peaking in mitosis. Inhibition of CDK4/CDK6 revealed proteasome-mediated Ki-67 degradation in G1 After cell-cycle exit, low-level Ki-67 expression persisted but was undetectable in fully quiescent differentiated cells or senescent cells. CDK4/CDK6 inhibition in vitro and in tumors in mice caused G1 cell-cycle arrest and eliminated Ki-67 mRNA in RB1-positive cells but had no effect in RB1-negative cells, which continued to proliferate and express Ki-67. Thus, Ki-67 expression varies due to cell-cycle regulation, but it remains a reliable readout for effects of CDK4/CDK6 inhibitors on cell proliferation. Cancer Res; 77(10); 2722-34. ©2017 AACR.

Cyclin-dependent kinase 6

Ki-67

10.1158/0008-5472.can-16-0707

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Citations (308)