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Studies of Mechanisms Involved in Coordinating Cell Growth and Genomic Duplication

Amy Louise Svitil

出版	San Diego State University, University of California, San Diego, 1993--Biology., 1993
URL	http://books.google.com.hk/books?id=jzSzd_3kp_gC&hl=&source=gbs_api

註釋

In the bacterium, Escherichia coli, the processes controlling the conversion of a mother cell into daughter cells, cell growth, DNA replication, and cell division, are highly coordinated; more than 99.97% of daughter cells successfully receive DNA. The rate of initiation at the origin of replication, oriC, controls the rate of replication in prokaryotic cells. Therefore, the coupling of replication to cell growth requires that the frequency of initiation from oriC be a function of growth rate. One method of controlling interinitiation time may be the state of methylation of GATC sites in or near oriC and in the dnaA promoter region. We examined the effect of removal of a protein methylation blocking factor, which has previously been shown to delay methylation of GATC sites, and found no effect on timing of initiation. Other elements, DnaA concentration and transcription from promoters adjacent to oriC, which may also be necessary for correct timing of DNA replication, are under stringent control. During amino acid starvation, the product of the relA gene, ppGpp synthetase I, synthesizes guanosine tetraphosphate (ppGpp), and concomitant with the increase in ppGpp, various physiological reactions occur in what is known as the stringent response. The nucleotide ppGpp is found in concentrations inversely proportional to growth rate, suggesting ppGpp may act as an effector molecule coupling growth rate with various cellular processes including initiation of DNA replication. We determined that relA overexpression, and thus ppGpp overexpression, causes a drastic inhibition of protein synthesis, which inhibits initiation of replication, and inhibits the accumulation of the carbon source glycerol into the cell. Cells that exhibit an abnormal number of chromosomes following completion of ongoing rounds of DNA replication have been believed to result from incorrect timing of initiation in the cell cycle. Cells deficient in RecA protein have this phenotype, but initiate DNA replication at the proper time in the cell cycle. We discovered that RecA protein is not required for correct timing of initiation of DNA replication, but instead is necessary for equal partitioning of the chromosome into daughter cells.