Ettensohn C A, McClay D R
Department of Zoology, Duke University, Durham, North Carolina 27706.
Dev Biol. 1988 Feb;125(2):396-409. doi: 10.1016/0012-1606(88)90220-5.
The mesoderm of the sea urchin embryo conventionally is divided into two populations of cells; the primary mesenchyme cells (PMCs), which produce the larval skeleton, and the secondary mesenchyme cells (SMCs), which differentiate into a variety of cell types but do not participate in skeletogenesis. In this study we examine the morphogenesis of embryos from which the PMCs have been removed microsurgically. We confirm the observation of Fukushi (1962) that embryos lacking PMCs form a complete skeleton, although in a delayed fashion. We demonstrate by microsurgical and cell marking experiments that the appearance of skeletogenic cells in such PMC-deficient embryos is due exclusively to the conversion of other cells to the PMC phenotype. Time-lapse video recordings of PMC-deficient embryos indicate that the converting cells are a subpopulation of late-ingressing SMCs. The conversion of these cells to the skeletogenic phenotype is accompanied by their de novo expression of cell surface determinants normally unique to PMCs, as shown by binding of wheat germ agglutinin and a PMC-specific monoclonal antibody. Cell transplantation and cell marking experiments have been carried out to determine the number of SMCs that convert when intermediate numbers of PMCs are present in the embryo. These experiments indicate that the number of converting SMCs is inversely proportional to the number of PMCs in the blastocoel. In addition, they show that PMCs and converted SMCs cooperate to produce a skeleton that is correct in both size and configuration. This regulatory system should shed light on the nature of cell-cell interactions that control cell differentiation and on the way in which evolutionary processes modify developmental programs.
海胆胚胎的中胚层传统上被分为两类细胞群体;一类是产生幼虫骨骼的初级间充质细胞(PMC),另一类是分化为多种细胞类型但不参与骨骼形成的次级间充质细胞(SMC)。在本研究中,我们研究了通过显微手术去除PMC后的胚胎的形态发生。我们证实了Fukushi(1962年)的观察结果,即缺乏PMC的胚胎尽管形成骨骼的时间延迟,但仍能形成完整的骨骼。我们通过显微手术和细胞标记实验证明,在这种缺乏PMC的胚胎中,成骨细胞的出现完全是由于其他细胞向PMC表型的转化。对缺乏PMC的胚胎进行的延时视频记录表明,转化细胞是晚期内陷SMC的一个亚群。这些细胞向成骨表型的转化伴随着它们从头表达通常仅PMC特有的细胞表面决定簇,这通过小麦胚凝集素和一种PMC特异性单克隆抗体的结合得以证明。已经进行了细胞移植和细胞标记实验,以确定当胚胎中存在中等数量的PMC时转化的SMC的数量。这些实验表明,转化的SMC的数量与囊胚腔中PMC的数量成反比。此外,它们还表明,PMC和转化的SMC共同协作产生大小和形态均正确的骨骼。这种调节系统应该能够阐明控制细胞分化的细胞间相互作用的本质,以及进化过程如何改变发育程序。