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MKLs: co-factors of serum response factor (SRF) in neuronal responses

Katarzyna Kalita1, Bozena Kuzniewska, Leszek Kaczmarek

  • 1Department of Molecular and Cellular Neurobiology, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland. k.kalita@nencki.gov.pl

The International Journal of Biochemistry & Cell Biology
|May 26, 2012
PubMed

Insights

Myocardin-related transcription factors (MRTFs), MKL1 and MKL2, are crucial co-activators of serum response factor (SRF) in developing neurons. Their inactivation impairs neuronal migration and neurite outgrowth, highlighting their role in brain development and plasticity.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Serum response factor (SRF) regulates activity-dependent gene expression in neurons.
  • SRF activation involves co-factors like ternary complex factors (TCFs) and myocardin-related transcription factors (MRTFs).

Purpose of the Study:

  • This review focuses on MKL1 and MKL2, key MRTF family members.
  • To elucidate the role of MKL1 and MKL2 as SRF co-activators in neuronal development and plasticity.

Main Methods:

  • Review of existing literature on MKL1 and MKL2 function.
  • Analysis of studies involving MKL inactivation or inhibition (e.g., using short-hairpin RNAs).

Main Results:

  • MKL1 and MKL2 are expressed in the brain and co-activate SRF-dependent gene expression.
  • Inactivation of MKLs leads to impaired neuronal migration and abnormal neurite outgrowth in developing mice.
  • Inhibition of MKL1 or MKL2 reduces dendritic processes and length, indicating a role in structural plasticity.

Conclusions:

  • MKL1 and MKL2 are essential co-activators for SRF function in the developing brain.
  • MKLs play a critical role in neuronal development, including migration and neurite outgrowth.
  • These findings suggest MKLs are key regulators of plasticity-related structural changes in neurons.

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