Analysis of epigenetic alterations to chromatin during development

Minard, Meghan E.; Jain, Abhinav K.; Barton, Michelle C.

doi:10.1002/dvg.20534

Cited by 45 publications

(28 citation statements)

References 145 publications

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“…In this model lncRNAs, while still tethered to the genome during their transcription, would act by recruiting DNA binding proteins into complexes that interact with ICRs generating anchoring points for structural proteins that would pull genomic regions together into transcriptional hotspots (Court et al, 2011;Horike et al, 2005). The disruption of this genomic architecture would lead to uncoordinated activation/silencing of imprinted genes (Minard et al, 2009;Zlatanova & Caiafa, 2009). In this framework, still to be clarified is the differential role played by the parental origins.…”

Section: Wwwintechopencommentioning

confidence: 99%

Genomic Imprinting in Human Placenta

Lambertini¹,

Lee²,

Marsit³

et al. 2012

Recent Advances in Research on the Human Placenta

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This book contains the total of 19 chapters, each of which is written by one or several experts in the corresponding field. The objective of this book is to provide a comprehensive and most updated overview of the human placenta, including current advances and future directions in the early detection, recognition, and management of placental abnormalities as well as the most common placental structure and functions, abnormalities, toxicology, infections, and pathologies. It also includes a highly controversial topic, therapeutic applications of the human placenta. A collection of articles presented by active investigators provides a clear update in the area of placental research for medical students, nurse practitioners, practicing clinicians, and biomedical researchers in the fields of obstetrics, pediatrics, family practice, genetics, and others who may be interested in human placentas.

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Section: Wwwintechopencommentioning

confidence: 99%

Genomic Imprinting in Human Placenta

Lambertini¹,

Lee²,

Marsit³

et al. 2012

Recent Advances in Research on the Human Placenta

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“…In general, methylation at H3K9, H3K27, and H4K20 correlates with transcriptional repression, while methylation at H3K4, H3K36, and H3K79 correlates with gene transcription (Kouzarides 2002;Peterson and Laniel 2004;Martin and Zhang 2005). In addition to its role in transcriptional regulation, methylation has also been linked to X inactivation, cell fate determination, terminal differentiation, and the spatiotemporal patterning of Hox genes (Cavalli 2006;Minard et al 2009). Moreover, aberrant histone methylation has also been linked to various human cancers (Feinberg et al 2002;Handel et al 2010).…”

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confidence: 99%

The diverse functions of Dot1 and H3K79 methylation

Nguyen¹,

Zhang²

2011

Genes Dev.

512

478

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DOT1 (disruptor of telomeric silencing; also called Kmt4) was initially discovered in budding yeast in a genetic screen for genes whose deletion confers defects in telomeric silencing. Since the discovery ∼10 years ago that Dot1 and its mammalian homolog, DOT1L (DOT1-Like), possess histone methyltransferase activity toward histone H3 Lys 79, great progress has been made in characterizing their enzymatic activities and the role of Dot1/DOT1L-mediated H3K79 methylation in transcriptional regulation, cell cycle regulation, and the DNA damage response. In addition, gene disruption in mice has revealed that mouse DOT1L plays an essential role in embryonic development, hematopoiesis, cardiac function, and the development of leukemia. The involvement of DOT1L enzymatic activity in leukemogenesis driven by a subset of MLL (mixed-lineage leukemia) fusion proteins raises the possibility of targeting DOT1L for therapeutic intervention.

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“…The packaging of DNA has significant consequences for the transcriptional state of the underlying DNA. Repression or activation of different regions of the genome through packaging as open euchromatin or as repressive heterochromatin is cell type specific (Fraser et al 2009;Minard et al 2009). Moreover, these transcriptional states must be maintained and passed on to daughter cells during mitosis.…”

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Multiple Functions for Drosophila Mcm10 Suggested Through Analysis of Two Mcm10 Mutant Alleles

et al. 2010

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DNA replication and the correct packaging of DNA into different states of chromatin are both essential processes in all eukaryotic cells. High-fidelity replication of DNA is essential for the transmission of genetic material to cells. Likewise the maintenance of the epigenetic chromatin states is essential to the faithful reproduction of the transcriptional state of the cell. It is becoming more apparent that these two processes are linked through interactions between DNA replication proteins and chromatin-associated proteins. In addition, more proteins are being discovered that have dual roles in both DNA replication and the maintenance of epigenetic states. We present an analysis of two Drosophila mutants in the conserved DNA replication protein Mcm10. A hypomorphic mutant demonstrates that Mcm10 has a role in heterochromatic silencing and chromosome condensation, while the analysis of a novel C-terminal truncation allele of Mcm10 suggests that an interaction with Mcm2 is not required for chromosome condensation and heterochromatic silencing but is important for DNA replication.T HE essential process of DNA replication does not occur in a vacuum; rather, it takes place within the context of the cell. More specifically, DNA replication occurs within the context of chromatin: an integrated network of DNA-associated proteins that have roles in packaging DNA, controlling transcription, and maintaining genome integrity. The maintenance and manipulation of these chromatin proteins are, like DNA replication, an essential process. The packaging of DNA has significant consequences for the transcriptional state of the underlying DNA. Repression or activation of different regions of the genome through packaging as open euchromatin or as repressive heterochromatin is cell type specific (Fraser et al. 2009;Minard et al. 2009). Moreover, these transcriptional states must be maintained and passed on to daughter cells during mitosis. If not passed on faithfully, genome instability and/or transcriptional misregulation can occur, both of which may lead to defects in cell proliferation, cancer, and other disease states ( Jones et al. 2007;Hirst and Marra 2009).By necessity, the process of DNA replication requires unencumbered access to the nitrogenous bases that make up the DNA strand. As a result, chromatin proteins must be removed. In the wake of the DNA replication fork this nascent DNA must be repackaged to recapitulate the previous chromatin state. While DNA replication benefits from complementary base pairing to build a DNA molecule through semiconservative replication, the reestablishment of epigenetic states occurs through more subtle and varied mechanisms (Groth et al. 2007). One central question in reconciling the processes of DNA replication and the establishment and/or maintenance of chromatin states is how are these processes linked? One model suggests that DNA replication proteins interact with separate chromatin establishment factors, thereby spatially linking the two processes. Supporting this model has ...

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Analysis of epigenetic alterations to chromatin during development

Cited by 45 publications

References 145 publications

Genomic Imprinting in Human Placenta

Genomic Imprinting in Human Placenta

The diverse functions of Dot1 and H3K79 methylation

Multiple Functions for Drosophila Mcm10 Suggested Through Analysis of Two Mcm10 Mutant Alleles

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