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首页> 外文期刊>Development >Phosphatidylserine receptor is required for the engulfment of dead apoptotic cells and for normal embryonic development in zebrafish.
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Phosphatidylserine receptor is required for the engulfment of dead apoptotic cells and for normal embryonic development in zebrafish.

机译:磷脂酰丝氨酸受体是死亡的凋亡细胞吞噬和斑马鱼正常胚胎发育所必需的。

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摘要

During development, the role of the phosphatidylserine receptor (PSR) in the removal of apoptotic cells that have died is poorly understood. We have investigated this role of PSR in developing zebrafish. Programmed cell death began during the shield stage, with dead cells being engulfed by a neighboring cell that showed a normal-looking nucleus and the nuclear condensation multi-micronuclei of an apoptotic cell. The zebrafish PSR engulfing receptor was cloned (zfpsr), and its nucleotide sequence was compared with corresponding sequences in Drosophila melanogaster (76% identity), human (74%), mouse (72%) and Caenorhabditis elegans (60%). The PSR receptor contained a jmjC domain (residues 143-206) that is a member of the cupin metalloenzyme superfamily, but in this case serves an as yet unknown function(s). psr knockdown by a PSR morpholino oligonucleotide led to accumulation of a large number of dead apoptotic cells in whole early embryo. These cells interfered with embryonic cell migration. In addition, normal development of the somite, brain, heart and notochord was sequentially disrupted up to 24 hours post-fertilization. Development could be rescued in defective embryos by injecting psr mRNA. These results are consistent with a PSR-dependent system in zebrafish embryos that engulfs apoptotic cells mediated by PSR-phagocytes during development, with the system assuming an important role in the normal development of tissues such as the brain, heart, notochord and somite.
机译:在开发过程中,人们对磷脂酰丝氨酸受体(PSR)在去除已死亡的凋亡细胞中的作用了解甚少。我们已经研究了PSR在开发斑马鱼中的作用。程序性细胞死亡始于屏蔽阶段,死细胞被邻近细胞吞噬,后者显示出正常外观的核和凋亡细胞的核浓缩多微核。克隆了斑马鱼PSR吞噬受体(zfpsr),并将其核苷酸序列与果蝇(76%相同),人(74%),小鼠(72%)和秀丽隐杆线虫(60%)中的相应序列进行了比较。 PSR受体包含一个jmjC域(残基143-206),该域是铜杯金属酶超家族的成员,但在这种情况下起着未知功能的作用。 PSR吗啉代寡核苷酸的psr敲低导致整个早期胚胎中大量死亡的凋亡细胞积聚。这些细胞干扰了胚胎细胞的迁移。此外,受精后长达24小时,豆sequentially,大脑,心脏和脊索的正常发育被依次破坏。可以通过注射psr mRNA在有缺陷的胚胎中挽救发育。这些结果与斑马鱼胚胎中依赖PSR的系统一致,该系统吞噬了在发育过程中由PSR吞噬细胞介导的凋亡细胞,并且该系统在诸如大脑,心脏,脊索和体节等组织的正常发育中起着重要作用。

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