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Updated: Aug 1, 2026

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
08:01

Stimulation of Notch Signaling in Mouse Osteoclast Precursors

Published on: February 28, 2017

Notch signaling modulates the nuclear localization of carboxy-terminal-phosphorylated smad2 and controls the

Takanori Abe1, Miho Furue, Akiko Kondow

  • 1Department of Biological Science, Graduate School of Science, The University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan.

Mechanisms of Development
|April 9, 2005
PubMed

Insights

Notch signaling delays loss of mesodermal competence in Xenopus embryos by maintaining Smad2 binding to Smad4, crucial for nuclear accumulation and mesodermal gene induction.

Area of Science:

  • Developmental Biology
  • Cell Signaling

Background:

  • Loss of mesodermal competence (LMC) is a poorly understood phenomenon in Xenopus development.
  • Prospective ectodermal cells lose responsiveness to inductive signals like activin A after gastrulation begins.
  • Notch signaling is known to delay LMC onset in animal caps, but the mechanism is unclear.

Purpose of the Study:

  • Investigate the mechanism by which Notch signaling delays LMC.
  • Determine the specific step in the activin signal transduction pathway affected by Notch signaling.

Main Methods:

  • Utilized Xenopus animal caps and whole embryos.
  • Examined the activin signal transduction pathway, focusing on ALK4, Smad2, and Smad4 interactions.
  • Compared control and Notch-activated conditions.

Main Results:

  • Activin A stimulation still phosphorylated Smad2 via ALK4 in both control and Notch-activated caps after LMC onset.
  • C-terminal phosphorylated Smad2 could bind Smad4 and accumulate in the nucleus only in Notch-activated caps.
  • LMC occurred because phosphorylated Smad2 lost its ability to bind Smad4 and enter the nucleus.

Conclusions:

  • Loss of mesodermal competence is caused by the failure of phosphorylated Smad2 to bind Smad4.
  • Notch signaling delays LMC by restoring the ability of phosphorylated Smad2 to bind Smad4, facilitating nuclear accumulation.

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