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Y-box binding protein-1 down-regulates expression of carbamoyl phosphate synthetase-I by suppressing CCAAT

Yen-Rong Chen1, Keisuke Sekine, Koji Nakamura

  • 1Institute of Molecular and Cellular Biosciences, The University of Tokyo, Japan.

Gastroenterology
|March 11, 2009
PubMed

Insights

Y-box binding protein-1 (YB-1) inhibits carbamoyl phosphate synthetase-I (CPS1) expression, impacting ammonia detoxification. This study reveals YB-1

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Genetics

Background:

  • Carbamoyl phosphate synthetase-I (CPS1) is crucial for urea cycle function; defects lead to hyperammonemia.
  • CPS1 liver expression is regulated by CCAAT enhancer-binding protein-alpha (C/EBPalpha) but is absent in fetal liver.

Purpose of the Study:

  • To elucidate the regulatory mechanism of CPS1 expression, particularly the factor involved in its absence in fetal liver.

Main Methods:

  • Microarray analysis identified Y-box binding protein-1 (YB-1) in mouse fetal liver.
  • Investigated YB-1's role in CPS1 regulation through overexpression studies and luciferase reporter assays.
  • Chromatin immunoprecipitation (ChIP) assays examined YB-1 recruitment to the CPS1 promoter in vivo.

Main Results:

  • YB-1 expression inversely correlated with CPS1 expression; YB-1 inhibited CPS1 and ammonia clearance in fetal liver.
  • Acute liver injury induced YB-1, suppressed CPS1, and increased serum ammonia levels.
  • YB-1 suppressed C/EBPalpha-mediated CPS1 transcription and was recruited to the CPS1 promoter in fetal and injured adult liver.

Conclusions:

  • Y-box binding protein-1 (YB-1) acts as a key regulator of ammonia detoxification.
  • YB-1 negatively regulates CPS1 expression by suppressing C/EBPalpha function.
Abstract

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