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Inactivation of Mre11 does not affect VSG gene duplication mediated by homologous recombination in Trypanosoma brucei

Research output: Contribution to Journal/Magazine › Journal article › peer-review

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Inactivation of Mre11 does not affect VSG gene duplication mediated by homologous recombination in Trypanosoma brucei. / Robinson, Nicholas P.; McCulloch, Richard; Conway, Colin et al.
In: Journal of Biological Chemistry, Vol. 277, No. 29, 19.07.2002, p. 26185-26193.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Robinson, NP, McCulloch, R, Conway, C, Browitt, A & Barry, JD 2002, 'Inactivation of Mre11 does not affect VSG gene duplication mediated by homologous recombination in Trypanosoma brucei', Journal of Biological Chemistry, vol. 277, no. 29, pp. 26185-26193. https://doi.org/10.1074/jbc.M203205200

APA

Robinson, N. P., McCulloch, R., Conway, C., Browitt, A., & Barry, J. D. (2002). Inactivation of Mre11 does not affect VSG gene duplication mediated by homologous recombination in Trypanosoma brucei. Journal of Biological Chemistry, 277(29), 26185-26193. https://doi.org/10.1074/jbc.M203205200

Vancouver

Robinson NP, McCulloch R, Conway C, Browitt A, Barry JD. Inactivation of Mre11 does not affect VSG gene duplication mediated by homologous recombination in Trypanosoma brucei. Journal of Biological Chemistry. 2002 Jul 19;277(29):26185-26193. doi: 10.1074/jbc.M203205200

Author

Robinson, Nicholas P. ; McCulloch, Richard ; Conway, Colin et al. / Inactivation of Mre11 does not affect VSG gene duplication mediated by homologous recombination in Trypanosoma brucei. In: Journal of Biological Chemistry. 2002 ; Vol. 277, No. 29. pp. 26185-26193.

Bibtex

@article{9026baf5038e4bb195e3f881ffc6fdbd,
title = "Inactivation of Mre11 does not affect VSG gene duplication mediated by homologous recombination in Trypanosoma brucei",
abstract = "We demonstrate, by gene deletion analysis, that Mre11 has a critical role in maintaining genomic integrity in Trypanosoma brucei. mre11(-/-) null mutant strains exhibited retarded growth but no delay or disruption of cell cycle progression. They showed also a weak hyporecombination phenotype and the accumulation of gross chromosomal rearrangements, which did not involve sequence translocation, telomere loss, or formation of new telomeres. The trypanosome mre11(-/-) strains were hypersensitive to phleomycin, a mutagen causing DNA double strand breaks (DSBs) but, in contrast to mre11(-/-) null mutants in other organisms and T. brucei rad51(-/-) null mutants, displayed no hypersensitivity to methyl methanesulfonate, which causes point mutations and DSBs. Mre11 therefore is important for the repair of chromosomal damage and DSBs in trypanosomes, although in this organism the intersection of repair pathways appears to differ from that in other organisms. Mre11 inactivation appears not to affect VSG gene switching during antigenic variation of a laboratory strain, which is perhaps surprising given the importance of homologous recombination during this process.",
keywords = "Amino Acid Sequence, Animals, Arabidopsis, DNA Damage, DNA Repair, Endodeoxyribonucleases, Exodeoxyribonucleases, Gene Duplication, Humans, Methyl Methanesulfonate, Phenotype, Phleomycins, Point Mutation, Saccharomyces cerevisiae Proteins, Sequence Alignment, Trypanosoma brucei brucei, Variant Surface Glycoproteins, Trypanosoma, Xenopus laevis, Journal Article, Research Support, Non-U.S. Gov't",
author = "Robinson, {Nicholas P.} and Richard McCulloch and Colin Conway and Alison Browitt and Barry, {J. David}",
year = "2002",
month = jul,
day = "19",
doi = "10.1074/jbc.M203205200",
language = "English",
volume = "277",
pages = "26185--26193",
journal = "Journal of Biological Chemistry",
issn = "0021-9258",
publisher = "American Society for Biochemistry and Molecular Biology Inc.",
number = "29",

}

RIS

TY - JOUR

T1 - Inactivation of Mre11 does not affect VSG gene duplication mediated by homologous recombination in Trypanosoma brucei

AU - Robinson, Nicholas P.

AU - McCulloch, Richard

AU - Conway, Colin

AU - Browitt, Alison

AU - Barry, J. David

PY - 2002/7/19

Y1 - 2002/7/19

N2 - We demonstrate, by gene deletion analysis, that Mre11 has a critical role in maintaining genomic integrity in Trypanosoma brucei. mre11(-/-) null mutant strains exhibited retarded growth but no delay or disruption of cell cycle progression. They showed also a weak hyporecombination phenotype and the accumulation of gross chromosomal rearrangements, which did not involve sequence translocation, telomere loss, or formation of new telomeres. The trypanosome mre11(-/-) strains were hypersensitive to phleomycin, a mutagen causing DNA double strand breaks (DSBs) but, in contrast to mre11(-/-) null mutants in other organisms and T. brucei rad51(-/-) null mutants, displayed no hypersensitivity to methyl methanesulfonate, which causes point mutations and DSBs. Mre11 therefore is important for the repair of chromosomal damage and DSBs in trypanosomes, although in this organism the intersection of repair pathways appears to differ from that in other organisms. Mre11 inactivation appears not to affect VSG gene switching during antigenic variation of a laboratory strain, which is perhaps surprising given the importance of homologous recombination during this process.

AB - We demonstrate, by gene deletion analysis, that Mre11 has a critical role in maintaining genomic integrity in Trypanosoma brucei. mre11(-/-) null mutant strains exhibited retarded growth but no delay or disruption of cell cycle progression. They showed also a weak hyporecombination phenotype and the accumulation of gross chromosomal rearrangements, which did not involve sequence translocation, telomere loss, or formation of new telomeres. The trypanosome mre11(-/-) strains were hypersensitive to phleomycin, a mutagen causing DNA double strand breaks (DSBs) but, in contrast to mre11(-/-) null mutants in other organisms and T. brucei rad51(-/-) null mutants, displayed no hypersensitivity to methyl methanesulfonate, which causes point mutations and DSBs. Mre11 therefore is important for the repair of chromosomal damage and DSBs in trypanosomes, although in this organism the intersection of repair pathways appears to differ from that in other organisms. Mre11 inactivation appears not to affect VSG gene switching during antigenic variation of a laboratory strain, which is perhaps surprising given the importance of homologous recombination during this process.

KW - Amino Acid Sequence

KW - Animals

KW - Arabidopsis

KW - DNA Damage

KW - DNA Repair

KW - Endodeoxyribonucleases

KW - Exodeoxyribonucleases

KW - Gene Duplication

KW - Humans

KW - Methyl Methanesulfonate

KW - Phenotype

KW - Phleomycins

KW - Point Mutation

KW - Saccharomyces cerevisiae Proteins

KW - Sequence Alignment

KW - Trypanosoma brucei brucei

KW - Variant Surface Glycoproteins, Trypanosoma

KW - Xenopus laevis

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1074/jbc.M203205200

DO - 10.1074/jbc.M203205200

M3 - Journal article

C2 - 12011090

VL - 277

SP - 26185

EP - 26193

JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

SN - 0021-9258

IS - 29

ER -