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The Journal of Neuroscience, November 16, 2005, 25(46):10803-10814; doi:10.1523/JNEUROSCI.2312-05.2005

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 Previous Article

Development/Plasticity/Repair
Gap Junctions Modulate Interkinetic Nuclear Movement in Retinal Progenitor Cells

Rachael A. Pearson,^1 * Nanna L. Lüneborg,¹ David L. Becker,² and Peter Mobbs¹

Departments of ¹Physiology and ²Anatomy and Developmental Biology, University College London, London WC1E 6BT, United Kingdom

During early retinal development, progenitor cells must divide repeatedly to expand the progenitor pool. During G₁ and G₂ of the cell cycle, progenitor cell nuclei migrate back-and-forth across the proliferative zone in a process termed interkinetic nuclear movement. Because division can only occur at the ventricular surface, factors that affect the speed of nuclear movement could modulate the duration of the cell cycle. Gap-junctional coupling and gap junction-dependent Ca²⁺ activity are common features of proliferating cells in the immature nervous system. Furthermore, both gap-junctional coupling and changes in [Ca²⁺]_i have been shown to be positively correlated with the migration of a number of immature cell types. Using time-lapse confocal microscopy, we describe the nature and rate of progenitor cell interkinetic nuclear movement. We show that nuclear movement is usually, but not always, associated with Ca²⁺ transients and that buffering of these transients with BAPTA slows movement. Furthermore, we show for the first time that gap-junctional communication is an important requirement for the maintenance of normal nuclear movement in retinal progenitor cells. Conventional blockers of gap junctions and transfection of cells with dominant-negative constructs of connexin 43 (Cx43) and Cx43-specific antisense oligodeoxynucleotides (asODNs) all act to slow interkinetic nuclear movement. The gap junction mimetic peptide Gap26 also acts to slow movement, an effect that we show may be attributable to the blockade of gap junction hemichannels.

Key words: Ca²⁺ waves; chick; hemichannel; proliferation; connexin43; antisense

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Received Feb 1, 2005; revised October 3, 2005; accepted October 5, 2005.

This article has been cited by other articles:

				J. E. Cook and D. L. Becker Gap-Junction Proteins in Retinal Development: New Roles for the "Nexus" Physiology, August 1, 2009; 24(4): 219 - 230. [Abstract] [Full Text] [PDF]

				X. Liu, K. Hashimoto-Torii, M. Torii, T. F. Haydar, and P. Rakic The role of ATP signaling in the migration of intermediate neuronal progenitors to the neocortical subventricular zone PNAS, August 19, 2008; 105(33): 11802 - 11807. [Abstract] [Full Text] [PDF]

				T. Weber, M. K. Corbett, L. M. L. Chow, M. B. Valentine, S. J. Baker, and J. Zuo Rapid cell-cycle reentry and cell death after acute inactivation of the retinoblastoma gene product in postnatal cochlear hair cells PNAS, January 15, 2008; 105(2): 781 - 785. [Abstract] [Full Text] [PDF]

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