Balanced SET levels favor the correct enhancer repertoire during cell fate acquisition

Nat Commun. 2023 Jun 3;14(1):3212. doi: 10.1038/s41467-023-39043-x.

Abstract

Within the chromatin, distal elements interact with promoters to regulate specific transcriptional programs. Histone acetylation, interfering with the net charges of the nucleosomes, is a key player in this regulation. Here, we report that the oncoprotein SET is a critical determinant for the levels of histone acetylation within enhancers. We disclose that a condition in which SET is accumulated, the severe Schinzel-Giedion Syndrome (SGS), is characterized by a failure in the usage of the distal regulatory regions typically employed during fate commitment. This is accompanied by the usage of alternative enhancers leading to a massive rewiring of the distal control of the gene transcription. This represents a (mal)adaptive mechanism that, on one side, allows to achieve a certain degree of differentiation, while on the other affects the fine and corrected maturation of the cells. Thus, we propose the differential in cis-regulation as a contributing factor to the pathological basis of SGS and possibly other the SET-related disorders in humans.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, N.I.H., Extramural

MeSH terms

  • Cell Differentiation / genetics
  • Chromatin / genetics
  • Enhancer Elements, Genetic* / genetics
  • Histones* / genetics
  • Histones* / metabolism
  • Humans
  • Promoter Regions, Genetic / genetics

Substances

  • Histones
  • Chromatin

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