POTASSIUM-DEPLETION AND HYPERTONIC MEDIUM REDUCE NON-COATED AND CLATHRIN-COATED PIT FORMATION, AS WELL AS ENDOCYTOSIS THROUGH THESE 2 GATES

POTASSIUM-DEPLETION AND HYPERTONIC MEDIUM REDUCE NON-COATED AND CLATHRIN-COATED PIT FORMATION, AS WELL AS ENDOCYTOSIS THROUGH THESE 2 GATES
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DOI:
10.1002/jcp.1041380311
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发表时间:
1989-03-01
影响因子:
5.6
通讯作者:
ORCI, L
ORCI, L
中科院分区:
生物学2区
文献类型:
--
作者:
CARPENTIER, JL;SAWANO, F;ORCI, L

文献摘要

被引文献

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细胞内钾消耗抑制受体介导的内吞过程发生通过网格蛋白包被坑。除了网格蛋白包被的凹坑路径外,没有典型网格蛋白包被的瓶状内陷最近被认为与受体介导的霍乱毒素内吞有关。这些凹坑被称为“非涂层”,以区别于典型的网格蛋白涂层凹坑。在本研究中,我们研究了“非包被”内陷是否像网格蛋白包被的凹穴一样对钾耗尽敏感,以及抑制受体介导的内吞作用的高渗介质是否也影响“非包被”内陷。我们发现1)缺钾和高渗介质都能减少细胞表面的“非包被”内陷;2)与缺钾相似,高渗培养基显著减少网格蛋白包埋坑的数量;3)这些变化伴随着霍乱毒素金内陷(通过“无涂层”内陷)以及α的内化(形态学测量)受到抑制。网格蛋白包覆凹坑吸收2-巨球蛋白金;4)此外,高渗培养基和缺钾都抑制了辣根过氧化物酶的摄取,过氧化物酶是一种液相内吞的标志。
Intracellular potassium depletion inhibits receptor-mediated endocytotic processes occurring through clathrin-coated pits. Besides the clathrin-coated pit route, flask-shaped invaginations that do not bear a typical clathrin coat have been recently implicated in receptor-mediated endocytosis of cholera toxin. These invaginations are called "non-coated" to distinguish them from the typical clathrin-coated pits. In the present study, we have investigated whether "noncoated" invaginations are sensitive, as are clathrin-coated pits, to potassium depletion and whether hypertonic medium, which inhibits receptor-mediated endocytosis, also affects "non-coated" invaginations. We found that 1) both potassium depletion and hypertonic medium reduce "non-coated" invaginations on the cell surface; 2) similar to potassium depletion, hypertonic medium markedly decreases the number of clathrin-coated pits; 3) these changes are accompanied by an inhibition of the internalization (measured morphologically) of cholera toxin-gold through "non-coated" invaginations, as well as of .alpha.2-macroglobulin-gold taken up by clathrin-coated pits; and 4) in addition, both the hypertonic medium and potassium depletion inhibit the uptake of horseradish peroxidase, a marker of fluid-phase endocytosis.