G1 phase regulation, area-specific cell cycle control, and cytoarchitectonics in the primate cortex

Neuron. 2005 Aug 4;47(3):353-64. doi: 10.1016/j.neuron.2005.06.032.

Abstract

We have investigated the cell cycle-related mechanisms that lead to the emergence of primate areas 17 and 18. These areas are characterized by striking differences in cytoarchitectonics and neuron number. We show in vivo that (1) area 17 precursors of supragranular neurons exhibit a shorter cell cycle duration, a reduced G1 phase, and a higher rate of cell cycle reentry than area 18 precursors; (2) area 17 and area 18 precursors show contrasting and specific levels of expression of cyclin E (high in area 17, low in area 18) and p27Kip1 (low in area 17, high in area 18); (3) ex vivo up- and downmodulation of cyclin E and p27Kip1 show that both regulators influence cell cycle kinetics by modifying rates of cell cycle progression and cell cycle reentry; (4) modeling the areal differences in cell cycle parameters suggests that they contribute to areal differences in numbers of precursors and neuron production.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Cycle / physiology*
  • Cell Cycle Proteins / metabolism
  • Cerebral Cortex / cytology*
  • Cerebral Cortex / embryology*
  • Cyclin E / metabolism
  • Cyclin-Dependent Kinase Inhibitor p27
  • Down-Regulation
  • Fetal Development
  • Fetus / metabolism
  • G1 Phase / physiology*
  • In Vitro Techniques
  • Kinetics
  • Macaca fascicularis / embryology*
  • Models, Neurological
  • Neurons / cytology
  • Time Factors
  • Tumor Suppressor Proteins / metabolism
  • Up-Regulation

Substances

  • Cell Cycle Proteins
  • Cyclin E
  • Tumor Suppressor Proteins
  • Cyclin-Dependent Kinase Inhibitor p27