The Dot1 Histone Methyltransferase and the Rad9 Checkpoint Adaptor Contribute to Cohesin-Dependent Double-Strand Break Repair by Sister Chromatid Recombination in <i>Saccharomyces cerevisiae</i>

Conde, Francisco; Refolio, Esther; Cordón-Preciado, Violeta; Cortés‐Ledesma, Felipe; Aragón, Luís; Aguilera, Andrés; San-Segundo, Pedro A.

doi:10.1534/genetics.109.101899

Cited by 61 publications

(48 citation statements)

References 43 publications

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“…A number of proteins, including cohesin, are required for maintaining chromosome structure and for efficient SCR. Interestingly, not only is Dot1 required for the recruitment of Rad9 to the DSB sites and for DNA resection, it also facilitates the recruitment of cohesin and efficient SCR (Conde et al 2009). …”

Section: Role Of Dot1 In Dna Repair and Cell Cycle Regulationmentioning

confidence: 99%

The diverse functions of Dot1 and H3K79 methylation

Nguyen¹,

Zhang²

2011

Genes Dev.

518

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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Section: Role Of Dot1 In Dna Repair and Cell Cycle Regulationmentioning

confidence: 99%

The diverse functions of Dot1 and H3K79 methylation

Nguyen¹,

Zhang²

2011

Genes Dev.

518

478

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“…In addition, H3K79 methylation mediated by Dot1L promotes nucleotide excision repair, and H3K79R mutation increases the binding of histone deacetylase complex to eliminate histone acetylation and reduce DNA lesion accessibility to repair enzymes (Chaudhuri et al, 2009;Tatum and Li, 2011). Moreover, Dot1L and H3K79me3 contribute to favorable sister chromatid exchange during HR and facilitate HR repair (Conde et al, 2009;Rossodivita et al, 2014). Furthermore, there is crosstalk between H3K79 methylation and other histone methylations.…”

Section: Methylationmentioning

confidence: 99%

Histone modifications in DNA damage response

Cao

Shen

Zhu

2016

Sci. China Life Sci.

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DNA damage is a relatively common event in eukaryotic cell and may lead to genetic mutation and even cancer. DNA damage induces cellular responses that enable the cell either to repair the damaged DNA or cope with the damage in an appropriate way. Histone proteins are also the fundamental building blocks of eukaryotic chromatin besides DNA, and many types of post-translational modifications often occur on tails of histones. Although the function of these modifications has remained elusive, there is ever-growing studies suggest that histone modifications play vital roles in several chromatin-based processes, such as DNA damage response. In this review, we will discuss the main histone modifications, and their functions in DNA damage response.DNA damage response, histone modifications, chromatin, DNA repair Citation:

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“…Me mark is constitutive and thought to be exposed upon damage (Conde et al 2009). Notably, Rad53 foci are Rad9-dependent, faint, and short-lived, which is consistent with the notion from mammalian cells that CHK2 (Rad53) must redistribute from the site of DNA damage upon phosphorylation to mediate a pan-nuclear checkpoint response (Lukas et al 2003).…”

Section: Choreography Of Focus Formationmentioning

confidence: 99%

Cell Biology of Mitotic Recombination

Lisby

Rothstein

2015

Cold Spring Harb Perspect Biol

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Homologous recombination provides high-fidelity DNA repair throughout all domains of life. Live cell fluorescence microscopy offers the opportunity to image individual recombination events in real time providing insight into the in vivo biochemistry of the involved proteins and DNA molecules as well as the cellular organization of the process of homologous recombination. Herein we review the cell biological aspects of mitotic homologous recombination with a focus on Saccharomyces cerevisiae and mammalian cells, but will also draw on findings from other experimental systems. Key topics of this review include the stoichiometry and dynamics of recombination complexes in vivo, the choreography of assembly and disassembly of recombination proteins at sites of DNA damage, the mobilization of damaged DNA during homology search, and the functional compartmentalization of the nucleus with respect to capacity of homologous recombination.

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The Dot1 Histone Methyltransferase and the Rad9 Checkpoint Adaptor Contribute to Cohesin-Dependent Double-Strand Break Repair by Sister Chromatid Recombination in Saccharomyces cerevisiae

Cited by 61 publications

References 43 publications

The diverse functions of Dot1 and H3K79 methylation

The diverse functions of Dot1 and H3K79 methylation

Histone modifications in DNA damage response

Cell Biology of Mitotic Recombination

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