ENS - MemoLife

Claudia Chica

Godfroid — 2017-11-07T15:55:08Z

Claudia Chica, Alexandra Louis, Hugues Roest Crollius, Vincent Colot, François Roudier.

ABSTRACT

Background :
Polycomb Repressive Complexes 2 (PRC2) are multi-protein chromatin modifiers that are evolutionarily conserved among eukaryotes and play key roles in the regulation of gene expression, notably through the trimethylation of lysine 27 of histone H3 (H3K27me3). Although PRC2-mediated gene regulation has been studied in many organisms, few studies have explored in depth the evolutionary conservation of PRC2 targets.
Results :
Here, we compare the H3K27me3 epigenomic profiles for the two closely related species Arabidopsis thaliana and Arabidopsis lyrata and the more distant species Arabis alpina, three Brassicaceae that diverged from each other within the past 24 million years. Using a robust set of gene orthologs present in the three species, we identify two classes of evolutionarily conserved PRC2 targets, which are characterized by either developmentally plastic or developmentally constrained H3K27me3 marking across species. Constrained H3K27me3 marking is associated with higher conservation of promoter sequence information content and higher nucleosome occupancy compared to plastic H3K27me3 marking. Moreover, gene orthologs with constrained H3K27me3 marking exhibit a higher degree of tissue specificity and tend to be involved in developmental functions, whereas gene orthologs with plastic H3K27me3 marking preferentially encode proteins associated with metabolism and stress responses. In addition, gene orthologs with constrained H3K27me3 marking are the predominant contributors to higher-order chromosome organization.
Conclusions :
Our findings indicate that developmentally plastic and constrained H3K27me3 marking define two evolutionarily conserved modes of PRC2-mediated gene regulation that are associated with distinct selective pressures operating at multiple scales, from DNA sequence to gene function and chromosome architecture.

More informations

Genome Biol. 2017 Oct 31 ;18(1):207. doi : 10.1186/s13059-017-1333-9.

Adel Al Jord

Godfroid — 2017-10-19T12:01:59Z

Abstract :

Cell division and differentiation depend on massive and rapid organelle remodeling. The mitotic oscillator, centered on the Cdk1-APC/C axis, spatiotemporally coordinates this reorganization in dividing cells. Here, we discovered that non-dividing cells could also implement this mitotic clock-like regulatory circuit to orchestrate subcellular reorganization associated with differentiation. We probed centriole amplification in differentiating mouse brain multiciliated cells. These post-mitotic progenitors fine-tuned mitotic oscillator activity to drive the orderly progression of centriole production, maturation and motile ciliation while avoiding the mitosis commitment threshold. Insufficient Cdk1 activity hindered differentiation, whereas excessive activity accelerated differentiation yet drove post-mitotic progenitors into mitosis. Thus, post-mitotic cells can redeploy and calibrate the mitotic oscillator to uncouple cytoplasmic from nuclear dynamics for organelle remodeling associated with differentiation.

More information

Science. 2017 Oct 5. pii : eaan8311. doi : 10.1126/science.aan8311

Jonathan Boulanger-Weill

Godfroid — 2017-06-12T15:19:23Z

Jonathan Boulanger-Weill, Virginie Candat, Adrien Jouary, Sebastián Romano, Verónica Pérez-Schuster, Germán Sumbre.

Highlights
• Newborn neurons show simple morphology and intrinsic activity but no visual responses
• Then they show correlated spontaneous activity with functionally mature local neurons
• Finally, they acquire receptive fields and complex dendritic arbors
• Removal of retinal inputs prevents the incorporation process

Summary
From development up to adulthood, the vertebrate brain is continuously supplied with newborn neurons that integrate into established mature circuits. However, how this process is coordinated during development remains unclear. Using two-photon imaging, GCaMP5 transgenic zebrafish larvae, and sparse electroporation in the larva's optic tectum, we monitored spontaneous and induced activity of large neuronal populations containing newborn and functionally mature neurons. We observed that the maturation of newborn neurons is a 4-day process. Initially, newborn neurons showed undeveloped dendritic arbors, no neurotransmitter identity, and were unresponsive to visual stimulation, although they displayed spontaneous calcium transients. Later on, newborn-labeled neurons began to respond to visual stimuli but in a very variable manner. At the end of the maturation period, newborn-labeled neurons exhibited visual tuning curves (spatial receptive fields and direction selectivity) and spontaneous correlated activity with neighboring functionally mature neurons. At this developmental stage, newborn-labeled neurons presented complex dendritic arbors and neurotransmitter identity (excitatory or inhibitory). Removal of retinal inputs significantly perturbed the integration of newborn neurons into the functionally mature tectal network. Our results provide a comprehensive description of the maturation of newborn neurons during development and shed light on potential mechanisms underlying their integration into a functionally mature neuronal circuit.

More information here

Current Biology. doi.org/10.1016/j.cub.2017.05.029. Published Online : June 01, 2017

Samuel Tozer

Godfroid — 2017-02-02T17:03:18Z

Samuel Tozer, Chooyoung Baek, Evelyne Fischer, Rosette Goiame and Xavier Morin

Highlights
• Centriolar satellites constitute a docking point for Mib1 at the daughter centriole
• Mib1 is inherited by the prospective neuron following asymmetric divisions
• Mib1 asymmetry regulates fate choices through unequal Notch activation in daughter cells
• In proliferative divisions, a Golgi apparatus pool of Mib1 compensates for the asymmetry

Summary
Unequal centrosome maturation correlates with asymmetric division in multiple cell types. Nevertheless, centrosomal fate determinants have yet to be identified. Here, we show that the Notch pathway regulator Mindbomb1 co-localizes asymmetrically with centriolar satellite proteins PCM1 and AZI1 at the daughter centriole in interphase. Remarkably, while PCM1 and AZI1 remain asymmetric during mitosis, Mindbomb1 is associated with either one or both spindle poles. Asymmetric Mindbomb1 correlates with neurogenic divisions and Mindbomb1 is inherited by the prospective neuron. By contrast, in proliferative divisions, a supplementary pool of Mindbomb1 associated with the Golgi apparatus in interphase is released during mitosis and compensates for Mindbomb1 centrosomal asymmetry. Finally, we show that preventing Mindbomb1 centrosomal association induces reciprocal Notch activation between sister cells and promotes symmetric divisions. Thus, we uncover a link between differential centrosome maturation and Notch signaling and reveal an unexpected compensatory mechanism involving the Golgi apparatus in restoring symmetry in proliferative divisions.

More information

Neuron, 2017. doi : 10.1016/j.neuron.2016.12.042