A scaffold lncRNA shapes the mitosis to meiosis switch

Vedrana Andric, Alicia Nevers, Ditipriya Hazra, Sylvie Auxilien, Alexandra Menant, Marc Graille, Benoit Palancade and Mathieu Rougemaille ()
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Vedrana Andric: Université Paris-Saclay, CEA, CNRS, Institute for Integrative Biology of the Cell (I2BC)
Alicia Nevers: Université Paris-Saclay, CEA, CNRS, Institute for Integrative Biology of the Cell (I2BC)
Ditipriya Hazra: Institut Polytechnique de Paris
Sylvie Auxilien: Université Paris-Saclay, CEA, CNRS, Institute for Integrative Biology of the Cell (I2BC)
Alexandra Menant: Université Paris-Saclay, CEA, CNRS, Institute for Integrative Biology of the Cell (I2BC)
Marc Graille: Institut Polytechnique de Paris
Benoit Palancade: Université de Paris, CNRS, Institut Jacques Monod
Mathieu Rougemaille: Université Paris-Saclay, CEA, CNRS, Institute for Integrative Biology of the Cell (I2BC)

Nature Communications, 2021, vol. 12, issue 1, 1-12

Abstract: Abstract Long non-coding RNAs (lncRNAs) contribute to the regulation of gene expression in response to intra- or extracellular signals but the underlying molecular mechanisms remain largely unexplored. Here, we identify an uncharacterized lncRNA as a central player in shaping the meiotic gene expression program in fission yeast. We report that this regulatory RNA, termed mamRNA, scaffolds the antagonistic RNA-binding proteins Mmi1 and Mei2 to ensure their reciprocal inhibition and fine tune meiotic mRNA degradation during mitotic growth. Mechanistically, mamRNA allows Mmi1 to target Mei2 for ubiquitin-mediated downregulation, and conversely enables accumulating Mei2 to impede Mmi1 activity, thereby reinforcing the mitosis to meiosis switch. These regulations also occur within a unique Mmi1-containing nuclear body, positioning mamRNA as a spatially-confined sensor of Mei2 levels. Our results thus provide a mechanistic basis for the mutual control of gametogenesis effectors and further expand our vision of the regulatory potential of lncRNAs.

Date: 2021
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DOI: 10.1038/s41467-021-21032-7

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