Phagosome-lysosome fusion inhibited by algal symbionts of Hydra viridis.
Phagosome-lysosome fusion inhibited by algal symbionts of Hydra viridis.
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hydra viridis的藻类共生体抑制了吞噬体 - 溶酶体融合。
DOI：
10.1083/jcb.94.1.56
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发表时间：
1982-07
影响因子：
7.8
通讯作者：
Muscatine, L
中科院分区：
文献类型：
--
作者：
Hohman, T C;McNeil, P L;Muscatine, L
某些种类的小球藻生活在淡水刺胞动物水螅的消化细胞内。当引入水螅肠道时，这些共生藻类被消化细胞吞噬，但避免宿主消化，并以相对恒定的数量在宿主细胞内持续存在。相反，热杀死的共生体在吞噬作用后迅速降解。活的共生体似乎持续存在，因为宿主溶酶体未能与含有活的共生体的吞噬体融合。无论是酸性磷酸酶，也没有铁蛋白通过溶酶体到吞噬体含有活的共生体，而这些溶酶体标记物中发现50%的空泡含有热杀死的共生体1小时后吞噬。在吞噬作用之前用聚阳离子多肽处理共生藻类消除了藻类的持久性，并扰乱了这些藻类在体外控制光合产物释放的能力。类似地，由于长时间黑暗和3-（3，4-二氯苯基）-1，1-二甲基脲（DCMU）处理而导致的光合作用的抑制以及因此光合产物的释放也消除了持久性。共生藻类不仅保护宿主免受消化攻击，而且还选择性地在宿主细胞内运输，从吞噬作用的顶端位置移动到永久居住的基部位置。这个过程也被聚阳离子多肽、DCMU和黑暗破坏。因此，藻类的持久性和运输可能是一个功能的产品从生活，光合作用共生体的释放。长春碱治疗宿主动物阻断宿主细胞内的藻类的运动，但没有扰乱藻类的持久性：藻类的持久性和运输的藻类可能是由相同的信号，但它们不是相互依赖的过程。
Certain species of Chlorella live within the digestive cells of the fresh water cnidarian Hydra viridis. When introduced into the hydra gut, these symbiotic algae are phagocytized by digestive cells but avoid host digestion and persist at relatively constant numbers within host cells. In contrast, heat-killed symbionts are rapidly degraded after phagocytosis. Live symbionts appear to persist because host lysosomes fail to fuse with phagosomes containing live symbionts. Neither acid phosphatase nor ferritin was delivered via lysosomes into phagosomes containing live symbionts, whereas these lysosomal markers were found in 50% of the vacuoles containing heat-killed symbionts 1 h after phagocytosis. Treatment of symbiotic algae before phagocytosis with polycationic polypeptides abolishes algal persistence and perturbs the ability of these algae to control the release of photosynthate in vitro. Similarly, inhibition of photosynthesis and hence of the release of photosynthetic products as a result of prolonged darkness and 3-(3,4- dichlorophenyl)-1,1-dimethyl urea (DCMU) treatment also abolishes persistence. Symbiotic algae are not only protected from host digestive attack but are also selectively transported within host cells, moving from the apical site of phagocytosis to a basal position of permanent residence. This process too is disrupted by polycationic polypeptides, DCMU and darkness. Both algal persistence and transport may, therefore, be a function of the release of products from living, photosynthesizing symbionts. Vinblastine treatment of host animals blocked the movement of algae within host cells but did not perturb algal persistence: algal persistence and the transport of algae may be initiated by the same signal, but they are not interdependent processes.