A dual role of dLsd1 in oogenesis: regulating developmental genes and repressing transposons

Author:

Lepesant Julie M J1,Iampietro Carole1,Galeota Eugenia2,Augé Benoit3,Aguirrenbengoa Marion1,Mercé Clemèntine14,Chaubet Camille1,Rocher Vincent1,Haenlin Marc3,Waltzer Lucas35,Pelizzola Mattia2ORCID,Di Stefano Luisa1

Affiliation:

1. LBCMCP, Centre de Biologie Intégrative (CBI), Université de Toulouse, CNRS, UPS, Toulouse 31062, France

2. Center for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT), Milan 20139, Italy

3. CBD, Centre de Biologie Intégrative (CBI), Université de Toulouse, CNRS, UPS, Toulouse 31062, France

4. School of Biological Sciences, University of Western Australia, Perth, WA 6009, Australia

5. Université Clermont Auvergne, CNRS, INSERM, GReD, Clermont-Ferrand F-63000, France

Abstract

Abstract The histone demethylase LSD1 is a key chromatin regulator that is often deregulated in cancer. Its ortholog, dLsd1 plays a crucial role in Drosophila oogenesis; however, our knowledge of dLsd1 function is insufficient to explain its role in the ovary. Here, we have performed genome-wide analysis of dLsd1 binding in the ovary, and we document that dLsd1 is preferentially associated to the transcription start site of developmental genes. We uncovered an unanticipated interplay between dLsd1 and the GATA transcription factor Serpent and we report an unexpected role for Serpent in oogenesis. Besides, our transcriptomic data show that reducing dLsd1 levels results in ectopic transposable elements (TE) expression correlated with changes in H3K4me2 and H3K9me2 at TE loci. In addition, our results suggest that dLsd1 is required for Piwi dependent TE silencing. Hence, we propose that dLsd1 plays crucial roles in establishing specific gene expression programs and in repressing transposons during oogenesis.

Funder

Fondation pour la Recherche Médicale

Agence Nationale de la Recherche

Marie Curie Career Integration Grant

Région Midi-Pyrénées

INSERM

ANR

Publisher

Oxford University Press (OUP)

Subject

Genetics

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