SUBCELLULAR DIFFERENTIATION ARRESTED IN ARTEMIA EMBRYOS UNDER ANOXIA - EVIDENCE SUPPORTING A REGULATORY ROLE FOR INTRACELLULAR PH
SUBCELLULAR DIFFERENTIATION ARRESTED IN ARTEMIA EMBRYOS UNDER ANOXIA - EVIDENCE SUPPORTING A REGULATORY ROLE FOR INTRACELLULAR PH
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DOI：
10.1002/jez.1402530308
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发表时间：
1990-03-01
影响因子：
--
通讯作者：
HAND, SC
中科院分区：
文献类型：
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作者：
HOFMANN, GE;HAND, SC
以前的工作已经清楚地证明，细胞内pH值（pHi）介导的代谢停滞在卤虫胚胎厌氧休眠。这项研究提供的证据表明，亚细胞分化过程中出现前的发展（PED）是由pHi的过渡，也报告了第一个详细的超微结构描述PED在这些胚胎。线粒体成熟、糖原场的形成和卵黄血小板结构的改变在有氧发育过程中是明显的（胚胎pHi ≥ 100）。7.9）。线粒体的成熟涉及两个群体的线粒体是空间分离的胚胎细胞中的细胞质和其他位于卵黄血小板内。后一种人群的鉴定部分基于DNA的组织化学染色。虽然这两种线粒体群体在PED期间结构成熟，但酶证据表明蛋黄内血小板群体没有功能。当胚胎在缺氧条件下（pHi ≤ 0.05）孵育时，在有氧发育过程中观察到的亚细胞形态发生事件被阻断。6.8)或需氧性酸中毒（通过人为将CO2升高至60%诱导的静止状态; pHi = 6.8）。暴露于这些实验处理中的任一种12小时的胚胎细胞与未分化的0小时胚胎的细胞基本相同。类似地，细胞色素c氧化酶比活性增加230%，超过12小时的有氧发展，但这种个体发育的增加被逮捕12小时的缺氧或有氧酸中毒。将酸化的胚返回到对照有氧条件下，导致酶增殖以与有氧对照值相同的速率恢复。当CO2浓度仅为11%时，在有氧酸中毒条件下，细胞色素c氧化酶活性的增殖也会受到类似的抑制。最后，碱化的pH值的胚胎缺氧条件下，通过添加氨的培养基中的细胞色素c氧化酶的水平增加37%，相对于那些缺氧条件下测量的结果。这些数据支持pH值依赖性调节的卤虫胚胎发育。
Previous work has clearly documented that intracellular pH (pHi) mediates metabolic arrest during anaerobic dormancy in Artemia embryo. This study provides evidence that subcellular differentiation during preemergence development (PED) is regulated by transitions in pHi and also reports the first detailed ultrastructural description of PED in these embryos. Mitochondrial maturation, elaboration of glycogen fields, and alteration in yolk platelet structure are clearly evident during aerobic development (embryo pHi .gtoreq. 7.9). Mitochondrial maturation involves two populations of mitochondria that are spatially segregated in embryonic cells-one in the cytoplasm and the other located inside of yolk platelets. Identification of the latter population is based in part on histochemical staining of DNA. While both mitochondrial populations mature structurally during PED, enzymatic evidence indicates that the intra-yolk platelet population is not functional. Subcellular morphogenetic events observed during aerobic development are blocked when embryos are incubated under anoxia (pHi .ltoreq. 6.8) or aerobic acidosis (a quiescent state induced by artificially elevating CO2 to 60%; pHi = 6.8). Embryonic cells exposed to either of these experimental treatments for 12 h are essentially identical to cells of the undifferentiated, hour 0 embryo. Analogously, cytochrome c oxidase specific activity increases 230% over 12 h of aerobic development, but this ontogenetic increase is arrested by 12 h of anoxia or aerobic acidosis. Returning the acidified embryos to control aerobic conditions causes enzyme proliferation to resume at rates identical to aerobic, control values. A similar arrest of the proliferation to cytochrome c oxidase activity is seen under aerobic acidosis when CO2 is present at only 11%. Finally, alkalinizing the pHi of embryos under anoxia by adding ammonia to the medium results in a 37% increase in cytochrome c oxidase levels relative to those measured under anoxia. These data support pHi-dependent regulation of development in preemergence Artemia embryos.