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    Rights statement: This is the author’s version of a work that was accepted for publication in Free Radical Biology and Medicine. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Free Radical Biology and Medicine, 96, 2016 DOI: 10.1016/j.freeradbiomed.2016.04.017

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Glutathione reductase gsr-1 is an essential gene required for Caenorhabditis elegans early embryonic development

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Glutathione reductase gsr-1 is an essential gene required for Caenorhabditis elegans early embryonic development. / Mora-Lorca, José Antonio; Sáenz-Narciso, Beatriz; Gaffney, Christopher J et al.
In: Free Radical Biology and Medicine, Vol. 96, 07.2016, p. 446-461.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Harvard

Mora-Lorca, JA, Sáenz-Narciso, B, Gaffney, CJ, Naranjo-Galindo, FJ, Pedrajas, JR, Guerrero-Gómez, D, Dobrzynska, A, Askjaer, P, Szewczyk, NJ, Cabello, J & Miranda-Vizuete, A 2016, 'Glutathione reductase gsr-1 is an essential gene required for Caenorhabditis elegans early embryonic development', Free Radical Biology and Medicine, vol. 96, pp. 446-461. https://doi.org/10.1016/j.freeradbiomed.2016.04.017

APA

Mora-Lorca, J. A., Sáenz-Narciso, B., Gaffney, C. J., Naranjo-Galindo, F. J., Pedrajas, J. R., Guerrero-Gómez, D., Dobrzynska, A., Askjaer, P., Szewczyk, N. J., Cabello, J., & Miranda-Vizuete, A. (2016). Glutathione reductase gsr-1 is an essential gene required for Caenorhabditis elegans early embryonic development. Free Radical Biology and Medicine, 96, 446-461. https://doi.org/10.1016/j.freeradbiomed.2016.04.017

Vancouver

Mora-Lorca JA, Sáenz-Narciso B, Gaffney CJ, Naranjo-Galindo FJ, Pedrajas JR, Guerrero-Gómez D et al. Glutathione reductase gsr-1 is an essential gene required for Caenorhabditis elegans early embryonic development. Free Radical Biology and Medicine. 2016 Jul;96:446-461. Epub 2016 Apr 24. doi: 10.1016/j.freeradbiomed.2016.04.017

Author

Mora-Lorca, José Antonio ; Sáenz-Narciso, Beatriz ; Gaffney, Christopher J et al. / Glutathione reductase gsr-1 is an essential gene required for Caenorhabditis elegans early embryonic development. In: Free Radical Biology and Medicine. 2016 ; Vol. 96. pp. 446-461.

Bibtex

@article{85617544c2ee4785936d7cf5c6b254bd,
title = "Glutathione reductase gsr-1 is an essential gene required for Caenorhabditis elegans early embryonic development",
abstract = "Glutathione is the most abundant thiol in the vast majority of organisms and is maintained in its reduced form by the flavoenzyme glutathione reductase. In this work, we describe the genetic and functional analysis of the Caenorhabditis elegans gsr-1 gene that encodes the only glutathione reductase protein in this model organism. By using green fluorescent protein reporters we demonstrate that gsr-1 produces two GSR-1 isoforms, one located in the cytoplasm and one in the mitochondria. gsr-1 loss of function mutants display a fully penetrant embryonic lethal phenotype characterized by a progressive and robust cell division delay accompanied by an aberrant distribution of interphasic chromatin in the periphery of the cell nucleus. Maternally expressed GSR-1 is sufficient to support embryonic development but these animals are short-lived, sensitized to chemical stress, have increased mitochondrial fragmentation and lower mitochondrial DNA content. Furthermore, the embryonic lethality of gsr-1 worms is prevented by restoring GSR-1 activity in the cytoplasm but not in mitochondria. Given the fact that the thioredoxin redox systems are dispensable in C. elegans, our data support a prominent role of the glutathione reductase/glutathione pathway in maintaining redox homeostasis in the nematode.",
keywords = "Caenorhabditis elegans, Embryonic development, Glutathione reductase, Mitochondria, Redox",
author = "Mora-Lorca, {Jos{\'e} Antonio} and Beatriz S{\'a}enz-Narciso and Gaffney, {Christopher J} and Naranjo-Galindo, {Francisco Jos{\'e}} and Pedrajas, {Jos{\'e} Rafael} and David Guerrero-G{\'o}mez and Agnieszka Dobrzynska and Peter Askjaer and Szewczyk, {Nathaniel J} and Juan Cabello and Antonio Miranda-Vizuete",
note = "This is the author{\textquoteright}s version of a work that was accepted for publication in Free Radical Biology and Medicine. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Free Radical Biology and Medicine, 96, 2016 DOI: 10.1016/j.freeradbiomed.2016.04.017",
year = "2016",
month = jul,
doi = "10.1016/j.freeradbiomed.2016.04.017",
language = "English",
volume = "96",
pages = "446--461",
journal = "Free Radical Biology and Medicine",
issn = "0891-5849",
publisher = "ELSEVIER SCIENCE INC",

}

RIS

TY - JOUR

T1 - Glutathione reductase gsr-1 is an essential gene required for Caenorhabditis elegans early embryonic development

AU - Mora-Lorca, José Antonio

AU - Sáenz-Narciso, Beatriz

AU - Gaffney, Christopher J

AU - Naranjo-Galindo, Francisco José

AU - Pedrajas, José Rafael

AU - Guerrero-Gómez, David

AU - Dobrzynska, Agnieszka

AU - Askjaer, Peter

AU - Szewczyk, Nathaniel J

AU - Cabello, Juan

AU - Miranda-Vizuete, Antonio

N1 - This is the author’s version of a work that was accepted for publication in Free Radical Biology and Medicine. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Free Radical Biology and Medicine, 96, 2016 DOI: 10.1016/j.freeradbiomed.2016.04.017

PY - 2016/7

Y1 - 2016/7

N2 - Glutathione is the most abundant thiol in the vast majority of organisms and is maintained in its reduced form by the flavoenzyme glutathione reductase. In this work, we describe the genetic and functional analysis of the Caenorhabditis elegans gsr-1 gene that encodes the only glutathione reductase protein in this model organism. By using green fluorescent protein reporters we demonstrate that gsr-1 produces two GSR-1 isoforms, one located in the cytoplasm and one in the mitochondria. gsr-1 loss of function mutants display a fully penetrant embryonic lethal phenotype characterized by a progressive and robust cell division delay accompanied by an aberrant distribution of interphasic chromatin in the periphery of the cell nucleus. Maternally expressed GSR-1 is sufficient to support embryonic development but these animals are short-lived, sensitized to chemical stress, have increased mitochondrial fragmentation and lower mitochondrial DNA content. Furthermore, the embryonic lethality of gsr-1 worms is prevented by restoring GSR-1 activity in the cytoplasm but not in mitochondria. Given the fact that the thioredoxin redox systems are dispensable in C. elegans, our data support a prominent role of the glutathione reductase/glutathione pathway in maintaining redox homeostasis in the nematode.

AB - Glutathione is the most abundant thiol in the vast majority of organisms and is maintained in its reduced form by the flavoenzyme glutathione reductase. In this work, we describe the genetic and functional analysis of the Caenorhabditis elegans gsr-1 gene that encodes the only glutathione reductase protein in this model organism. By using green fluorescent protein reporters we demonstrate that gsr-1 produces two GSR-1 isoforms, one located in the cytoplasm and one in the mitochondria. gsr-1 loss of function mutants display a fully penetrant embryonic lethal phenotype characterized by a progressive and robust cell division delay accompanied by an aberrant distribution of interphasic chromatin in the periphery of the cell nucleus. Maternally expressed GSR-1 is sufficient to support embryonic development but these animals are short-lived, sensitized to chemical stress, have increased mitochondrial fragmentation and lower mitochondrial DNA content. Furthermore, the embryonic lethality of gsr-1 worms is prevented by restoring GSR-1 activity in the cytoplasm but not in mitochondria. Given the fact that the thioredoxin redox systems are dispensable in C. elegans, our data support a prominent role of the glutathione reductase/glutathione pathway in maintaining redox homeostasis in the nematode.

KW - Caenorhabditis elegans

KW - Embryonic development

KW - Glutathione reductase

KW - Mitochondria

KW - Redox

U2 - 10.1016/j.freeradbiomed.2016.04.017

DO - 10.1016/j.freeradbiomed.2016.04.017

M3 - Journal article

C2 - 27117030

VL - 96

SP - 446

EP - 461

JO - Free Radical Biology and Medicine

JF - Free Radical Biology and Medicine

SN - 0891-5849

ER -