"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
Contact :nadine.laguette@igmm.cnrs.fr

IGMM External seminar

"Reappraising transcriptional enhancers"

Contact julie.carnesecchi@igmm.cnrs.fr

http://gompel.org

CRBM external seminar

wtf evolution

Contact: dominique.helmlinger@crbm.cnrs.fr

"The hidden SINEs of recovery"

Contact : jean-christophe.andrau@igmm.cnrs.fr

Repeat element RNAs integrate neuronal growth after injury. Neuronal growth and regeneration are regulated by specific gene transcription and translation programs that integrate mRNA localization, local protein synthesis, retrograde signaling and transcription factor (TF) activity. While the role of protein coding genes in these processes is well studied, that of regulatory RNAs is little understood. In a screen to identify RNA polyadenylation changes in mouse dorsal root ganglia (DRG) sensory neurons following sciatic nerve injury, we found the upregulation of polyadenylatedB2-SINE repeat elements. Employing long-read paired-end RNA-seq and ATAC-seq analyses we pinpointed the upregulation to a subset of B2-SINE loci that undergo injury-induced chromatin accessible remodeling. This transcriptional upregulation was specific to injured peripheral sensory neurons and did not occur 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.

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