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      Transcriptional reprogramming in cellular quiescence

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          Most cells in nature are not actively dividing, yet are able to return to the cell cycle given the appropriate environmental signals. There is now ample evidence that quiescent G0 cells are not shut-down but still metabolically and transcriptionally active. Quiescent cells must maintain a basal transcriptional capacity to maintain transcripts and proteins necessary for survival. This implies a tight control over RNA polymerases: RNA pol II for mRNA transcription during G0, but especially RNA pol I and RNA pol III to maintain an appropriate level of structural RNAs, raising the possibility that specific transcriptional control mechanisms evolved in quiescent cells. In accordance with this, we recently discovered that RNA interference is necessary to control RNA polymerase I transcription during G0. While this mini-review focuses on yeast model organisms ( Saccharomyces cerevisiae and Schizosaccharomyces pombe), parallels are drawn to other eukaryotes and mammalian systems, in particular stem cells.

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          Viable offspring derived from fetal and adult mammalian cells.

          Fertilization of mammalian eggs is followed by successive cell divisions and progressive differentiation, first into the early embryo and subsequently into all of the cell types that make up the adult animal. Transfer of a single nucleus at a specific stage of development, to an enucleated unfertilized egg, provided an opportunity to investigate whether cellular differentiation to that stage involved irreversible genetic modification. The first offspring to develop from a differentiated cell were born after nuclear transfer from an embryo-derived cell line that had been induced to become quiescent. Using the same procedure, we now report the birth of live lambs from three new cell populations established from adult mammary gland, fetus and embryo. The fact that a lamb was derived from an adult cell confirms that differentiation of that cell did not involve the irreversible modification of genetic material required for development to term. The birth of lambs from differentiated fetal and adult cells also reinforces previous speculation that by inducing donor cells to become quiescent it will be possible to obtain normal development from a wide variety of differentiated cells.
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            Models, mechanisms and clinical evidence for cancer dormancy.

            Patients with cancer can develop recurrent metastatic disease with latency periods that range from years even to decades. This pause can be explained by cancer dormancy, a stage in cancer progression in which residual disease is present but remains asymptomatic. Cancer dormancy is poorly understood, resulting in major shortcomings in our understanding of the full complexity of the disease. Here, I review experimental and clinical evidence that supports the existence of various mechanisms of cancer dormancy including angiogenic dormancy, cellular dormancy (G0-G1 arrest) and immunosurveillance. The advances in this field provide an emerging picture of how cancer dormancy can ensue and how it could be therapeutically targeted.
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              Molecular regulation of stem cell quiescence.

              Subsets of mammalian adult stem cells reside in the quiescent state for prolonged periods of time. This state, which is reversible, has long been viewed as dormant and with minimal basal activity. Recent advances in adult stem cell isolation have provided insights into the epigenetic, transcriptional and post-transcriptional control of quiescence and suggest that quiescence is an actively maintained state in which signalling pathways are involved in maintaining a poised state that allows rapid activation. Deciphering the molecular mechanisms regulating adult stem cell quiescence will increase our understanding of tissue regeneration mechanisms and how they are dysregulated in pathological conditions and in ageing.

                Author and article information

                RNA Biol
                RNA Biol
                RNA Biology
                Taylor & Francis
                12 May 2017
                12 May 2017
                : 14
                : 7
                : 843-853
                [a ]Cold Spring Harbor Laboratory, Cold Spring Harbor , NY, USA
                [b ]Genome Dynamics Unit, UMR 3525 CNRS, Institut Pasteur, 25–28 rue du Docteur Roux , Paris, France
                [c ]Howard Hughes Medical Institute—Gordon and Betty Moore Foundation (HHMI-GBM) Investigator , NY, USA
                Author notes
                CONTACT Robert Martienssen martiens@ 123456cshl.edu Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor , NY, 11724 USA
                © 2017 The Author(s). Published with license by Taylor & Francis Group, LLC

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License ( http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.

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                Figures: 2, Tables: 0, Equations: 0, References: 164, Pages: 11
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