IJM News since 2010
C’est avec un grand regret que nous avons appris le décès le 29 décembre dernier de Jacques Ricard qui fut directeur de l’Institut Jacques Monod de 1992 à 1996 et professeur d’Enzymologie à l’Université Paris-Diderot. Il a été également directeur du Centre de Biochimie et de Biologie Moléculaire du CNRS à Marseille de 1980 à 1991, membre de l’Académie Internationale de Philosophie des Sciences et membre correspondant de l’Académie des Sciences. Nous lui devons en particulier d’avoir structuré l’Institut Jacques Monod en départements, qui fut le mode de fonctionnement jusqu’en 2008 et d’avoir été l’artisan d’une orientation « Biologie cellulaire » forte à l’Institut. Ses travaux ont été fondateurs dans le domaine de l’enzymologie, notamment en ce qui concerne la régulation des enzymes via leurs interactions avec leurs substrats et métabolites ainsi que leur environnement cellulaire.
In an article published in December in eLife, the Dumont team at the Institut Jacques Monod shows that the kinase BUB-1 controls chromosome segregation by modulating the activity of various kinetochore components. Surprisingly, this function of BUB-1 is independent of its kinase activity.
Regeneration, the ability of some animals to restore a lost or damaged body part is a fascinating process that has intrigued biologists since centuries. The annelid Platynereis dumerilii is one such animals possessing remarkable regeneration abilities. This marine worm is indeed able to reform various parts of its body following amputation, notably its appendages and its posterior part. The latter contains both various differentiated structures and stem cells responsible of the growth of the animals. In a paper published this month in Developmental Biology, Anabelle Planques and members of the “Stem cells, Development and Evolution” team at the Institut Jacques Monod, in collaboration with a researcher form the University of Coruña (Spain), characterized Platynereis caudal regeneration. They have shown that posterior regeneration is a very rapid process, requiring cell proliferation and during which several genes, known to be markers of stem cells in various models, are expressed. The origin of the cells involved in regeneration of missing structures has been partly uncovered, suggesting a major role of dedifferentiation of cells abutting the amputation site. This pioneer study of Platynereis regeneration paves the way to the identification of mechanisms controlling this process in this species and open new perspectives for the understanding of its evolution at the metazoan scale.
Male genitals evolve very quickly in animals. Studying the mechanisms underlying their evolution is crucial to understand the phenomenon of speciation. However, the genes involved in genital differences between species are poorly known. A work published in the journal Current Biology in October, resulting from a collaboration between the Jacques Monod Institute, the CNRS, the Paris Museum, the EGCE laboratory of Gif-sur-Yvette and two teams in the United States, constitutes a first step forward in Drosophila. The mutation of a single letter in the DNA contributes to both the loss of sensory organs under the phallus and the increase in size of a sexual comb located on the legs. This is the first time that a single mutation is observed to contribute to the evolution of two organs between species.
It is now well established that formins are central players in the regulation of the dynamics of almost all actin networks in cells. But how their activities are modulated by biochemistry and mechanics is far less well understood. Researchers from the ‘Regulation of Actin Assembly Dynamics’ team of the Institut Jacques Monod have studied in vitro actin filament elongation induced by mDia1 and mDia2 mammalian formins. This work, published in eLife, has shown that filament length can be increased by the presence of profilin, a protein that forms binary complexes with actin, but is highly diminished if a pulling force is applied between formins and actin filaments. How cells limit formin dissociation under tension is now a key question for future studies.
The DNA of every cell is constantly undergoing damage, and the cell cannot survive without actively repairing these lesions using specialized molecular systems. Defects in DNA repair systems are frequently associated with the apparition of cancers. Among the most complex forms of damage that DNA must be rescued from involve double-strand breaks in the double helix. In humans these breaks are repaired by a system comprised of no less than six distinct proteins. So as to understand how this multitude of proteins can assemble in a timely fashion into a functional system, the lab of T. Strick (Institut Jacques Monod and Ecole normale supérieure) has developped new nanotechnologcial approaches which allow for real-time observation of repair of DNA double-strand breaks. This study highlights the functional redundancy which allows this system to function in a robust and efficient manner despite its molecular complexity. It paves the way for quantitative analysis of new therapeutic molecules targeting this process. This study was published on May 21st 2018 in Nature Structural and Molecular Biology.
Si de nombreuses activités cellulaires mettent en jeu des édifices protéiques formés de plusieurs sous-unités, les régulations contrôlant leur homéostasie restent mal connues. Un groupe de chercheurs, mené par Benoit Palancade à l’Institut Jacques Monod, a utilisé le complexe du pore nucléaire (NPC) comme paradigme pour déchiffrer les mécanismes qui assurent la biogénèse de tels assemblages, et maintiennent leur stœchiométrie. Leurs travaux, publiés dans la revue Nature communications, révèlent une boucle de régulation par laquelle la biogenèse des sous-unités du NPC est ajustée en fonction de l’intégrité du complexe.
In an article published on April 23rd, and featured on the cover of Developmental Cell, the team Minc at Institut Jacques Monod establishes a new live imaging method to study the dynamics of cell wall assembly in living cells.
Lipid droplets (LDs) are essential cellular organelles, but how proteins that regulate LD function are targeted to this compartment is poorly understood. In an article by Copic et al., published on April 6 in Nature Communications, the Jackson-Verbavatz team has used a remarkable LD protein, perilipin 4, as a model to study how proteins interact with LDs. They demonstrate both in vitro and in cells that the extremely long amphipathic helix of perilipin 4 can directly bind to the neutral lipid core of LDs, acting as a coat that prevents unregulated LD growth.
Nicolas MINC is leader of the group “Cellular Spatial Organization” at the Institut Jacques Monod