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Julian Blow is a molecular biologist, Professor of Chromosome Maintenance, and also the Dean of the School of Life Sciences, University of Dundee, Scotland.
Blow graduated with a BSc in Medical Sciences from the University of Edinburgh in 1984. He then earned his PhD in DNA replication from the University of Cambridge in 1987. Following his PhD, in 1988, he worked as a postdoctoral research fellow at the University of Oxford. In 1991 he established his own laboratory at the ICRF Clare Hall Laboratories before being promoted to Senior Scientist in 1996. The following year he moved to the University of Dundee as a Principal Investigator. In 2012 he became Director of the Centre for Gene Regulation and Expression. In 2014, he was made Director of Research for the School of Life Sciences and then, in 2016, he was appointed Dean of the School of Life Sciences. [1]
Blow’s research focuses on understanding how chromosomes are replicated and the molecular biology behind how this is regulated. Primarily, his research investigates mechanisms that ensure the eukaryotic genome is precisely replicated during the eukaryotic cell division cycle so that no section of DNA is left un-replicated nor replicated more than once. An important part of this control involves replication origins being “licensed” early in the cell cycle to allow for replication in the upcoming S phase. [2] This process is important in advancing our understanding of cancer, as the unchecked proliferative capacity of cancers may arise from their having lost their ability to down-regulate the licensing system. [3] In addition to this, Blow has contributions extending to: a potential "constant" number for DNA replication robustness, [4] methods for examining extracts from the African clawed toad (Xenopus laevis) that support cell cycle progression [5] and a potential method for reprogramming somatic cells to a pluripotent state. [6] As of July 2020, he has written 148 papers and has 12,141 citations on these papers. [7]
Blow has received many awards, among these being the British Association for Cancer Research / Zeneca "Young Scientist of the Year" [17] (1996), Wellcome Trust Senior Investigator Award (2011) and in 2018, in collaboration with the Näthke lab, they were selected for a special collection of “outstanding” 2017/early 2018 Journal of Cell Biology articles focused on Stem Cells and Development. [18] He was elected a Member of the European Molecular Biology Organization in 1999, Research Fellow of the Lister Institute Jenner-Centenary (1991-1996), Fellow of the Royal Society of Edinburgh (FRSE) in 2002, and Fellow of the Academy of Medical Sciences (FMedSci) in 2012. [19]
This article incorporates text from this source, which is in the public domain : https://scholar.google.com/
The cell cycle, or cell-division cycle, is the sequential series of events that take place in a cell that causes it to divide into two daughter cells. These events include the growth of the cell, duplication of its DNA and some of its organelles, and subsequently the partitioning of its cytoplasm, chromosomes and other components into two daughter cells in a process called cell division.
A pre-replication complex (pre-RC) is a protein complex that forms at the origin of replication during the initiation step of DNA replication. Formation of the pre-RC is required for DNA replication to occur. Complete and faithful replication of the genome ensures that each daughter cell will carry the same genetic information as the parent cell. Accordingly, formation of the pre-RC is a very important part of the cell cycle.
G2 phase, Gap 2 phase, or Growth 2 phase, is the third subphase of interphase in the cell cycle directly preceding mitosis. It follows the successful completion of S phase, during which the cell’s DNA is replicated. G2 phase ends with the onset of prophase, the first phase of mitosis in which the cell’s chromatin condenses into chromosomes.
Endoreduplication is replication of the nuclear genome in the absence of mitosis, which leads to elevated nuclear gene content and polyploidy. Endoreduplication can be understood simply as a variant form of the mitotic cell cycle (G1-S-G2-M) in which mitosis is circumvented entirely, due to modulation of cyclin-dependent kinase (CDK) activity. Examples of endoreduplication characterised in arthropod, mammalian, and plant species suggest that it is a universal developmental mechanism responsible for the differentiation and morphogenesis of cell types that fulfill an array of biological functions. While endoreduplication is often limited to specific cell types in animals, it is considerably more widespread in plants, such that polyploidy can be detected in the majority of plant tissues. Polyploidy and aneuploidy are common phenomena in cancer cells. Given that oncogenesis and endoreduplication likely involve subversion of common cell cycle regulatory mechanisms, a thorough understanding of endoreduplication may provide important insights for cancer biology.
DNA replication licensing factor MCM6 is a protein that in humans is encoded by the MCM6 gene. MCM6 is one of the highly conserved mini-chromosome maintenance proteins (MCM) that are essential for the initiation of eukaryotic genome replication.
Cell cycle checkpoints are control mechanisms in the eukaryotic cell cycle which ensure its proper progression. Each checkpoint serves as a potential termination point along the cell cycle, during which the conditions of the cell are assessed, with progression through the various phases of the cell cycle occurring only when favorable conditions are met. There are many checkpoints in the cell cycle, but the three major ones are: the G1 checkpoint, also known as the Start or restriction checkpoint or Major Checkpoint; the G2/M checkpoint; and the metaphase-to-anaphase transition, also known as the spindle checkpoint. Progression through these checkpoints is largely determined by the activation of cyclin-dependent kinases by regulatory protein subunits called cyclins, different forms of which are produced at each stage of the cell cycle to control the specific events that occur therein.
Geminin, DNA replication inhibitor, also known as GMNN, is a protein in humans encoded by the GMNN gene. A nuclear protein present in most eukaryotes and highly conserved across species, numerous functions have been elucidated for geminin including roles in metazoan cell cycle, cellular proliferation, cell lineage commitment, and neural differentiation. One example of its function is the inhibition of Cdt1.
In molecular biology, origin recognition complex (ORC) is a multi-subunit DNA binding complex that binds in all eukaryotes and archaea in an ATP-dependent manner to origins of replication. The subunits of this complex are encoded by the ORC1, ORC2, ORC3, ORC4, ORC5 and ORC6 genes. ORC is a central component for eukaryotic DNA replication, and remains bound to chromatin at replication origins throughout the cell cycle.
Eukaryotic DNA replication is a conserved mechanism that restricts DNA replication to once per cell cycle. Eukaryotic DNA replication of chromosomal DNA is central for the duplication of a cell and is necessary for the maintenance of the eukaryotic genome.
The minichromosome maintenance protein complex (MCM) is a DNA helicase essential for genomic DNA replication. Eukaryotic MCM consists of six gene products, Mcm2–7, which form a heterohexamer. As a critical protein for cell division, MCM is also the target of various checkpoint pathways, such as the S-phase entry and S-phase arrest checkpoints. Both the loading and activation of MCM helicase are strictly regulated and are coupled to cell growth cycles. Deregulation of MCM function has been linked to genomic instability and a variety of carcinomas.
DNA replication licensing factor MCM2 is a protein that in humans is encoded by the MCM2 gene.
CDT1 is a protein that in humans is encoded by the CDT1 gene. It is a licensing factor that functions to limit DNA from replicating more than once per cell cycle.
Histone acetyltransferase KAT7 is an enzyme that in humans is encoded by the KAT7 gene. It specifically acetylates H4 histones at the lysine12 residue (H4K12) and is necessary for origin licensing and DNA replication. KAT7 associates with origins of replication during G1 phase of the cell cycle through complexing with CDT1. Geminin is thought to inhibit the acetyltransferase activity of KAT7 when KAT7 and CDT1 are complexed together.
The table conveys different eukaryotes, and Cyclin-CDK complexes needed for the species to initiate DNA replication, which occurs in the S-phases.
In cell biology, eukaryotes possess a regulatory system that ensures that DNA replication occurs only once per cell cycle.
The G2-M DNA damage checkpoint is an important cell cycle checkpoint in eukaryotic organisms that ensures that cells don't initiate mitosis until damaged or incompletely replicated DNA is sufficiently repaired. Cells with a defective G2-M checkpoint will undergo apoptosis or death after cell division if they enter the M phase before repairing their DNA. The defining biochemical feature of this checkpoint is the activation of M-phase cyclin-CDK complexes, which phosphorylate proteins that promote spindle assembly and bring the cell to metaphase.
DNA re-replication is an undesirable and possibly fatal occurrence in eukaryotic cells in which the genome is replicated more than once per cell cycle. Rereplication is believed to lead to genomic instability and has been implicated in the pathologies of a variety of human cancers. To prevent rereplication, eukaryotic cells have evolved multiple, overlapping mechanisms to inhibit chromosomal DNA from being partially or fully rereplicated in a given cell cycle. These control mechanisms rely on cyclin-dependent kinase (CDK) activity. DNA replication control mechanisms cooperate to prevent the relicensing of replication origins and to activate cell cycle and DNA damage checkpoints. DNA rereplication must be strictly regulated to ensure that genomic information is faithfully transmitted through successive generations.
Jonathon Noë Joseph Pines is Head of the Cancer Biology Division at the Institute of Cancer Research in London. He was formerly a senior group leader at the Gurdon Institute at the University of Cambridge.
Induced cell cycle arrest is the use of a chemical or genetic manipulation to artificially halt progression through the cell cycle. Cellular processes like genome duplication and cell division stop. It can be temporary or permanent. It is an artificial activation of naturally occurring cell cycle checkpoints, induced by exogenous stimuli controlled by an experimenter.
Xenopus egg extract is a lysate that is prepared by crushing the eggs of the African clawed frog Xenopus laevis. It offers a powerful cell-free system for studying various cell biological processes, including cell cycle progression, nuclear transport, DNA replication and chromosome segregation. It is also called Xenopus egg cell-free system or Xenopus egg cell-free extract.
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