Cell · 2025
Repeat-element RNAs integrate a neuronal growth circuit.
СтатьяНазвание и аннотация: Перевод в очереди
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Zahavi Eitan Erez, Koppel Indrek, Kawaguchi Riki, Oses-Prieto Juan A, Briner Adam, Monavarfeshani Aboozar, Dalla Costa Irene, van Niekerk Erna, Lee Jinyoung, Matoo Samaneh, Hegarty Shane, Donahue Ryan J, Sahoo Pabitra K, Ben-Dor Shifra, Feldmesser Ester, Ryvkin Julia, Leshkowitz Dena, Perry Rotem Ben-Tov, Cheng Yuyan, Farber Eli, Abraham Ofri, Samra Nitzan, Okladnikov Nataliya, Alber Stefanie, Albus Christin A, Rishal Ida, Ulitsky Igor, Tuszynski Mark H, Twiss Jeffery L, He Zhigang, Burlingame Alma L, Fainzilber Mike
Аннотация
Neuronal growth and regeneration are regulated by local translation of mRNAs in axons. We examined RNA polyadenylation changes upon sensory neuron injury and found upregulation of a subset of polyadenylated B2-SINE repeat elements, hereby termed GI-SINEs (growth-inducing B2-SINEs). GI-SINEs are induced from ATF3 and other AP-1 promoter-associated extragenic loci in injured sensory neurons but are not upregulated in lesioned retinal ganglion neurons. Exogenous GI-SINE expression elicited axonal growth in injured sensory, retinal, and corticospinal tract neurons. GI-SINEs interact with ribosomal proteins and nucleolin, an axon-growth-regulating RNA-binding protein, to regulate translation in neuronal cytoplasm. Finally, antisense oligos against GI-SINEs perturb sensory neuron outgrowth and nucleolin-ribosome interactions. Thus, a specific subfamily of transposable elements is integral to a physiological circuit linking AP-1 transcription with localized RNA translation.