Ramachandran R K, Seid C A, Lee H, Tomlinson C R
Department of Biology, University of Houston, TX 77204-5513.
Mech Dev. 1993 Nov;44(1):33-40. doi: 10.1016/0925-4773(93)90014-o.
Development and LpS1 transcription in Lytechinus embryos are arrested at the mesenchyme blastula stage when collagen deposition is inhibited by the lathrytic agent beta-aminopropionitrile (BAPN) or by proline analogs. We found that human recombinant platelet derived growth factor-BB (PDGF-BB) and transforming growth factor-alpha (TGF-alpha) synergistically rescue collagen disrupted/developmentally arrested L. pictus and L. variegatus embryos so that development and RNA accumulation of LpS1 proceed. In addition, nonspecific antagonists of PDGF block gastrulation and LpS1 RNA accumulation. The embryos recover and LpS1 RNA accumulation resumes when the antagonists are removed. These data suggest that a growth factor mediated pathway, associated with the ECM, is required for sea urchin gastrulation, spiculogenesis, and LpS1 gene activation.
当溶菌剂β-氨基丙腈(BAPN)或脯氨酸类似物抑制胶原蛋白沉积时,海胆胚胎中的发育和LpS1转录在间充质囊胚阶段停滞。我们发现,人重组血小板衍生生长因子-BB(PDGF-BB)和转化生长因子-α(TGF-α)协同拯救胶原蛋白破坏/发育停滞的花斑海胆和杂色海胆胚胎,从而使LpS1的发育和RNA积累得以继续。此外,PDGF的非特异性拮抗剂会阻断原肠胚形成和LpS1 RNA积累。去除拮抗剂后,胚胎恢复,LpS1 RNA积累恢复。这些数据表明,与细胞外基质相关的生长因子介导途径是海胆原肠胚形成、骨针形成和LpS1基因激活所必需的。