The cardiac neural crest gene MafB ectopically directs CXCR4 expression in the trunk neural crest

Saori Tani-Matsuhana1, Yuga Kawata1, Kunio Inoue1

  • 1Department of Biology, Graduate School of Science, Kobe University, 1-1 Rokkodaicho, Nada-ku, Kobe, 657-8501, Japan.

Developmental Biology
|December 24, 2022
PubMed

Insights

MafB, Ets1, and Sox8 genes are crucial for cardiac neural crest identity. Their expression in trunk neural crest cells induces cell migration properties, essential for cardiovascular development.

Area of Science:

  • Developmental Biology
  • Molecular Biology
  • Genetics

Background:

  • Cardiac neural crest cells originate from the hindbrain and are vital for cardiovascular system formation.
  • These cells migrate to the heart via the CXCR/SDF1 signaling pathway.
  • The septation of the outflow tract is a unique contribution of cardiac neural crest cells.

Purpose of the Study:

  • To investigate the effect of ectopic MafB gene expression on trunk neural crest cells.
  • To identify key genes involved in conferring cardiac neural crest identity, particularly cell migration properties.

Main Methods:

  • Analysis of MafB cis-regulatory element activity in different neural crest cell types.
  • Forced expression of cardiac neural crest genes (MafB, Ets1, Sox8) in trunk neural crest cells.
  • Assessment of ectopic Sox10E2 enhancer and CXCR4 expression.

Main Results:

  • MafB activates its own cis-regulatory element in enteric and trunk neural crest cells.
  • Co-expression of Ets1 and Sox8, with or without MafB, induced ectopic Sox10E2 enhancer activity in trunk neural crest cells.
  • MafB, Ets1, and Sox8 co-expression induced ectopic CXCR4 expression, conferring SDF1 signal responsiveness.

Conclusions:

  • MafB, Ets1, and Sox8 are essential for establishing cardiac neural crest cell identity.
  • These genes play a critical role in regulating cell migration properties of neural crest cells.
  • The findings provide insights into the molecular mechanisms governing neural crest cell fate and migration.