HP1 builds heterochromatin and silences genes without H3K9 methylation
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A study published in Molecular Cell on October 22, 2026, reports that in C. elegans the HP1 homolog HPL-2 can form heterochromatin foci, repress genes, and restrict organogenesis without relying on H3K9 methylation, long considered the mark that recruits HP1 proteins to chromatin. Delaney et al. show that HP1/HPL-2 and the H3K9 methyltransferase SETDB1/MET-2 assemble heterochromatin foci by binding distinct cofactors, and that it is these foci, rather than H3K9me3 itself, that track with transcriptional silencing. The findings reframe HP1 as an active, methylation-independent driver of heterochromatin formation rather than a passive reader of the H3K9me mark. How the distinct cofactors are identified and whether the mechanism extends to other organisms remain open questions.
Written by a model from the reports · updated 3 hours ago
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Delaney et al. report that in C. elegans the HP1 homolog HPL-2 can form heterochromatin foci, silence genes, and restrict organogenesis independently of H3K9 methylation. HP1/HPL-2 and the H3K9 methyltransferase SETDB1/MET-2 form heterochromatin foci by binding distinct cofactors, and it is these foci, rather than H3K9me3, that track with silencing activity.
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