Redundant mechanisms explains the majority of transcription silencing downstream of DNA methylation

DNA methylation is a conserved epigenetic modification crucial for silencing genes and transposable elements (TEs). However, the mechanisms that cause silencing remain unclear, partly because methyl reader protein mutants in both plants and animals show minimal transcriptional changes. To explore the possibility of redundancy among these silencing mechanisms, we generated combinatorial mutants of H1.1, H1.2, ADCP1, MOM1, MBD2, MBD5, and MBD6 lacking key methyl readers and related silencing pathways. We observed massive derepression of genes and TEs at DNA-methylated loci, showing that these pathways account for 73% of silencing compared to DNA methylation-free mutants. To assess whether TE derepression resulted in higher TE mobilization, we generated PacBio HiFi sequencing data for two lines of h1.1 h1.2 adcp1 mom1 mbd2 mbd5 mbd6 mutants (hhammmm-1 and hhammmm-2), h1.1 h1.2 adcp1 mutant and wild type as a control.