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Fluid phase endocytosis in wild-type...

Wang, Ru Hung.

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Fluid phase endocytosis in wild-type and mutant Chinese hamster ovary cells.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Fluid phase endocytosis in wild-type and mutant Chinese hamster ovary cells./
作者:	Wang, Ru Hung.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 1990,
面頁冊數:	153 p.
附註:	Source: Dissertation Abstracts International, Volume: 51-11, Section: B, page: 5170.
Contained By:	Dissertation Abstracts International51-11B.
標題:	Molecular biology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9111464

Fluid phase endocytosis in wild-type and mutant Chinese hamster ovary cells.
Wang, Ru Hung.

Fluid phase endocytosis in wild-type and mutant Chinese hamster ovary cells. - Ann Arbor : ProQuest Dissertations & Theses, 1990 - 153 p.

Source: Dissertation Abstracts International, Volume: 51-11, Section: B, page: 5170.

Thesis (Ph.D.)--The University of Texas at Dallas, 1990.

Several aspects of fluid-phase endocytosis were studied in wild-type and in mutant Chinese hamster ovary (CHO) cells. These include: (1) the fate of endocytosed fluid in wild-type CHO cells; (2) the effects of impaired secretory function on fluid-phase endocytosis in mutant V.24.1 cells; and (3) the isolation of mutants defective in fluid-phase endocytosis.Subjects--Topical Terms:

517296
Molecular biology.

Fluid phase endocytosis in wild-type and mutant Chinese hamster ovary cells.
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100 1 $a Wang, Ru Hung. $3 3427621
245 1 0 $a Fluid phase endocytosis in wild-type and mutant Chinese hamster ovary cells.
260 1 $a Ann Arbor : $b ProQuest Dissertations & Theses, $c 1990
300 $a 153 p.
500 $a Source: Dissertation Abstracts International, Volume: 51-11, Section: B, page: 5170.
500 $a Supervisor: Rockford K. Draper.
502 $a Thesis (Ph.D.)--The University of Texas at Dallas, 1990.
520 $a Several aspects of fluid-phase endocytosis were studied in wild-type and in mutant Chinese hamster ovary (CHO) cells. These include: (1) the fate of endocytosed fluid in wild-type CHO cells; (2) the effects of impaired secretory function on fluid-phase endocytosis in mutant V.24.1 cells; and (3) the isolation of mutants defective in fluid-phase endocytosis.
520 $a Three populations of vesicles which are involved in fluid-phase endocytosis, namely endosomes, buoyant lysosomes, and dense lysosomes, were separated based on differences in their buoyant densities by centrifuging postnuclear supernatants with 17% and 27% Percoll. Results of pulse-chase experiments using horseradish peroxidase (HRP) and FITC-dextran as fluid markers revealed that endocytosed material appears first in endosomes en route to buoyant and dense lysosomes. Low temperature and conditions that elevate vesicular pH inhibited the accumulation of fluid in dense, but not buoyant lysosomes. In addition, several properties of the two lysosomal populations also indicated that buoyant lysosomes are distinct from dense lysosomes.
520 $a Mutant V.24.1 defines the End4 complementation group of temperature-sensitive CHO cell mutants selected for resistance to protein toxins. Further characterization of this mutant revealed a severe defect in the secretory pathway: (1) Secretion of total soluble proteins into the medium was strongly inhibited. (2) The hemagglutinin of influenza virus failed to reach the plasma membrane and remained sensitive to endoglycosidase H digestion, indicating that it had not reached the medial Golgi compartment. (3) Transferrin receptors were also retained in the endoglycosidase H sensitive form. The effect of the lesion on fluid-phase endocytosis was investigated by measuring the accumulation and recycling of horseradish peroxidase at the restrictive temperature. Accumulation was inhibited by 50% while recycling was nearly normal, implying that the rate of fluid-phase endocytosis was reduced. Moreover, the delivery of endocytosed material to lysosomes was partially impaired. However, the clathrin-coated pit pathway of endocytosis was not affected, as indicated by a normal transferrin cycle (Colbaugh et al., 1989, J. Cell Biol. 108:2211-2219). Thus, the secretory lesion correlates with reduced fluid-phase endocytosis without impairing the clathrin-dependent pathway of receptor-mediated endocytosis.
520 $a A novel method was developed for isolating mutants defective in fluid-phase endocytosis based on the lethal effects of diaminobenzidine polymerization catalyzed by HRP taken up by fluid-phase endocytosis. A mutant defective in fluid-phase endocytosis, termed HRP-1, was isolated using the new technique. At the restrictive temperature, the rate of fluid-phase endocytosis was reduced as much as 70% in HRP-1 cells at the restrictive temperature. In addition, this mutant acquired resistance to diphtheria toxin and modeccin at high temperature, consistent with a defect in the endocytic pathway.
590 $a School code: 0382.
650 4 $a Molecular biology. $3 517296
650 4 $a Cellular biology. $3 3172791
690 $a 0307
690 $a 0379
710 2 $a The University of Texas at Dallas. $3 1018411
773 0 $t Dissertation Abstracts International $g 51-11B.
790 $a 0382
791 $a Ph.D.
792 $a 1990
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9111464