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TACC3-TSC2 maintains nuclear envelope structure and controls cell division

Laia Gómez-Baldó1, Stephan Schmidt, Christopher A Maxwell

  • 1Translational Research Laboratory, Catalan Institute of Oncology, Bellvitge Biomedical Research Institute, Barcelona, Spain.

Cell Cycle (Georgetown, Tex.)
|March 19, 2010
PubMed

Insights

Transforming acidic coiled-coil (TACC) proteins, like TACC3, interact with tuberous sclerosis complex 2 (TSC2), revealing novel roles in cell structure and division. This finding offers new insights into TSC and LAM pathogenesis.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • Tuberous sclerosis complex (TSC) proteins (TSC1/TSC2) are known regulators of translation and cell growth.
  • The role of TSC proteins in cellular structure and cell cycle regulation is not fully understood.
  • Transforming acidic coiled-coil (TACC) domain proteins are involved in centrosome-associated structures and processes.

Purpose of the Study:

  • To investigate the interaction between TACC3 and TSC2.
  • To elucidate the role of TACC3 and TSC2 in cellular structures and cell division.
  • To explore the implications for lymphangioleiomyomatosis (LAM) and TSC syndrome.

Main Methods:

  • Interactome mapping to identify TACC3 binding partners.
  • Co-localization and co-purification studies with nuclear envelope components.
  • Analysis of cell division, including spindle pole localization, abscission, and binucleation in Tacc3- and Tsc2-deficient cells.

Main Results:

  • TACC3 interactome mapping identified TSC2 and 15 other proteins, including ch-TOG/CKAP5 and FAM161B.
  • TACC3 and TSC2 co-localize with nuclear envelope components, and their deficiency causes nuclear envelope morphological alterations.
  • TACC3 is essential for proper phospho-Ser939 TSC2 localization during cell division, and Tacc3/Tsc2 deficiency leads to abscission defects and increased binucleation.

Conclusions:

  • TACC3 links to novel structural and cell division functions of TSC2.
  • TSC2 acts epistatically to TACC3 in cell division regulation, converging on the CHFR-mediated mitotic checkpoint.
  • These findings provide potential explanations for the clinical manifestations of LAM and TSC, including the differential severity of TSC1 versus TSC2 mutations.

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