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首页> 外文期刊>Journal of bacteriology >Synthesis of Nucleic Acid and Protein in L Cells Infected with the Agent of Meningopneumonitis
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Synthesis of Nucleic Acid and Protein in L Cells Infected with the Agent of Meningopneumonitis

机译:脑膜炎性脑炎病原菌感染的L细胞中核酸和蛋白质的合成

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Schechter, Esther M. (The University of Chicago, Chicago, Ill.). Synthesis of nucleic acid and protein in L cells infected with the agent of meningopneumonitis. J. Bacteriol. >91:2069–2080. 1966.—Synthesis of deoxyribonucleic acid (DNA), 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 C14-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.
机译:Schechter,Esther M.(伊利诺伊州芝加哥大学,芝加哥大学)。感染脑膜肺炎的L细胞中核酸和蛋白质的合成。 J.细菌。 > 91: 2069-2080。 1966年。通过测量H 3 -的掺入率,比较了未感染的L细胞和感染脑膜炎的L细胞中脱氧核糖核酸(DNA),核糖核酸(RNA)和蛋白质的合成。在脑膜炎性脑炎生长周期的连续5小时内,胞苷和C 14 -赖氨酸分解为核,细胞质和药剂级分。脑膜肺炎DNA,RNA和蛋白质的合成首先在感染后15到20小时的标记期间内就很明显了,这是在药剂增殖开始后不久。试剂DNA,RNA和蛋白质的合成速率在短时间内呈对数增长,然后下降。然而,在整个脑膜肺炎生长周期的其余时间内,同位素掺入所有三个脑膜肺炎大分子的速率均维持在接近最大值的水平。这些数据最容易解释为二元裂变引起的脑膜肺炎病原体增殖。 L细胞对感染的反应是DNA和RNA合成速率降低以及细胞死亡速率提高。宿主蛋白的合成不受影响。感染的L细胞中核酸合成的抑制可能涉及宿主与寄生虫之间对核酸前体的竞争。 L细胞的不同亚系在其核酸合成机制被感染破坏的程度上差异很大。被感染的L细胞的细胞质中含有新合成的DNA和RNA,不能被认为是完整的脑膜肺炎细胞。该核酸可能是由于脆性细胞内形式的脑膜肺炎药的崩解引起的。

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