DEVELOPMENTAL POTENTIAL OF MUSCLE-CELL PROGENITORS AND THE MYOGENIC FACTOR SUM-1 IN THE SEA-URCHIN EMBRYO

被引:25
作者
VENUTI, JM
GAN, L
KOZLOWSKI, MT
KLEIN, WH
机构
[1] Department of Biochemistry and Molecular Biology, The University of Texas M.D. Anderson Cancer Center, Houston
关键词
SEA URCHIN EMBRYO; MYOGENESIS; MYOGENIC REGULATORY FACTOR;
D O I
10.1016/0925-4773(93)90051-X
中图分类号
Q [生物科学];
学科分类号
07 [理学]; 0710 [生物学]; 09 [农学];
摘要
During sea urchin development, esophageal muscle arises from secondary mesenchyme cells, descendants of the vegetal plate that delaminate from the coelomic epithelium at the end of gastrulation. In lithium-induced exogastrulae, where vegetal plate descendants evert rather than invaginate, myogenesis occurs normally, indicating that myocyte progenitors do not have to be near the future stomodeum for differentiation to occur. Vegetal plate descendants isolated along with the extracellular matrix at different times during gastrulation produce differentiated myocytes in culture as monitored by staining with a myosin heavy chain antibody. Vegetal isolates prepared at mid-gastrulation or later consistently produce differentiated myocytes whose form and position resembled their counterparts in the intact embryo, whereas vegetal isolates prepared a few hours earlier while capable of gut differentiation, as evidenced by the de novo synthesis of the endodermal surface marker Endo 1, did not produce differentiated myocytes. These results suggest that sometime after early gastrulation, a subset of secondary mesenchyme cells are competent to differentiate into muscle cells. RNase protection assays showed that the accumulation of sea urchin myogenic factor (SUM-1) mRNA is likely to be coincident with the earliest demonstrable commitment of myogenic precursors. Premature expression of SUM-1 coding sequences in mesenchyme blastulae resulted in the activation of muscle-specific enhancer elements, demonstrating that SUM-1 can function precociously in the early embryo. However, SUM-1 expressed in this manner did not activate the endogenous MHC gene, nor induce premature or ectopic production of muscle cells.
引用
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页码:3 / 14
页数:12
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