Knockout of ERK5 causes multiple defects in placental and embryonic development

Lijun Yan1, Julia Carr, Peter R Ashby

  • 1MRC Protein Phosphorylation Unit, University of Dundee, Dundee, DD1 5EH, UK. l.yan@dundee.ac.uk

BMC Developmental Biology
|December 17, 2003
PubMed
Abstract

Insights

Extracellular signal-regulated kinase 5 (ERK5) is vital for embryonic development. ERK5 knockout mice exhibit developmental defects and embryonic lethality around day 10.5, underscoring its essential role.

Area of Science:

  • Molecular Biology
  • Developmental Biology
  • Genetics

Background:

  • Extracellular signal-regulated kinase 5 (ERK5) is part of the mitogen-activated protein kinase family.
  • ERK5 is activated by mitogenic or stressful stimuli.
  • The precise physiological function of ERK5 in cellular processes remains largely undetermined.

Purpose of the Study:

  • To elucidate the physiological function of ERK5 in mammalian development.
  • To investigate the consequences of ERK5 gene inactivation in vivo.

Main Methods:

  • Gene targeting was employed to create ERK5 knockout mice (ERK5-/-).
  • In situ hybridization was used to analyze the expression patterns of ERK5 and its activator MKK5.
  • Embryonic development was monitored from E9.5 to E10.5 for morphological and cellular abnormalities.

Main Results:

  • ERK5 knockout mice exhibited embryonic lethality around embryonic day 10.5 (E10.5).
  • Significant expression of ERK5 and MKK5 was observed in the embryonic head and trunk at E10.5.
  • ERK5-/- embryos displayed increased apoptosis in cephalic mesenchyme, hindgut abnormalities, and defects in vascular remodeling, cardiac development, and placental formation.

Conclusions:

  • ERK5 is indispensable for early embryonic development in mice.
  • The study highlights ERK5's critical role in vascular system development.
  • ERK5 is essential for maintaining cell survival during embryogenesis.