"Machine learning model and other computational approaches to predict the balance of protein aggregation, gelation and solubility"

IGMM External Seminar

“Too knotty to resist: Twisted DNA behavior attracts Smc5/6”

Aurélie a obtenu son master en biochimie, biologie moléculaire et cellulaire à l’UC Louvain (Louvain-la-Neuve, Belgique). En 2014, elle a entamé une thèse dedoctorat dans le laboratoire de la Professeure Anabelle Decottignies à l’Institut de Duve (Bruxelles, Belgique), où elle a étudié la régulation transcriptionnelle des télomères humains ainsi que le mécanisme ALTernatif de maintien de leur longueur dans les cellules cancéreuses. En 2018, elle a rejoint le laboratoire du Professeur Michel Strubin à l’Université de Genève (Suisse) en tant que chercheuse postdoctorale, afin d’explorer les bases moléculaires responsables de la liaison préférentielle du complexe Smc5/6 àl’ADN extrachromosomique dans les cellules de mammifères. Depuis 2025, elle occupe un poste de maître-assistante et développe un programme de recherche indépendant visant à élucider les mécanismes moléculaires parlesquels le complexe Smc5/6 réprime spécifiquement la transcription de l’ADN extrachromosomique.

Title : "Reappraising transcriptional enhancers" 
Contact : julie.carnesecchi@igmm.cnrs.fr
 http://gompel.org/

CRBM and BIOLUM external seminar

wtf evolution

Contact: dominique.helmlinger@crbm.cnrs.fr

Title : "The hidden SINEs of recovery"
Contact : jean-christophe.andrau@igmm.cnrs.fr 

"The hidden SINEs of recovery"

Repeat element RNAs integrate neuronal growth after injury

Neuronal growth and regeneration are regulated by specific genetranscription and translation programs that integrate mRNA localization, localprotein synthesis, retrograde signaling and transcription factor (TF) activity.While the role of protein coding genes in these processes is well studied, thatof regulatory RNAs is little understood. In a screen to identify RNApolyadenylation changes in mouse dorsal root ganglia (DRG) sensory neuronsfollowing sciatic nerve injury, we found the upregulation of polyadenylatedB2-SINE repeat elements. Employing long-read paired-end RNA-seq and ATAC-seqanalyses we pinpointed the upregulation to a subset of B2-SINE loci thatundergo injury-induced chromatin accessible remodeling. This transcriptionalupregulation was specific to injured peripheral sensory neurons and did notoccur retinal ganglion cells following optic nerve crush. Importantly,expression of B2-SINE RNA in retinal and cortical neurons, whose intrinsicability to regenerate is poorer than that of DRG neurons, significantlyimproved their regrowth after nerve injury. Hence, we termed this subset ofinjury-induced, DRG specific elements GI-SINE (growth-inducing B2-SINE).GI-SINEs are induced as discrete transcriptional units from theinjury-activated and pro-regenerative ATF3 and other AP-1 TFs associated loci.GI-SINE RNA interacts with ribosomal proteins and nucleolin, anaxon-growth-regulating RNA binding protein, to regulate translation in neuronalcytoplasm. Finally, antisense oligos against GI-SINEs perturb sensory neuronoutgrowth and nucleolin-ribosome interactions. Thus, we identify a subfamily oftransposable element RNAs that is integral in a signaling circuit regulatingneuronal regrowth, suggesting similar elements can be utilized as regulatedregenerative effectors in other physiological contexts.

Conférence invitée CRBM 
Salle Marcel Dorée
contact: Claude.prigent@crbm.cnrs.fr 
https://earnshawlab.com/prof-bill-earnshaw/