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Missing-in-metastasis MIM/MTSS1 promotes actin assembly at intercellular junctions and is required for integrity of

Juha Saarikangas1, Pieta K Mattila, Markku Varjosalo

  • 1Institute of Biotechnology, PO Box 56, University of Helsinki, 00014 Finland.

Journal of Cell Science
|March 17, 2011
PubMed

Insights

MIM protein maintains kidney epithelial cell junctions, crucial for kidney function. MIM deficiency causes severe urinary defects and renal failure, highlighting its role in maintaining tissue integrity.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Renal Physiology

Background:

  • MIM/MTSS1 regulates plasma membrane dynamics and is implicated in cancer metastasis.
  • MIM interacts with membranes via its I-BAR domain and actin monomers via its WH2 domain.
  • Previous studies suggested MIM potentiates Sonic hedgehog (Shh) signaling.

Purpose of the Study:

  • To investigate the physiological role of MIM protein in vivo and in vitro.
  • To determine the function of MIM in kidney epithelial cells and its impact on renal function.
  • To clarify MIM's role in Shh signaling during embryonic development.

Main Methods:

  • Generation and analysis of MIM mutant mice.
  • In vitro studies using cultured kidney epithelial (MDCK) cells.
  • Assessment of kidney function, epithelial integrity, and actin dynamics.

Main Results:

  • Full-length MIM protein is dispensable for embryonic development.
  • MIM-deficient mice exhibit severe urinary concentration defects due to compromised intercellular junctions.
  • MIM localizes to adherens junctions in kidney cells, promoting Arp2/3-mediated actin assembly.
  • MIM's function is dependent on its interaction with membranes and actin monomers.
  • MIM does not appear crucial for Shh signaling during embryogenesis.

Conclusions:

  • MIM is essential for maintaining the integrity of intercellular contacts in kidney epithelia.
  • MIM modulates the actin cytoskeleton and plasma membrane interplay to ensure proper kidney function.
  • MIM deficiency leads to renal failure, underscoring its critical role in renal health.

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