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A mammalian monothiol glutaredoxin, Grx3, is critical for cell cycle progression during embryogenesis

Glutaredoxins (Grxs) have been shown to be critical in maintaining redox homeostasis in living cells. Recently, an emerging subgroup of Grxs with one cysteine residue in the putative active motif (monothiol Grxs) has been identified. However, the biological and physiological functions of this group... Full description

Journal Title: FEBS Journal July 2011, Vol.278(14), pp.2525-2539
Main Author: Cheng, Ning‐Hui
Other Authors: Zhang, Wei , Chen, Wei‐Qin , Jin, Jianping , Cui, Xiaojiang , Butte, Nancy F. , Chan, Lawrence , Hirschi, Kendal D.
Format: Electronic Article Electronic Article
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ID: ISSN: 1742-464X ; E-ISSN: 1742-4658 ; DOI: 10.1111/j.1742-4658.2011.08178.x
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recordid: wj10.1111/j.1742-4658.2011.08178.x
title: A mammalian monothiol glutaredoxin, Grx3, is critical for cell cycle progression during embryogenesis
format: Article
creator:
  • Cheng, Ning‐Hui
  • Zhang, Wei
  • Chen, Wei‐Qin
  • Jin, Jianping
  • Cui, Xiaojiang
  • Butte, Nancy F.
  • Chan, Lawrence
  • Hirschi, Kendal D.
subjects:
  • Cell Cycle
  • Embryogenesis
  • Glutaredoxin
  • Mouse
  • Oxidative Stress
ispartof: FEBS Journal, July 2011, Vol.278(14), pp.2525-2539
description: Glutaredoxins (Grxs) have been shown to be critical in maintaining redox homeostasis in living cells. Recently, an emerging subgroup of Grxs with one cysteine residue in the putative active motif (monothiol Grxs) has been identified. However, the biological and physiological functions of this group of proteins have not been well characterized. Here, we characterize a mammalian monothiol Grx (Grx3, also termed TXNL2/PICOT) with high similarity to yeast ScGrx3/ScGrx4. In yeast expression assays, mammalian Grx3s were localized to the nuclei and able to rescue growth defects of cells. Furthermore, Grx3 inhibited iron accumulation in yeast cells and suppressed the sensitivity of mutant cells to exogenous oxidants. In mice, mRNA was ubiquitously expressed in developing embryos, adult tissues and organs, and was induced during oxidative stress. Mouse embryos absent of grew smaller with morphological defects and eventually died at 12.5 days of gestation. Analysis in mouse embryonic fibroblasts revealed that cells had impaired growth and cell cycle progression at the G/M phase, whereas the DNA replication during the S phase was not affected by deletion. Furthermore, Grx3‐knockdown HeLa cells displayed a significant delay in mitotic exit and had a higher percentage of binucleated cells. Therefore, our findings suggest that the mammalian Grx3 has conserved functions in protecting cells against oxidative stress and deletion of in mice causes early embryonic lethality which could be due to defective cell cycle progression during late mitosis. Structured digital abstract •   and   by   Mammalian monothiol Grx3 is able to rescue growth defects of yeast mutant cells and to protect cells against oxidative stress. Disruption of causes early embryo death. Mouse embryonic fibroblasts from null mice display impaired growth and cell cycle progression at the G2/M phase. The defective cell cycle progression during late mitosis may account for early embryonic lethality.
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source:
identifier: ISSN: 1742-464X ; E-ISSN: 1742-4658 ; DOI: 10.1111/j.1742-4658.2011.08178.x
fulltext: fulltext
issn:
  • 1742-464X
  • 1742464X
  • 1742-4658
  • 17424658
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titleA mammalian monothiol glutaredoxin, Grx3, is critical for cell cycle progression during embryogenesis
creatorCheng, Ning‐Hui ; Zhang, Wei ; Chen, Wei‐Qin ; Jin, Jianping ; Cui, Xiaojiang ; Butte, Nancy F. ; Chan, Lawrence ; Hirschi, Kendal D.
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descriptionGlutaredoxins (Grxs) have been shown to be critical in maintaining redox homeostasis in living cells. Recently, an emerging subgroup of Grxs with one cysteine residue in the putative active motif (monothiol Grxs) has been identified. However, the biological and physiological functions of this group of proteins have not been well characterized. Here, we characterize a mammalian monothiol Grx (Grx3, also termed TXNL2/PICOT) with high similarity to yeast ScGrx3/ScGrx4. In yeast expression assays, mammalian Grx3s were localized to the nuclei and able to rescue growth defects of cells. Furthermore, Grx3 inhibited iron accumulation in yeast cells and suppressed the sensitivity of mutant cells to exogenous oxidants. In mice, mRNA was ubiquitously expressed in developing embryos, adult tissues and organs, and was induced during oxidative stress. Mouse embryos absent of grew smaller with morphological defects and eventually died at 12.5 days of gestation. Analysis in mouse embryonic fibroblasts revealed that cells had impaired growth and cell cycle progression at the G/M phase, whereas the DNA replication during the S phase was not affected by deletion. Furthermore, Grx3‐knockdown HeLa cells displayed a significant delay in mitotic exit and had a higher percentage of binucleated cells. Therefore, our findings suggest that the mammalian Grx3 has conserved functions in protecting cells against oxidative stress and deletion of in mice causes early embryonic lethality which could be due to defective cell cycle progression during late mitosis. Structured digital abstract •   and   by   Mammalian monothiol Grx3 is able to rescue growth defects of yeast mutant cells and to protect cells against oxidative stress. Disruption of causes early embryo death. Mouse embryonic fibroblasts from null mice display impaired growth and cell cycle progression at the G2/M phase. The defective cell cycle progression during late mitosis may account for early embryonic lethality.
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titleA mammalian monothiol glutaredoxin, Grx3, is critical for cell cycle progression during embryogenesis
descriptionGlutaredoxins (Grxs) have been shown to be critical in maintaining redox homeostasis in living cells. Recently, an emerging subgroup of Grxs with one cysteine residue in the putative active motif (monothiol Grxs) has been identified. However, the biological and physiological functions of this group of proteins have not been well characterized. Here, we characterize a mammalian monothiol Grx (Grx3, also termed TXNL2/PICOT) with high similarity to yeast ScGrx3/ScGrx4. In yeast expression assays, mammalian Grx3s were localized to the nuclei and able to rescue growth defects of cells. Furthermore, Grx3 inhibited iron accumulation in yeast cells and suppressed the sensitivity of mutant cells to exogenous oxidants. In mice, mRNA was ubiquitously expressed in developing embryos, adult tissues and organs, and was induced during oxidative stress. Mouse embryos absent of grew smaller with morphological defects and eventually died at 12.5 days of gestation. Analysis in mouse embryonic fibroblasts revealed that cells had impaired growth and cell cycle progression at the G/M phase, whereas the DNA replication during the S phase was not affected by deletion. Furthermore, Grx3‐knockdown HeLa cells displayed a significant delay in mitotic exit and had a higher percentage of binucleated cells. Therefore, our findings suggest that the mammalian Grx3 has conserved functions in protecting cells against oxidative stress and deletion of in mice causes early embryonic lethality which could be due to defective cell cycle progression during late mitosis. Structured digital abstract •   and   by   Mammalian monothiol Grx3 is able to rescue growth defects of yeast mutant cells and to protect cells against oxidative stress. Disruption of causes early embryo death. Mouse embryonic fibroblasts from null mice display impaired growth and cell cycle progression at the G2/M phase. The defective cell cycle progression during late mitosis may account for early embryonic lethality.
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abstractGlutaredoxins (Grxs) have been shown to be critical in maintaining redox homeostasis in living cells. Recently, an emerging subgroup of Grxs with one cysteine residue in the putative active motif (monothiol Grxs) has been identified. However, the biological and physiological functions of this group of proteins have not been well characterized. Here, we characterize a mammalian monothiol Grx (Grx3, also termed TXNL2/PICOT) with high similarity to yeast ScGrx3/ScGrx4. In yeast expression assays, mammalian Grx3s were localized to the nuclei and able to rescue growth defects of cells. Furthermore, Grx3 inhibited iron accumulation in yeast cells and suppressed the sensitivity of mutant cells to exogenous oxidants. In mice, mRNA was ubiquitously expressed in developing embryos, adult tissues and organs, and was induced during oxidative stress. Mouse embryos absent of grew smaller with morphological defects and eventually died at 12.5 days of gestation. Analysis in mouse embryonic fibroblasts revealed that cells had impaired growth and cell cycle progression at the G/M phase, whereas the DNA replication during the S phase was not affected by deletion. Furthermore, Grx3‐knockdown HeLa cells displayed a significant delay in mitotic exit and had a higher percentage of binucleated cells. Therefore, our findings suggest that the mammalian Grx3 has conserved functions in protecting cells against oxidative stress and deletion of in mice causes early embryonic lethality which could be due to defective cell cycle progression during late mitosis. Structured digital abstract •   and   by   Mammalian monothiol Grx3 is able to rescue growth defects of yeast mutant cells and to protect cells against oxidative stress. Disruption of causes early embryo death. Mouse embryonic fibroblasts from null mice display impaired growth and cell cycle progression at the G2/M phase. The defective cell cycle progression during late mitosis may account for early embryonic lethality.
copOxford, UK
pubBlackwell Publishing Ltd
doi10.1111/j.1742-4658.2011.08178.x
pages2525-2539
date2011-07