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© The Rockefeller University Press, 0021-9525/2003/8/361 $5.00
The Journal of Cell Biology, Volume 162, Number 3, 361-361

Neural progenitors play favorites

Apoptotic cells (green) are PAR-4 positive (red).

Programmed cell death is essential for preventing hyperproliferation during normal embryonic brain development and is also critical to the pathogenesis of several neurodegenerative diseases. Using mouse embryonic stem cells to model neuronal differentiation, Bieberich et al. (page 469) now show that when neural progenitor cells divide, only one progeny cell survives due to asymmetric distribution of pro- and anti-apoptotic factors between daughter cells.

In the developing mouse brain, apoptosis often correlates with the presence of the lipid ceramide and the protein PAR-4, and current models predict that neuronal apoptosis follows soon after cell division. The authors found that, in neuronal progenitors derived from embryonic stem cells, PAR-4 and the intermediate filament protein nestin (a marker of neural progenitors) are asymmetrically distributed after mitosis. One daugher cell inherits high PAR-4 and low nestin levels, and undergoes apoptosis. The other daughter inherits low PAR-4 and high nestin levels, and survives. Ceramide apparently induces apoptosis in the PAR-4–positive cell but not in the nestin-positive cell, possibly through active destruction of ceramide in the surviving daughter. The authors are now trying to determine how ceramide and PAR-4 interact to induce cell death and also hope to identify the mechanism that ensures asymmetric inheritance of PAR-4 and nestin.

Alan W. Dove

alanwdove{at}earthlink.net

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This Article Full Text (PDF, 642K) PPT slides of all figures Alert me when this article is cited Services Email this article Similar articles in this journal Alert me to new content in the JCB Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Dove, A. W. Search for Related Content PubMed Articles by Dove, A. W. Related Collections Related Article Social Bookmarking                            What's this?