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A Study of Chinese Hamster Cell Mutants with Defects in Oxidative Energy Metabolism.

Record Type:	Language materials, manuscript : Monograph/item
Title/Author:	A Study of Chinese Hamster Cell Mutants with Defects in Oxidative Energy Metabolism./
Author:	Soderberg, Kathy Lynne.
Description:	1 online resource (192 pages)
Notes:	Source: Dissertations Abstracts International, Volume: 41-07, Section: B.
Contained By:	Dissertations Abstracts International41-07B.
Subject:	Biology. -
Online resource:	click for full text (PQDT)
ISBN:	9798662329300

A Study of Chinese Hamster Cell Mutants with Defects in Oxidative Energy Metabolism.
Soderberg, Kathy Lynne.

A Study of Chinese Hamster Cell Mutants with Defects in Oxidative Energy Metabolism. - 1 online resource (192 pages)

Source: Dissertations Abstracts International, Volume: 41-07, Section: B.

Thesis (Ph.D.)--University of California, San Diego, 1980.

Includes bibliographical references

This thesis describes the isolation and characterization of mutant cells of Chinese hamster cell lines which are defective in proteins of the Krebs cycle or electron transport chain. Based on the known nutritional requirements of one such mutant, fortuitously isolated, a selection scheme was devised which enriched for the survival of mutants in a mixed culture. Using this procedure, a large number of mutants were isolated from mutagenized populations of the cell lines CCL16 and V79. A representative fraction of the newly isolated mutants were tested and most proved unable to respire while all lacked significant Krebs cycle activity. Thirty-five of the mutants were analyzed pair-wise in cell-cell fusions to determine whether the defects of individual diploid cells could be complemented in tetraploid hybrids. It was found that the mutations under study were all recessive and defined seven complementation groups. One mutant failed to complement two separate complementation groups and may be defective in two genes affecting complex I of the electron transport chain. Biochemical characterization of another mutant, CCL16-B9, has shown that the cell lacks activity for the Krebs cycle enzyme succinate dehydrogenase. Studies with antibody directed against the large subunit of this enzyme demonstrated that the mutant has retained cross-reacting material within its mitochondria, evidence that would indicate a missense mutation in a structural gene for this enzyme. The mutant was used in interspecies hybridization experiments to map the normal locus of this defective gene to the human genome. It was found that the presence of human chromosome 1 in hybrids resulted in complementation of the defect of CCL16-B9 and that loss of this chromosome correlated with the hybrids' return to respiration-defective character. We therefore believe that human chromosome 1 contains a locus for a structural gene of succinate dehydrogenase.

Electronic reproduction.
Ann Arbor, Mich. :
ProQuest,
2024

Mode of access: World Wide Web

ISBN: 9798662329300Subjects--Topical Terms:

599573
Biology.
Index Terms--Genre/Form:

554714
Electronic books.

A Study of Chinese Hamster Cell Mutants with Defects in Oxidative Energy Metabolism.
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245 1 2 $a A Study of Chinese Hamster Cell Mutants with Defects in Oxidative Energy Metabolism.
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300 $a 1 online resource (192 pages)
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500 $a Source: Dissertations Abstracts International, Volume: 41-07, Section: B.
500 $a Publisher info.: Dissertation/Thesis.
502 $a Thesis (Ph.D.)--University of California, San Diego, 1980.
504 $a Includes bibliographical references
520 $a This thesis describes the isolation and characterization of mutant cells of Chinese hamster cell lines which are defective in proteins of the Krebs cycle or electron transport chain. Based on the known nutritional requirements of one such mutant, fortuitously isolated, a selection scheme was devised which enriched for the survival of mutants in a mixed culture. Using this procedure, a large number of mutants were isolated from mutagenized populations of the cell lines CCL16 and V79. A representative fraction of the newly isolated mutants were tested and most proved unable to respire while all lacked significant Krebs cycle activity. Thirty-five of the mutants were analyzed pair-wise in cell-cell fusions to determine whether the defects of individual diploid cells could be complemented in tetraploid hybrids. It was found that the mutations under study were all recessive and defined seven complementation groups. One mutant failed to complement two separate complementation groups and may be defective in two genes affecting complex I of the electron transport chain. Biochemical characterization of another mutant, CCL16-B9, has shown that the cell lacks activity for the Krebs cycle enzyme succinate dehydrogenase. Studies with antibody directed against the large subunit of this enzyme demonstrated that the mutant has retained cross-reacting material within its mitochondria, evidence that would indicate a missense mutation in a structural gene for this enzyme. The mutant was used in interspecies hybridization experiments to map the normal locus of this defective gene to the human genome. It was found that the presence of human chromosome 1 in hybrids resulted in complementation of the defect of CCL16-B9 and that loss of this chromosome correlated with the hybrids' return to respiration-defective character. We therefore believe that human chromosome 1 contains a locus for a structural gene of succinate dehydrogenase.
533 $a Electronic reproduction. $b Ann Arbor, Mich. : $c ProQuest, $d 2024
538 $a Mode of access: World Wide Web
650 4 $a Biology. $3 599573
655 7 $a Electronic books. $2 local $3 554714
690 $a 0306
710 2 $a ProQuest Information and Learning Co. $3 1178819
710 2 $a University of California, San Diego. $3 1187935
773 0 $t Dissertations Abstracts International $g 41-07B.
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=8018798 $z click for full text (PQDT)