Evolutionary conservation of the CDK targets in eukaryotic DNA replication initiation

Zegerman, Philip

doi:10.1007/s00412-014-0500-y

Cited by 38 publications

(30 citation statements)

References 108 publications

(170 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Pre-RC assembly "licenses" the origin for potential activation in the subsequent S phase (Siddiqui et al 2013). As cells progress into S phase, the activity of cyclin-dependent kinases (CDKs) and Dbf4-dependent kinases (DDKs) stimulates the recruitment of proteins, including Cdc45 and GINS, to the origin that are required to form an active Cdc45/Mcm2-7/GINS (CMG) helicase complex to initiate DNA unwinding, facilitate formation of the replisome, and prime DNA synthesis (Zegerman 2015). The activation of replication origins during S phase is in part regulated by limiting concentrations of key activating factors (Mantiero et al 2011;Tanaka et al 2011;Collart et al 2013).…”

mentioning

confidence: 99%

DNA replication origins—where do we begin?

2016

View full text Add to dashboard Cite

For more than three decades, investigators have sought to identify the precise locations where DNA replication initiates in mammalian genomes. The development of molecular and biochemical approaches to identify start sites of DNA replication (origins) based on the presence of defining and characteristic replication intermediates at specific loci led to the identification of only a handful of mammalian replication origins. The limited number of identified origins prevented a comprehensive and exhaustive search for conserved genomic features that were capable of specifying origins of DNA replication. More recently, the adaptation of origin-mapping assays to genome-wide approaches has led to the identification of tens of thousands of replication origins throughout mammalian genomes, providing an unprecedented opportunity to identify both genetic and epigenetic features that define and regulate their distribution and utilization. Here we summarize recent advances in our understanding of how primary sequence, chromatin environment, and nuclear architecture contribute to the dynamic selection and activation of replication origins across diverse cell types and developmental stages.

show abstract

mentioning

confidence: 99%

DNA replication origins—where do we begin?

2016

View full text Add to dashboard Cite

show abstract

“…This step is also referred to as pre-replication complex (pre-RC) formation. In the subsequent S phase, DBF4-dependent kinase (DDK) and cyclin-dependent kinases (CDKs) trigger the recruitment of additional replication proteins to the origins, leading to the remodeling of inactive MCM2–7 complexes to active CMG (CDC45–MCM–GINS) replicative helicase complexes, and to the initiation of DNA synthesis at bidirectional replication forks [18,20,21]. According to a recent model, DNA polymerase α (Pol α) and primase complex initiate DNA synthesis, and Polδ and Polε continue lagging and leading DNA strand synthesis, respectively [22].…”

Section: Replication Origins For the Duplication Of Telomeric Dnamentioning

confidence: 99%

DNA Replication Origins and Fork Progression at Mammalian Telomeres

Higa¹,

Fujita²,

Yoshida³

2017

Genes

View full text Add to dashboard Cite

Telomeres are essential chromosomal regions that prevent critical shortening of linear chromosomes and genomic instability in eukaryotic cells. The bulk of telomeric DNA is replicated by semi-conservative DNA replication in the same way as the rest of the genome. However, recent findings revealed that replication of telomeric repeats is a potential cause of chromosomal instability, because DNA replication through telomeres is challenged by the repetitive telomeric sequences and specific structures that hamper the replication fork. In this review, we summarize current understanding of the mechanisms by which telomeres are faithfully and safely replicated in mammalian cells. Various telomere-associated proteins ensure efficient telomere replication at different steps, such as licensing of replication origins, passage of replication forks, proper fork restart after replication stress, and dissolution of post-replicative structures. In particular, shelterin proteins have central roles in the control of telomere replication. Through physical interactions, accessory proteins are recruited to maintain telomere integrity during DNA replication. Dormant replication origins and/or homology-directed repair may rescue inappropriate fork stalling or collapse that can cause defects in telomere structure and functions.

show abstract

“…Regardless, it is clear that the cooperation between the two kinases is essential for genome duplication. As the individual functions of CDK and DDK during replication initiation in proliferating cells have been the subject of excellent reviews (for example, see [3,4]), we will focus on aspects that are specific to the meiotic cycle.…”

Section: Genome Duplication In Mitosis and Meiosismentioning

confidence: 99%

“…The mechanisms that drive both mitosis and meiosis are tightly controlled, and this relies on the functions of two conserved types of serine-threonine kinases, the cyclin-dependent kinases (CDK) and the Dbf4-dependent kinase (DDK) (reviewed in [3,4]). In a mitotic cycle, CDK activity regulates cell cycle progression, with essential roles at its major transitions: G1/S (DNA replication) and G2/M (chromosome segregation) [5].…”

Section: Introductionmentioning

confidence: 99%

“…As a number of reviews have addressed the activities of these kinases in proliferating cells [3,4,23], we will pay special attention to the modification of their roles during sexual reproduction. First, we will present evidence for quantitative models for how CDK and DDK activities ensure the temporal progression of mitotic and meiotic events.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Roles of CDK and DDK in Genome Duplication and Maintenance: Meiotic Singularities

Gómez‐Escoda

2017

Genes

View full text Add to dashboard Cite

Cells reproduce using two types of divisions: mitosis, which generates two daughter cells each with the same genomic content as the mother cell, and meiosis, which reduces the number of chromosomes of the parent cell by half and gives rise to four gametes. The mechanisms that promote the proper progression of the mitotic and meiotic cycles are highly conserved and controlled. They require the activities of two types of serine-threonine kinases, the cyclin-dependent kinases (CDKs) and the Dbf4-dependent kinase (DDK). CDK and DDK are essential for genome duplication and maintenance in both mitotic and meiotic divisions. In this review, we aim to highlight how these kinases cooperate to orchestrate diverse processes during cellular reproduction, focusing on meiosis-specific adaptions of their regulation and functions in DNA metabolism.

show abstract

Evolutionary conservation of the CDK targets in eukaryotic DNA replication initiation

Cited by 38 publications

References 108 publications

DNA replication origins—where do we begin?

DNA replication origins—where do we begin?

DNA Replication Origins and Fork Progression at Mammalian Telomeres

Roles of CDK and DDK in Genome Duplication and Maintenance: Meiotic Singularities

Contact Info

Product

Resources

About