NEJ1 controls non-homologous end joining in Saccharomyces cerevisiae

Maria Valencia; Marc Bentele; Moreshwar B. Vaze; Gernot Herrmann; Eliayhu Kraus; Sang Eun Lee; Primo Schär; James E. Haber

doi:10.1038/414666a

NEJ1 controls non-homologous end joining in Saccharomyces cerevisiae

Maria Valencia, Marc Bentele, Moreshwar B. Vaze, Gernot Herrmann, Eliayhu Kraus, Sang Eun Lee, Primo Schär, James E. Haber

Department of Molecular Medicine

Research output: Contribution to journal › Article › peer-review

185 Scopus citations

Abstract

Broken DNA ends are rejoined by non-homologous end-joining (NHEJ) pathways requiring the Ku proteins (Ku70, Ku80), DNA ligase IV and its associated protein Lif1/Xrcc4 (ref. 1). In mammalian meiotic cells, Ku protein levels are much lower than in somatic cells, apparently reducing the capacity of meiotic cells to carry out NHEJ and thereby promoting homologous recombination. In Saccharomyces cerevisiae, NHEJ is also down-regulated in meiosis-competent MATa/MATα diploid cells in comparison with diploids or haploids expressing only MATa or MATα^3,4;. Diploids expressing both MATa and MATα show enhanced mitotic homologous recombination. Here we report that mating-type-dependent regulation of NHEJ in budding yeast is caused in part by transcriptional repression of both LIF1 and the gene NEJ1 (YLR265C) - identified from microarray screening of messenger RNAs. Deleting NEJ1 reduces NHEJ 100-fold in MATa or MATα haploids. Constitutive expression of NEJ1, but not expression of LIF1, restores NHEJ in MATa/MATα cells. Nej1 regulates the subcellular distribution of Lif1. A green fluorescent protein (GFP) - Lif1 fusion protein accumulates in the nucleus in cells expressing NEJ1 but is largely cytoplasmic when NEJ1 is repressed.

Original language	English (US)
Pages (from-to)	666-669
Number of pages	4
Journal	Nature
Volume	414
Issue number	6864
DOIs	https://doi.org/10.1038/414666a
State	Published - Dec 6 2001

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@article{9049da58571543378ab46dd586f631b5,

title = "NEJ1 controls non-homologous end joining in Saccharomyces cerevisiae",

abstract = "Broken DNA ends are rejoined by non-homologous end-joining (NHEJ) pathways requiring the Ku proteins (Ku70, Ku80), DNA ligase IV and its associated protein Lif1/Xrcc4 (ref. 1). In mammalian meiotic cells, Ku protein levels are much lower than in somatic cells, apparently reducing the capacity of meiotic cells to carry out NHEJ and thereby promoting homologous recombination. In Saccharomyces cerevisiae, NHEJ is also down-regulated in meiosis-competent MATa/MATα diploid cells in comparison with diploids or haploids expressing only MATa or MATα3,4;. Diploids expressing both MATa and MATα show enhanced mitotic homologous recombination. Here we report that mating-type-dependent regulation of NHEJ in budding yeast is caused in part by transcriptional repression of both LIF1 and the gene NEJ1 (YLR265C) - identified from microarray screening of messenger RNAs. Deleting NEJ1 reduces NHEJ 100-fold in MATa or MATα haploids. Constitutive expression of NEJ1, but not expression of LIF1, restores NHEJ in MATa/MATα cells. Nej1 regulates the subcellular distribution of Lif1. A green fluorescent protein (GFP) - Lif1 fusion protein accumulates in the nucleus in cells expressing NEJ1 but is largely cytoplasmic when NEJ1 is repressed.",

author = "Maria Valencia and Marc Bentele and Vaze, {Moreshwar B.} and Gernot Herrmann and Eliayhu Kraus and Lee, {Sang Eun} and Primo Sch{\"a}r and Haber, {James E.}",

note = "Funding Information: We are grateful for collaboration with A. Gasch, P. Brown and D. Botstein to analyse mRNA abundance under various conditions, and for their generosity in declining to be authors on this paper. S.E.L. is a Hildegarde A. Becher Foundation fellow of The Leukemia and Lymphoma Society. G.H. was supported by the Deutsche Forschungsgesellschaft (DFG). This work was supported by a grant of the Swiss National Science Foundation to M.B. and P.S. and DOE and National Institutes of Health grants to J.E.H.",

year = "2001",

month = dec,

day = "6",

doi = "10.1038/414666a",

language = "English (US)",

volume = "414",

pages = "666--669",

journal = "Nature",

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publisher = "Nature Publishing Group",

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T1 - NEJ1 controls non-homologous end joining in Saccharomyces cerevisiae

AU - Valencia, Maria

AU - Bentele, Marc

AU - Vaze, Moreshwar B.

AU - Herrmann, Gernot

AU - Kraus, Eliayhu

AU - Lee, Sang Eun

AU - Schär, Primo

AU - Haber, James E.

N1 - Funding Information: We are grateful for collaboration with A. Gasch, P. Brown and D. Botstein to analyse mRNA abundance under various conditions, and for their generosity in declining to be authors on this paper. S.E.L. is a Hildegarde A. Becher Foundation fellow of The Leukemia and Lymphoma Society. G.H. was supported by the Deutsche Forschungsgesellschaft (DFG). This work was supported by a grant of the Swiss National Science Foundation to M.B. and P.S. and DOE and National Institutes of Health grants to J.E.H.

PY - 2001/12/6

Y1 - 2001/12/6

N2 - Broken DNA ends are rejoined by non-homologous end-joining (NHEJ) pathways requiring the Ku proteins (Ku70, Ku80), DNA ligase IV and its associated protein Lif1/Xrcc4 (ref. 1). In mammalian meiotic cells, Ku protein levels are much lower than in somatic cells, apparently reducing the capacity of meiotic cells to carry out NHEJ and thereby promoting homologous recombination. In Saccharomyces cerevisiae, NHEJ is also down-regulated in meiosis-competent MATa/MATα diploid cells in comparison with diploids or haploids expressing only MATa or MATα3,4;. Diploids expressing both MATa and MATα show enhanced mitotic homologous recombination. Here we report that mating-type-dependent regulation of NHEJ in budding yeast is caused in part by transcriptional repression of both LIF1 and the gene NEJ1 (YLR265C) - identified from microarray screening of messenger RNAs. Deleting NEJ1 reduces NHEJ 100-fold in MATa or MATα haploids. Constitutive expression of NEJ1, but not expression of LIF1, restores NHEJ in MATa/MATα cells. Nej1 regulates the subcellular distribution of Lif1. A green fluorescent protein (GFP) - Lif1 fusion protein accumulates in the nucleus in cells expressing NEJ1 but is largely cytoplasmic when NEJ1 is repressed.

AB - Broken DNA ends are rejoined by non-homologous end-joining (NHEJ) pathways requiring the Ku proteins (Ku70, Ku80), DNA ligase IV and its associated protein Lif1/Xrcc4 (ref. 1). In mammalian meiotic cells, Ku protein levels are much lower than in somatic cells, apparently reducing the capacity of meiotic cells to carry out NHEJ and thereby promoting homologous recombination. In Saccharomyces cerevisiae, NHEJ is also down-regulated in meiosis-competent MATa/MATα diploid cells in comparison with diploids or haploids expressing only MATa or MATα3,4;. Diploids expressing both MATa and MATα show enhanced mitotic homologous recombination. Here we report that mating-type-dependent regulation of NHEJ in budding yeast is caused in part by transcriptional repression of both LIF1 and the gene NEJ1 (YLR265C) - identified from microarray screening of messenger RNAs. Deleting NEJ1 reduces NHEJ 100-fold in MATa or MATα haploids. Constitutive expression of NEJ1, but not expression of LIF1, restores NHEJ in MATa/MATα cells. Nej1 regulates the subcellular distribution of Lif1. A green fluorescent protein (GFP) - Lif1 fusion protein accumulates in the nucleus in cells expressing NEJ1 but is largely cytoplasmic when NEJ1 is repressed.

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DO - 10.1038/414666a

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VL - 414

SP - 666

EP - 669

JO - Nature

JF - Nature

IS - 6864

ER -

NEJ1 controls non-homologous end joining in Saccharomyces cerevisiae

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