Michel Cohen‐Tannoudji

The paper identifies transposable element insertions that repurpose immune endonucleases to cause hybrid embryo death in mice, contributing to reproductive isolation.

This study investigates how GATA6, a pioneer transcription factor, drives Primitive Endoderm differentiation by remodeling chromatin and interacting with other TFs.

This study investigates the evolutionary dynamics of Schlafen genes in rodents and primates, identifying recurrent positive selection and structural innovations linked to immune functions.

This study identifies PI3K/AKT signaling as an upstream regulator that enables ICM formation and specifies both epiblast and primitive endoderm lineages in mouse embryos.

This study shows Nr5a2 is essential for morula development in mice, as its absence causes embryonic arrest, lineage specification issues, and genome instability.

The paper identifies H3K9me3 at the Nanog locus as a repressive mark that marks differentiation commitment and enables primitive endoderm fate acquisition in ES cells.

The paper identifies a genetic circuitry where OCT4 activates an antisense lncRNA that represses Suv39h1, linking H3K9 methylation levels to pluripotency in mouse ES cells.

This study identifies a Nanog-dependent gene cluster that initiates epiblast specification in early mouse embryos, revealing a primary heterogeneity independent of NANOG, GATA6, and FGF signaling.

This paper introduces a genetic switch called iOn that enables the identification of genomic integration events by triggering gene expression upon insertion, improving transgenesis in stem cells and model organisms.

The paper shows that CTCF and Esrrb maintain nucleosome positioning at gene regulatory regions during DNA replication and mitosis in mouse ES cells.

The paper investigates how transcription factors maintain gene regulatory information during mitosis by comparing fixation methods and analyzing nucleosome organization.

The paper develops an automated tool for annotating embryo morphokinetic parameters, showing high concordance with manual annotation in human and mouse embryos.

The paper shows that FGF/ERK inhibition during a short time window can convert ICM cells into epiblast, requiring transcription and proteasome degradation.