THE POTENTIAL TO DIFFERENTIATE EPIDERMIS IS UNEQUALLY DISTRIBUTED IN THE AB LINEAGE DURING EARLY EMBRYONIC-DEVELOPMENT IN C-ELEGANS

Citation
Sb. Gendreau et al., THE POTENTIAL TO DIFFERENTIATE EPIDERMIS IS UNEQUALLY DISTRIBUTED IN THE AB LINEAGE DURING EARLY EMBRYONIC-DEVELOPMENT IN C-ELEGANS, Developmental biology, 166(2), 1994, pp. 770-781
Citations number
38
Categorie Soggetti
Developmental Biology",Biology
Journal title
ISSN journal
00121606
Volume
166
Issue
2
Year of publication
1994
Pages
770 - 781
Database
ISI
SICI code
0012-1606(1994)166:2<770:TPTDEI>2.0.ZU;2-K
Abstract
In the early Caenorhabditis elegans embryo most of the ectoderm arises from the AB blastomere, one of the six founder cells. We report that nonequivalent blastomeres are generated at the third division round in the AB lineage. Each AB granddaughter divides to produce one cell tha t has the potential to make abundant epidermis and one that instead pr oduces primarily nervous system. This unequal distribution of the pote ntial to make epidermis occurs in an AB granddaughter that is isolated by laser-ablation of all other cells or during the development of an isolated AB blastomere in culture. The fidelity of this event is norma lly masked by a signal from the MS founder cell, which induces mesoder m in particular AB descendants. When MS induction is prevented by lase r cell-ablation or by a mutation in the glp-1 gene, the epidermal fate map of the AB great granddaughters becomes left-right symmetrical. Ce ll lineage analyses demonstrate that, in fact, the AB lineage becomes entirely left-right symmetrical in the absence of MS induction. This a ccounts for the extra epidermal cells previously observed in a glp-1 m utant. Our results suggest that epidermal differentiation in the nemat ode may be controlled by a cell-autonomous mechanism that differential ly allocates epidermal potential during AB development and that MS ind uction generates the left-right asymmetry in the fates of AB descendan ts in part by overriding this potential. (C) 1994 Academic Press, Inc.