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Impaired manganese metabolism causes mitotic misregulation.

Manganese is an essential trace element, whose intracellular levels need to be carefully regulated. Mn(2+) acts as a cofactor for many enzymes and excess of Mn(2+) is toxic. Alterations in Mn(2+) homeostasis affect metabolic functions and mutations in the human Mn(2+)/Ca(2+) transporter ATP2C1 have been linked to Hailey-Hailey disease. By deletion of the yeast orthologue PMR1 we have studied the impact of Mn(2+) on cell cycle progression and show that an excess of cytosolic Mn(2+) alters S-phase transit, induces transcriptional up-regulation of cell cycle regulators, bypasses the need for S-phase cell cycle checkpoints and predisposes to genomic instability. On the other hand, we find that depletion of the Golgi Mn(2+) pool requires a functional morphology checkpoint to avoid the formation of polyploid cells.

Pubmed ID: 22493290


  • García-Rodríguez N
  • Díaz de la Loza Mdel C
  • Andreson B
  • Monje-Casas F
  • Rothstein R
  • Wellinger RE


The Journal of biological chemistry

Publication Data

May 25, 2012

Associated Grants

  • Agency: NIGMS NIH HHS, Id: GM50237
  • Agency: NIGMS NIH HHS, Id: R37 GM050237

Mesh Terms

  • Blotting, Western
  • Cell Cycle
  • Flow Cytometry
  • Genomic Instability
  • Homeostasis
  • Manganese
  • Mitosis