Interkinetic nuclear migration: reciprocal activities of dynein and kinesin

Abstract

A hallmark of neurogenesis in vertebrate is the apical-basal fluctuation of radial glia nuclei. Such a phenomenon, called INM, has been known for decades and is closely associated with mitosis but still puzzles scientists. An impressive step in the molecular understanding of INM has recently been achieved by Tsai and coworkers. Using RNA interference associated with time-lapse imaging, these authors demonstrated a dual motor system that can push/pull the nuclei accordingly with the cell cycle stages.

Figure 1

Molecular mechanisms of INM. Position of the RGPC's nucleus in the VZ depends on the phase of the cell cycle. The nucleus stays at the pial surface until the end of the S phase. During the G₂ phase Dyn transport the nucleus along uniformly directed microtubules toward the ventricular surface, where it undergoes mitosis (M phase). This nuclear movement is fast, but intermittent. After mitosis, at the G₁ phase the nucleus is driven back to the pial surface by Kin. Unlike basal-to-apical INM, apical-to-basal nuclear translocation is slower, but continuous in time. The centrosomes remain at the ventricular surface during the whole cycle.