- 1 Cell Cycle
- 2 2015
- 3 2014
- 4 2013
- 5 2012
- 6 2011
- 7 2008
- 8 Cell Press Videos
<pubmed limit=5>Cell Cycle</pubmed> <pubmed limit=5>Cell Cycle Regulation</pubmed>
Intrinsic and extrinsic mechanisms regulating satellite cell function
Development. 2015 May 1;142(9):1572-1581. Review
Dumont NA1, Wang YX2, Rudnicki MA3.
Abstract Muscle stem cells, termed satellite cells, are crucial for skeletal muscle growth and regeneration. In healthy adult muscle, satellite cells are quiescent but poised for activation. During muscle regeneration, activated satellite cells transiently re-enter the cell cycle to proliferate and subsequently exit the cell cycle to differentiate or self-renew. Recent studies have demonstrated that satellite cells are heterogeneous and that subpopulations of satellite stem cells are able to perform asymmetric divisions to generate myogenic progenitors or symmetric divisions to expand the satellite cell pool. Thus, a complex balance between extrinsic cues and intrinsic regulatory mechanisms is needed to tightly control satellite cell cycle progression and cell fate determination. Defects in satellite cell regulation or in their niche, as observed in degenerative conditions such as aging, can impair muscle regeneration. Here, we review recent discoveries of the intrinsic and extrinsic factors that regulate satellite cell behaviour in regenerating and degenerating muscles. © 2015. Published by The Company of Biologists Ltd. KEYWORDS: Aging; Asymmetric division; Cell cycle regulation; Muscle stem cell; Myogenesis; Quiescence; Regeneration; Satellite cell; Self-renewal; Skeletal muscle PMID 25922523
Connecting the nucleolus to the cell cycle and human disease
FASEB J. 2014 Apr 30. [Epub ahead of print]
Tsai RY1, Pederson T. Author information
Abstract Long known as the center of ribosome synthesis, the nucleolus is connected to cell cycle regulation in more subtle ways. One is a surveillance system that reacts promptly when rRNA synthesis or processing is impaired, halting cell cycle progression. Conversely, the nucleolus also acts as a first-responder to growth-related stress signals. Here we review emerging concepts on how these "infraribosomal" links between the nucleolus and cell cycle progression operate in both forward and reverse gears. We offer perspectives on how new cancer therapeutic designs that target this infraribosomal mode of cell growth control may shape future clinical progress.-Tsai, R. Y. L., Pederson, T. Connecting the nucleolus to the cell cycle and human disease. KEYWORDS: cancer, cell cycle, ribosome synthesis
DNA methylation dynamics during the mammalian life cycle
Philos Trans R Soc Lond B Biol Sci. 2013 Jan 5;368(1609):20110328. doi: 10.1098/rstb.2011.0328.
Hackett JA, Surani MA. Source Wellcome Trust/Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, UK.
DNA methylation is dynamically remodelled during the mammalian life cycle through distinct phases of reprogramming and de novo methylation. These events enable the acquisition of cellular potential followed by the maintenance of lineage-restricted cell identity, respectively, a process that defines the life cycle through successive generations. DNA methylation contributes to the epigenetic regulation of many key developmental processes including genomic imprinting, X-inactivation, genome stability and gene regulation. Emerging sequencing technologies have led to recent insights into the dynamic distribution of DNA methylation during development and the role of this epigenetic mark within distinct genomic contexts, such as at promoters, exons or imprinted control regions. Additionally, there is a better understanding of the mechanistic basis of DNA demethylation during epigenetic reprogramming in primordial germ cells and during pre-implantation development. Here, we discuss our current understanding of the developmental roles and dynamics of this key epigenetic system.
The University has a system for automated recording of lectures called Lectopia. Lectopia requires login using your student number and unipass. I will be adding the link to each iLecture Audio following the Lecture. Due to the automated recording method, most lectures begin 4-5 minutes into MP3 recordings and occasionally stop before the end of the lecture.
Lecture 14 Audio Lecture Date: 2013-05-07 Lecture Time: 15:00 Venue: WW LG02 Speaker: Dr Mark Hill
Phosphorylation network dynamics in the control of cell cycle transitions
J Cell Sci. 2012 Oct 15;125(Pt 20):4703-11. doi: 10.1242/jcs.106351.
Fisher D, Krasinska L, Coudreuse D, Novák B. Source Institut de Génétique Moléculaire de Montpellier, IGMM, CNRS UMR, Université Montpellier I and II, France. email@example.com Abstract Fifteen years ago, it was proposed that the cell cycle in fission yeast can be driven by quantitative changes in the activity of a single protein kinase complex comprising a cyclin - namely cyclin B - and cyclin dependent kinase 1 (Cdk1). When its activity is low, Cdk1 triggers the onset of S phase; when its activity level exceeds a specific threshold, it promotes entry into mitosis. This model has redefined our understanding of the essential functional inputs that organize cell cycle progression, and its main principles now appear to be applicable to all eukaryotic cells. But how does a change in the activity of one kinase generate ordered progression through the cell cycle in order to separate DNA replication from mitosis? To answer this question, we must consider the biochemical processes that underlie the phosphorylation of Cdk1 substrates. In this Commentary, we discuss recent findings that have shed light on how the threshold levels of Cdk1 activity that are required for progression through each phase are determined, how an increase in Cdk activity generates directionality in the cell cycle, and why cell cycle transitions are abrupt rather than gradual. These considerations lead to a general quantitative model of cell cycle control, in which opposing kinase and phosphatase activities have an essential role in ensuring dynamic transitions.
Cell cycle regulation in hematopoietic stem cells
J Cell Biol. 2011 Nov 28;195(5):709-20. doi: 10.1083/jcb.201102131.
Pietras EM, Warr MR, Passegué E. Source Department of Medicine, Division of Hematology/Oncology, The Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research, University of California, San Francisco, San Francisco, CA 94143, USA. Abstract Hematopoietic stem cells (HSCs) give rise to all lineages of blood cells. Because HSCs must persist for a lifetime, the balance between their proliferation and quiescence is carefully regulated to ensure blood homeostasis while limiting cellular damage. Cell cycle regulation therefore plays a critical role in controlling HSC function during both fetal life and in the adult. The cell cycle activity of HSCs is carefully modulated by a complex interplay between cell-intrinsic mechanisms and cell-extrinsic factors produced by the microenvironment. This fine-tuned regulatory network may become altered with age, leading to aberrant HSC cell cycle regulation, degraded HSC function, and hematological malignancy.
Beyrouthy MJ, Alexander KE, Baldwin A, Whitfield ML, Bass HW, et al. (2008) Identification of G1-Regulated Genes in Normally Cycling Human Cells. PLoS ONE 3(12): e3943. doi:10.1371/journal.pone.0003943 http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0003943
Cell Press Videos
Polymerization Pulls (George von Dassow, University of Oregon) http://www.youtube.com/watch?v=W89cD0YkHfw&feature=player_embedded http://www.youtube.com/v/W89cD0YkHfw
Ready, Set, Replicate (Teresa Davoli, Eros Lazzerini Denchi, Titia de Lange) http://www.youtube.com/watch?v=gucJ9TwHNtA&feature=player_embedded http://www.youtube.com/v/gucJ9TwHNtA