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c-Jun NH2-terminal kinase is required for lineage-specific differentiation but not stem cell self-renewal

Ping Xu1, Roger J Davis

  • 1Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA. roger.davis@umassmed.edu

Molecular and Cellular Biology
|January 13, 2010
PubMed

Insights

The c-Jun NH(2)-terminal kinase (JNK) is crucial for embryonic stem cell differentiation. While JNK is not essential for stem cell proliferation or self-renewal, its absence leads to rapid senescence and impaired lineage development.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Genetics

Background:

  • c-Jun NH(2)-terminal kinase (JNK) signaling pathways are involved in cellular proliferation and stress responses.
  • While individual JNK1 or JNK2 gene deficiencies are tolerated in mice, combined deficiencies lead to embryonic lethality.
  • Previous studies indicated that loss of JNK kinase function induces senescence.

Purpose of the Study:

  • To investigate the role of JNK in embryonic stem (ES) cell proliferation and differentiation.
  • To determine if JNK is required for the self-renewal capacity of ES cells.

Main Methods:

  • Isolation of embryonic stem cells from wild-type and JNK-deficient (Jnk1(-/-)Jnk2(-/-)) mice.
  • Assessment of ES cell self-renewal, proliferation rates, and lineage-specific differentiation potential.
  • Utilized conditional gene ablation and chemical genetic approaches in prior studies.

Main Results:

  • JNK-deficient ES cells exhibited normal self-renewal capabilities.
  • JNK-deficient ES cells proliferated at a faster rate compared to wild-type ES cells.
  • Significant defects in lineage-specific differentiation were observed in JNK-deficient ES cells.

Conclusions:

  • JNK signaling is not essential for the proliferation or self-renewal of mouse embryonic stem cells.
  • JNK plays a critical regulatory role in promoting proper lineage-specific differentiation of ES cells.
  • The absence of JNK function in ES cells leads to impaired differentiation capacity.

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