Compensation for the Lost Prospective Central Nervous System by Expansion of the Prospective Epidermis in the ‘16-Cell’ Embryos of Xenopus laevis Lacking All Animal Dorsal Blastomeres
Compensation for the Lost Prospective Central Nervous System by Expansion of the Prospective Epidermis in the ‘16-Cell’ Embryos of Xenopus laevis Lacking All Animal Dorsal Blastomeres
复制标题
通过扩张缺乏所有动物背卵裂球的非洲爪蟾“16细胞”胚胎中的预期表皮来补偿失去的预期中枢神经系统
DOI:
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发表时间:
1999
期刊:
影响因子:
--
通讯作者:
M. Koga
中科院分区:
文献类型:
--
作者:
M. Koga
Abstract In the normal embryo of Xenopus laevis, the central nervous system (CNS) and epidermis, a pair of main ectodermal tissues, are derived mainly from the animal dorsal (AD) and animal ventral (AV) blastomeres, respectively. The defect embryo, from which all AD blastomeres have been removed at the 16-cell stage, can develop into a normally proportioned embryo, i.e., a regulated embryo, despite the striking deficiency of the prospective CNS. To compare the contribution of the AV blastomeres to the CNS and epidermis between the normal and regulated embryos, each of the AV blastomeres was labelled by a tracer injection at the 16-cell stage, and a clonal domain originating from the labelled blastomere in these ectodermal tissues was examined. By the removal of the AD blastomeres, the clonal domains of the each AV blastomeres were expanded in a dorsal direction, and covered the regions not only in the epidermis just as in normal embryos but also in the CNS extending from the anterior to the posterior end, respectively. Most of the lost prospective regions of the AD blastomeres in the ectodermal tissues were compensated not by the descendants of all the remained blastomeres in the defect embryo, but by the progeny of the AV blastomeres extending dorsally. These facts suggest that compensation for the lost prospective CNS owes mainly to the regulation in the prospective ectoderm, and spreading of the prospective ectoderm is progressively directed after the 16-cell stage by interaction with other parts of the embryo.
影响因子:
2.7
作者:
MOODY, SA
通讯作者:
MOODY, SA
影响因子:
2.7
作者:
MOODY, SA
通讯作者:
MOODY, SA
影响因子:
2.7
作者:
Gimlich,RL;Braun,J
通讯作者:
Braun,J