Cell cycle regulation of the psoriasis associated gene CCHCR1 by transcription factor E2F1

PLoS One. 2023 Dec 21;18(12):e0294661. doi: 10.1371/journal.pone.0294661. eCollection 2023.

Abstract

The coiled-coil alpha-helical rod protein 1 (CCHCR1) was first identified as a candidate gene in psoriasis and has lately been found to be associated with a wide range of clinical conditions including COVID-19. CCHCR1 is located within P-bodies and centrosomes, but its exact role in these two subcellular structures and its transcriptional control remain largely unknown. Here, we showed that CCHCR1 shares a bidirectional promoter with its neighboring gene, TCF19. This bidirectional promoter is activated by the G1/S-regulatory transcription factor E2F1, and both genes are co-induced during the G1/S transition of the cell cycle. A luciferase reporter assay suggests that the short intergenic sequence, only 287 bp in length, is sufficient for the G1/S induction of both genes, but the expression of CCHCR1 is further enhanced by the presence of exon 1 from both TCF19 and CCHCR1. This research uncovers the transcriptional regulation of the CCHCR1 gene, offering new perspectives on its function. These findings contribute to the broader understanding of diseases associated with CCHCR1 and may serve as a foundational benchmark for future research in these vital medical fields.

MeSH terms

  • Cell Cycle
  • E2F Transcription Factors / metabolism
  • E2F1 Transcription Factor* / genetics
  • E2F1 Transcription Factor* / metabolism
  • Gene Expression Regulation
  • Humans
  • Intracellular Signaling Peptides and Proteins / metabolism
  • Psoriasis* / genetics
  • Psoriasis* / metabolism
  • Transcription Factors / genetics
  • Transcription Factors / metabolism

Substances

  • E2F1 Transcription Factor
  • Intracellular Signaling Peptides and Proteins
  • E2F Transcription Factors
  • TCF19 protein, human
  • Transcription Factors
  • CCHCR1 protein, human
  • E2F1 protein, human

Grants and funding

The author(s) received no specific funding for this work.