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Impaired manganese metabolism causes mitotic misregulation.

http://www.ncbi.nlm.nih.gov/pubmed/22493290

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 RIS Download

Mesh terms: Blotting, Western | Cell Cycle | Flow Cytometry | Genomic Instability | Homeostasis | Manganese | Mitosis

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Associated grants

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

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