Notch transactivates Rheb to maintain the multipotency of TSC-null cells

Nat Commun. 2017 Nov 29;8(1):1848. doi: 10.1038/s41467-017-01845-1.

Abstract

Differentiation abnormalities are a hallmark of tuberous sclerosis complex (TSC) manifestations; however, the genesis of these abnormalities remains unclear. Here we report on mechanisms controlling the multi-lineage, early neuronal progenitor and neural stem-like cell characteristics of lymphangioleiomyomatosis (LAM) and angiomyolipoma cells. These mechanisms include the activation of a previously unreported Rheb-Notch-Rheb regulatory loop, in which the cyclic binding of Notch1 to the Notch-responsive elements (NREs) on the Rheb promoter is a key event. This binding induces the transactivation of Rheb. The identified NRE2 and NRE3 on the Rheb promoter are important to Notch-dependent promoter activity. Notch cooperates with Rheb to block cell differentiation via similar mechanisms in mouse models of TSC. Cell-specific loss of Tsc1 within nestin-expressing cells in adult mice leads to the formation of kidney cysts, renal intraepithelial neoplasia, and invasive papillary renal carcinoma.

Publication types

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

MeSH terms

  • Angiomyolipoma / metabolism
  • Angiomyolipoma / pathology*
  • Animals
  • Cell Differentiation / genetics
  • Cell Differentiation / physiology
  • Female
  • Humans
  • Lung Neoplasms / metabolism
  • Lung Neoplasms / pathology*
  • Lymphangioleiomyomatosis / metabolism
  • Lymphangioleiomyomatosis / pathology*
  • Male
  • Mice, SCID
  • Mice, Transgenic
  • Neural Crest / metabolism
  • Neural Crest / pathology
  • Promoter Regions, Genetic
  • Ras Homolog Enriched in Brain Protein / genetics
  • Ras Homolog Enriched in Brain Protein / metabolism*
  • Receptor, Notch1 / genetics
  • Receptor, Notch1 / metabolism*
  • Transcription Factor HES-1 / genetics
  • Transcription Factor HES-1 / metabolism
  • Tuberous Sclerosis / metabolism
  • Tuberous Sclerosis Complex 1 Protein
  • Tuberous Sclerosis Complex 2 Protein
  • Tumor Suppressor Proteins / genetics
  • Xenograft Model Antitumor Assays

Substances

  • NOTCH1 protein, human
  • RHEB protein, human
  • Ras Homolog Enriched in Brain Protein
  • Receptor, Notch1
  • TSC1 protein, human
  • Transcription Factor HES-1
  • Tsc1 protein, mouse
  • Tuberous Sclerosis Complex 1 Protein
  • Tuberous Sclerosis Complex 2 Protein
  • Tumor Suppressor Proteins
  • HES1 protein, human