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      The Inherent Asymmetry of DNA Replication

      1 , 1 , 1
      Annual Review of Cell and Developmental Biology
      Annual Reviews

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          Abstract

          <p class="first" id="P1">Our understanding of the structure of DNA has helped pave the way for tremendous advancements in understanding the mechanisms of DNA replication. Semiconservative DNA replication has provided an elegant solution to the fundamental problem of how life is able to proliferate in a way that allows cells, organisms, and populations to survive and replicate many times over. Somewhat lost, however, in our admiration for this elegant mechanism is an appreciation for the asymmetries that inevitably occur in the process of DNA replication. As we will discuss in this review, these asymmetries arise as a consequence of the structure of the DNA molecule and the enzymatic mechanism DNA synthesis. Furthermore, increasing evidence suggests that these asymmetries are utilized as mechanisms to drive diverse processes ranging from adaptation and evolution, to cell fate decisions related to patterning and development. </p>

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          Most cited references127

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          Transcription factors: from enhancer binding to developmental control.

          Developmental progression is driven by specific spatiotemporal domains of gene expression, which give rise to stereotypically patterned embryos even in the presence of environmental and genetic variation. Views of how transcription factors regulate gene expression are changing owing to recent genome-wide studies of transcription factor binding and RNA expression. Such studies reveal patterns that, at first glance, seem to contrast with the robustness of the developmental processes they encode. Here, we review our current knowledge of transcription factor function from genomic and genetic studies and discuss how different strategies, including extensive cooperative regulation (both direct and indirect), progressive priming of regulatory elements, and the integration of activities from multiple enhancers, confer specificity and robustness to transcriptional regulation during development.
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            PCNA, the maestro of the replication fork.

            Inheritance requires genome duplication, reproduction of chromatin and its epigenetic information, mechanisms to ensure genome integrity, and faithful transmission of the information to progeny. Proliferating cell nuclear antigen (PCNA)-a cofactor of DNA polymerases that encircles DNA-orchestrates several of these functions by recruiting crucial players to the replication fork. Remarkably, many factors that are involved in replication-linked processes interact with a particular face of PCNA and through the same interaction domain, indicating that these interactions do not occur simultaneously during replication. Switching of PCNA partners may be triggered by affinity-driven competition, phosphorylation, proteolysis, and modification of PCNA by ubiquitin and SUMO.
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              Cohesin: its roles and mechanisms.

              The cohesin complex is a major constituent of interphase and mitotic chromosomes. Apart from its role in mediating sister chromatid cohesion, it is also important for DNA double-strand-break repair and transcriptional control. The functions of cohesin are regulated by phosphorylation, acetylation, ATP hydrolysis, and site-specific proteolysis. Recent evidence suggests that cohesin acts as a novel topological device that traps chromosomal DNA within a large tripartite ring formed by its core subunits.
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                Author and article information

                Journal
                Annual Review of Cell and Developmental Biology
                Annu. Rev. Cell Dev. Biol.
                Annual Reviews
                1081-0706
                1530-8995
                October 06 2017
                October 06 2017
                : 33
                : 1
                : 291-318
                Affiliations
                [1 ]Department of Biology, The Johns Hopkins University, Baltimore, Maryland 21218;, ,
                Article
                10.1146/annurev-cellbio-100616-060447
                5695668
                28800257
                f4906c10-e4c2-4529-b2f6-127af4a8937c
                © 2017

                http://www.annualreviews.org/licenses/tdm

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