Journal
CELL CYCLE
Volume 14, Issue 12, Pages 1938-1947Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15384101.2015.1026487
Keywords
cell division; LCMT1; methylation; mitotic spindle; PME-1
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Funding
- National Science Foundation [MCB1243645]
- Div Of Molecular and Cellular Bioscience
- Direct For Biological Sciences [1243645] Funding Source: National Science Foundation
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Leucine carboxyl methyltransferase-1 (LCMT1) and protein phosphatase methylesterase-1 (PME-1) are essential enzymes that regulate the methylation of the protein phosphatase 2A catalytic subunit (PP2AC). LCMT1 and PME-1 have been linked to the regulation of cell growth and proliferation, but the underlying mechanisms have remained elusive. We show here an important role for an LCMT1-PME-1 methylation equilibrium in controlling mitotic spindle size. Depletion of LCMT1 or overexpression of PME-1 led to long spindles. In contrast, depletion of PME-1, pharmacological inhibition of PME-1 or overexpression of LCMT1 led to short spindles. Furthermore, perturbation of the LCMT1-PME-1 methylation equilibrium led to mitotic arrest, spindle assembly checkpoint activation, defective cell divisions, induction of apoptosis and reduced cell viability. Thus, we propose that the LCMT1-PME-1 methylation equilibrium is critical for regulating mitotic spindle size and thereby proper cell division.
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