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Long-range chromosomal interactions increase and mark repressed gene expression during adipogenesis.

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Long-range interactions (LRIs) increase during adipogenesis, marking repressed genomic regions crucial for cell-type specific gene regulation in obesity research.

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Area of Science:

  • Genomics
  • Epigenetics
  • Cell Biology

Background:

  • Obesity involves altered adipose tissue function, particularly adipogenesis (preadipocyte to adipocyte differentiation).
  • Epigenetic factors significantly influence adipogenesis, driven by environmental influences in obesity.
  • Promoter Capture Hi-C (pCHi-C) identifies interactions between gene promoters and regulatory elements, but often excludes long-range interactions (LRIs >1 Mb).

Purpose of the Study:

  • To investigate the role of LRIs in adipogenesis.
  • To analyze epigenetic regulation of adipogenesis using pCHi-C and RNA-seq data.
  • To identify novel regulatory mechanisms influencing obesity through LRIs.

Main Methods:

  • Utilized Promoter Capture Hi-C (pCHi-C) and bulk/single-nucleus RNA-sequencing.
  • Analyzed preadipocyte differentiation into adipocytes.
  • Investigated reproducibility and frequency of LRIs during adipogenesis.

Main Results:

  • LRIs are reproducible and increase over 2-fold during adipogenesis.
  • Genomic loci with LRIs show epigenetic repression and lower gene expression.
  • LRI regions contain repressed preadipocyte genes and lack active adipocyte genes during differentiation.
  • Identified a potential LRI-mediated regulatory mechanism at the *LYPLAL1*/*TGFB2* obesity locus.

Conclusions:

  • LRIs mark repressed genomic regions that become more prevalent during adipogenesis.
  • LRIs are critical for cell-type specific repression required for adipogenesis.
  • LRIs can refine long-range *cis*-eQTL analysis to identify obesity-related regulatory variants.