Pearson, R.A.;
Lüneborg, N.L.;
Becker, D.L.;
Mobbs, P.;
(2005)
Gap junctions modulate interkinetic nuclear movement in retinal progenitor cells.
Journal of Neuroscience
, 25
(46)
pp. 10803-10814.
10.1523/JNEUROSCI.2312-05.2005.
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Abstract
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.
| Type: | Article |
|---|---|
| Title: | Gap junctions modulate interkinetic nuclear movement in retinal progenitor cells |
| Open access status: | An open access version is available from UCL Discovery |
| DOI: | 10.1523/JNEUROSCI.2312-05.2005 |
| Publisher version: | http://dx.doi.org/10.1523/JNEUROSCI.2312-05.2005 |
| Language: | English |
| Additional information: | Published by the Society of Neuroscience This work is licensed under the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. The license allows you to copy, distribute, and transmit the work, as well as adapting it. However, you must attribute the work to the author (but not in any way that suggests that they endorse you or your use of the work), and cannot use the work for commercial purposes without prior permission of the author. If you alter or build upon this work, you can distribute the resulting work only under the same or similar license to this one. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/ or send a letter to Creative Commons, 444 Castro Street, Suite 900, Mountain View, California, 94041, USA. |
| Keywords: | Ca2+ waves, chick, hemichannel, proliferation, connexin43, antisense |
| URI: | https://discovery.ucl.ac.uk/id/eprint/9685 |
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