ERP137538 PRJEB52795 22febab7-4de6-4f81-9fb6-7790699d1484 Complex interplay between Plant Mobile Domain and Microrchidia silencing pathways Silencing of transposable elements (TEs) is an essential process to maintain genomic integrity within the cell. In Arabidopsis, together with canonical epigenetic pathways such as DNA methylation and modifications of histone tails, the plant mobile domain (PMD) proteins MAINTENANCE OF MERISTEMS (MAIN) and MAIN-LIKE 1 (MAIL1) are involved in TE silencing. Additionally, the MICRORCHIDIA (MORC) ATPases, including MORC1 are important cellular factors repressing TEs. Here, we describe the genetic interaction and connection between the PMD and MORC pathways by showing that MORC1 expression is impaired in main and mail1 mutants. This suggests that at least for a subset of TEs, silencing defects observed in pmd mutants could be the consequence of MORC1 downregulation. Transcriptomic analyses of higher-order mutant plants combining pmd and morc1 mutations as well as pmd mutants in which MORC1 expression is restored confirm this hypothesis. Thus, TE silencing defects observed in the pmd main and mail1 mutants can be partially explained by MORC1 downregulation. Plant Mobile Domain proteins are required for Microrchidia 1 expression to fulfil transposon silencing Silencing of transposable elements (TEs) is an essential process to maintain genomic integrity within the cell. In Arabidopsis, together with canonical epigenetic pathways such as DNA methylation and modifications of histone tails, the plant mobile domain (PMD) proteins MAINTENANCE OF MERISTEMS (MAIN) and MAIN-LIKE 1 (MAIL1) are involved in TE silencing. Additionally, the MICRORCHIDIA (MORC) ATPases, including MORC1 are important cellular factors repressing TEs. Here, we describe the genetic interaction and connection between the PMD and MORC pathways by showing that MORC1 expression is impaired in main and mail1 mutants. This suggests that at least for a subset of TEs, silencing defects observed in pmd mutants could be the consequence of MORC1 downregulation. Transcriptomic analyses of higher-order mutant plants combining pmd and morc1 mutations as well as pmd mutants in which MORC1 expression is restored confirm this hypothesis. Thus, TE silencing defects observed in the pmd main and mail1 mutants can be partially explained by MORC1 downregulation. ENA-FIRST-PUBLIC 2023-01-06 ENA-LAST-UPDATE 2023-01-06