Methylation of DNA and dimethylated histone H3 Lys9 (H3K9me2) are marks for epigenetic silencing, leading to higher-order compaction of chromatin. These methylation marks are usually enriched in regions containing transposable elements and DNA repeats, and a deficiency in DNA methyltransferases can result in loss of silencing. Now Jacobsen and colleagues uncover a novel mechanism regulating gene silencing in Arabidopsis thaliana, involving alterations in chromosome superstructure. Using the normally silenced SDC gene with a GFP fusion as a reporter, the authors identified two genes, AtMORC1 and AtMORC6, whose mutations led to loss of SDC silencing. RNA sequencing analyses showed that the derepression effect of the AtMORC gene mutations was also observed for transposable elements and other silenced loci. However, DNA methylation and H3K9me2 levels, as assessed by whole-genome bisulfite sequencing and ChIP-seq respectively, were not affected in atmorc1 or atmorc6 mutants. AtMORC1 and AtMORC6 have close orthologs in higher eukaryotes, and the proteins belong to a broader family of ATPases that includes bacterial DNA gyrase and the mismatch-repair protein MutL. This family had been previously proposed to manipulate DNA superstructures and to remodel chromatin in eukaryotes. Based on this idea, the authors examined chromatin compaction in atmorc1 and atmorc6 by microscopy and observed decondensation of the chromocenters, nuclear bodies where pericentromeric heterochromatin usually localizes. They then used Hi-C analysis to examine genome-wide chromatin interactions, finding that pericentromeric heterochromatin made many more contacts with the rest of the genome in an atmorc6 mutant than in the wild type. AtMORC1 and AtMORC6 proteins seem to localize to the outside of chromocenters. Altogether, these observations led the authors to propose that AtMORC1 and AtMORC6 enforce silencing of pericentromeric heterochromatin by regulating its architecture and promoting its compaction. Interestingly, this silencing mechanism seems to be conserved in worms: the authors showed that knockdown of the single ortholog morc-1 in Caenorhabditis elegans led to derepression of a silenced reporter gene, and previous observations in the mouse knockout are consistent with a role of Morc-1 in silencing of transposable elements during spermatogenesis. (Science 336, 1448–1451, 2012)