DNA Replication: An Annotated Bibliography 1.B

1.Baker, T. A. Replication arrest. Cell. 80:521-524; 1995, February 24.

This brief article reviews different ways of halting DNA replication. DNA synthesis occurs at chromosomal replication forks. The enzymes involved typically replicate DNA at a rate of about 1,000 base pairs per second. Thus, there must be ways of stopping the process. Replication termination systems generally consist of protein-DNA complexes. Various termination proteins make contact with the DNA at specific sites. These complexes specifically inhibit DNA helicases (i.e., the proteins responsible for replication fork movement). Such termination machinery ultimately represents a mechanism by which DNA replication can be controlled after initiation.

2.Blow, J. J. Preventing re-replication of DNA in a single cell cycle: Evidence for a replication licensing factor. The Journal of Cell Biology. 122:993-1002; 1993, September.

This 10-page paper describes an investigation into a possible DNA replication licensing factor. It notes that Xenopus egg extracts which have been treated with the protein kinase inhibitor, 6-dimethylaminopurine, do not exhibit DNA replication initiation. Moreover, a specific protein thought to be a replication factor is rendered nonfunctional by the treatments. This factor normally becomes rapidly activated on exit from metaphase. Then, before the nuclear envelope has been completely formed (i.e., early G1), it may mod

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airpin molecules. The sequence of this arrangement is governed by the nucleotide sequence of an assembler strand. This code strand could presumably consist of DNA. Each of the hairpin molecules carries an amino acid at the bottom of one of its legs; further, the proximity of the different amino acids facilitates their eventual linkage. The author postulates that because of copying errors such sequences would have only temporary value. However, with the formation of beneficial oligopeptides, replication would eventually be improved. 6.Kunkel, T. A.; Roberts, J. D.; Thomas, D. C.; Nguyen, D. C. The "fine structure" of DNA replication fidelity. In: Bohr, V. A.; Wasserman, K.; Kraemer, K. H., eds. DNA Repair Mechanisms. Copenhagen, Denmark: Munksgaard; 1992; pp. 189-199. These 11 pages actually represent a subsection in a book on DNA repair. They begin by reviewing the overall processes involved in DNA replication. Various replication error pathways are also mentioned. The most thoroughly studied such pathway results in a substitution error. This occurs when noncomplementary nucleotides are matched. In addition, another common error pathway involves template-primer misalignment. This can cause deletion, addition,
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Some common words found in the essay are:
Society Microbiology, Cell Biology, Biophysica Acta, Annotated Bibliography, Harvey Lectures, FEBS Letters, Denmark Munksgaard, Francis Crick, Damaged DNA, August Naegeli, dna replication, replication licensing, dna repair, licensing factor, replication licensing factor, escherichia coli, mismatch repair, dna synthesis, polymerase iii, cell cycle, dna polymerase, dna polymerase iii, dna replication fidelity, replication licensing factors, dna repair mechanisms,
Approximate Word count = 1423
Approximate Pages = 6 (250 words per page)