Nucleic Acid Metabolism in L Cells Infected with a Member of the Psittacosis Group

Schechter, Esther M.; Tribby, Ilse I. E.; Moulder, James W.

doi:10.1126/science.145.3634.819

Cited by 8 publications

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“…The titer of both intracellular and extracellular infections began to rise 10 hr after infection, and reached its peak at 40 hr. Growth of the meningopneumonitis agent in the cloned L cells differed from that in the uncloned L cells used previously (28) in that multiplication continued for about 10 hr longer, reached a terminal titer more than 1 log higher, and resulted in a slower rate of killing of the host cells.…”

Section: Growth Ofthe Meningopneumonitis Agent In Clonementioning

confidence: 66%

“…Table 6 compares the effect of meningopneumonitis infection on incorporation of labeled precursors into the RNA and DNA of the nuclei of uncloned and cloned L cells. The data on uncloned cells were obtained with a P32-orthophosphate label (28), but more recent use of a H3-cytidine label has yielded identical results. The effect of infection on nucleic acid synthesis in the two closely related L cell lines differed greatly.…”

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confidence: 91%

“…Thus, the profound inhibition of nuclear DNA synthesis and rapid death of the host cell, first found in the uncloned L cells by Schechter,Tribby,and Moulder (28), has turned out to be an extreme case of the effect of infection on the host cell. I. I. E. Tribby (personal communication) has isolated from the original L cell line received in this laboratory several clones differing in susceptibility to infection with the meningopneumonitis agent, generation time, and pattern of (28).…”

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confidence: 99%

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Synthesis of Nucleic Acid and Protein in L Cells Infected with the Agent of Meningopneumonitis

Schechter

1966

J Bacteriol

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ribonucleic acid (RNA), and protein in uninfected L cells and in L cells infected with the meningopneumonitis agent was compared by measuring rates of incorporation of H3-cytidine and C'4-lysine into nuclear, cytoplasmic, and agent fractions in successive 5-hr periods during the meningopneumonitis growth cycle. Synthesis of meningopneumonitis DNA, RNA, and protein was first clearly evident in the labeling period 15 to 20 hr after infection, soon after initiation of agent multiplication. The rates of synthesis of agent DNA, RNA, and protein increased logarithmically for a brief period and then declined. However, rates of isotope incorporation into all three meningopneumonitis macromolecules were sustained at near maximal values throughout the remainder of the meningopneumonitis growth cycle. These data are most readily interpreted in terms of multiplication of the meningopneumonitis agent by binary fission. The L cell response to infection was a decreased rate of DNA and RNA synthesis and an accelerated rate of cell death. Host protein synthesis was unaffected. The inhibition of nucleic acid synthesis in infected L cells probably involved competition between host and parasite for nucleic acid precursors. Different sublines of L cells varied greatly in the degree to which their nucleic acid-synthesizing mechanisms were damaged by infection. The cytoplasm of infected L cells contained newly synthesized DNA and RNA that could not be accounted for as intact meningopneumonitis cells. This nucleic acid probably arose from disintegration of the fragile intracellular forms of the meningopneumonitis agent. Microorganisms of the psittacosis group contain both deoxyribonucleic acid (DNA) and ribonucleic acid (RNA) (20, 31, 32), multiply by binary fission within membrane-bound vacuoles in the cytoplasm of their host cells (1, 10), and degrade glucose and pyruvate (37, 38) by enzymes that are qualitatively different from those of the corresponding enzymes of their host (22). These observations, together with many others, as reviewed by Moulder (21), indicate that the growth of a psittacosis agent within a host cell represents an intimate interaction of two organisms, each with its own set of macromolecule-synthesizing enzyme systems. Schechter, Tribby, and Moulder (28) used p32_ orthophosphate to follow the synthesis of nucleic acids in L cells infected with the agent of meningopneumonitis. Cell fractionation methods were employed to distinguish between synthesis of men-ingopneumonitis nucleic acids in the cytoplasm and host nucleic acids in the nucleus. This paper describes further investigations on macromolecule synthesis in meningopneumonitis-infected L cells in which nucleic acids were labeled with H3cytidine and proteins with C'4-lysine. Particular attention was paid to the course of synthesis of meningopneumonitis DNA, RNA, and protein and to the effect of meningopneumonitis multiplication on the synthesis of macromolecules by the L cell. MATERIALS AND METHODS Growth of L cells. Strain L cells (6, 27) obtained from H. M....

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Section: Growth Ofthe Meningopneumonitis Agent In Clonementioning

confidence: 66%

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confidence: 91%

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confidence: 99%

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Synthesis of Nucleic Acid and Protein in L Cells Infected with the Agent of Meningopneumonitis

Schechter

1966

J Bacteriol

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“…Members of the genus Chlamydia inhibit macromolecular synthesis in their host cells, particularly the synthesis of deoxyribonucleic acid (DNA); DNA synthesis is inhibited first and to a greater extent than synthesis of ribonucleic acid (RNA) and protein (42,43). The host genome is not degraded during the early stages of infection (25), so that loss of the template is not responsible for the inhibition.…”

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“…The host genome is not degraded during the early stages of infection (25), so that loss of the template is not responsible for the inhibition. Crocker and his associates (6) suggested that the inhibition of host DNA synthesis results from competition between the host cell and the parasite for cytoplasmic resources, whereas Schechter et al (43) and Schechter (42) postulated a specific inhibitory action on the part of the parasite.…”

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Inhibition of Thymidine Kinase Activity and Deoxyribonucleic Acid Synthesis in L Cells Infected with the Meningopneumonitis Agent

Lin

1968

J Bacteriol

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The activities of enzymes related to deoxyribonucleic acid (DNA) synthesis were studied in uninfected L cells and in L cells infected with Chlamydia psittaci (strain meningopneumonitis). The meningopneumonitis agent multiplied normally but failed to induce the synthesis of thymidine kinase in LM (TK-) cells which contain no thymidine kinase in the uninfected state. It was concluded that this microorganism has no thymidine kinase of its own and that it does not depend on the functioning of the host enzyme for synthesizing its DNA. Exposure of clone 5b L cells to the meningopneumonitis agent was followed by a decline in their thymidine kinase activity to nearly zero levels, whereas the levels of uridine kinase and thymidylate synthetase remained unchanged. Inhibition of thymidine kinase activity in L cells occurred soon after infection and required new protein synthesis by the meningopneumonitis agent. This inhibition occurred before inhibition of host DNA synthesis, but it was not an essential prelude to the latter inhibition. On the basis of this and previous investigations and in light of present knowledge of the mammalian cell cycle, it was postulated that the meningopneumonitis agent inhibits macromolecular synthesis in L cells by preventing the initiation of a new cell cycle.

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Biochemie der Regeneration

Bern

1969

Handbuch Der Allgemeinen Pathologie

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Nucleic Acid Metabolism in L Cells Infected with a Member of the Psittacosis Group

Cited by 8 publications

References 9 publications

Synthesis of Nucleic Acid and Protein in L Cells Infected with the Agent of Meningopneumonitis

Synthesis of Nucleic Acid and Protein in L Cells Infected with the Agent of Meningopneumonitis

Inhibition of Thymidine Kinase Activity and Deoxyribonucleic Acid Synthesis in L Cells Infected with the Meningopneumonitis Agent

Biochemie der Regeneration

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