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Failure to Degrade Poly(ADP-Ribose) Causes Increased Sensitivity to Cytotoxicity and Early Embryonic Lethality

by Wattler, Sigrid , Dawson, Ted M. , Koh, David W. , Dawson, Valina L. , Snyder, Solomon H. , Poitras, Marc F. , Stöger, Tobias , Sasaki, Masayuki , Nehls, Michael C. , Lawler, Ann M. , Poirier, Guy G.

in Alleles / Animals / Apoptosis / Biological Sciences / Blastocyst / Blastocyst - cytology / Blastocyst - metabolism / Cell death / Cell growth / Cell Proliferation / Cellular biology / Cultured cells / Cytotoxicity / Delta cells / DNA damage / Embryo Loss - chemically induced / Embryo Loss - embryology / Embryo Loss - enzymology / Embryo Loss - metabolism / Embryonic growth stage / Embryos / Enzymes / Female / Genetics / Glycoside Hydrolases - deficiency / Glycoside Hydrolases - genetics / Glycoside Hydrolases - metabolism / Methylnitronitrosoguanidine - pharmacology / Methylnitronitrosoguanidine - toxicity / Mice / Mice, Knockout / Poly (ADP-Ribose) Polymerase-1 / Poly Adenosine Diphosphate Ribose - metabolism / Poly(ADP-ribose) Polymerases - metabolism / Pregnancy / Proteins / Stem cells / Trophoblasts - cytology / Trophoblasts - metabolism / Vitamin K 3 - pharmacology / Vitamin K 3 - toxicity

2004

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Failure to Degrade Poly(ADP-Ribose) Causes Increased Sensitivity to Cytotoxicity and Early Embryonic Lethality

2004

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Failure to Degrade Poly(ADP-Ribose) Causes Increased Sensitivity to Cytotoxicity and Early Embryonic Lethality

2004

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Journal Article

Failure to Degrade Poly(ADP-Ribose) Causes Increased Sensitivity to Cytotoxicity and Early Embryonic Lethality

Wattler, Sigrid,

Dawson, Ted M.,

Koh, David W.,

Dawson, Valina L.,

Snyder, Solomon H.,

Poitras, Marc F.,

Stöger, Tobias,

Sasaki, Masayuki,

Nehls, Michael C.,

Lawler, Ann M.,

Poirier, Guy G.

2004

Overview

The metabolism of poly(ADP-ribose) (PAR) is critical for genomic stability in multicellular eukaryotes. Here, we show that the failure to degrade PAR by means of disruption of the murine poly(ADP-ribose) glycohydrolase (PARG) gene unexpectedly causes early embryonic lethality and enhanced sensitivity to genotoxic stress. This lethality results from the failure to hydrolyze PAR, because PARG null embryonic day (E) 3.5 blastocysts accumulate PAR and concurrently undergo apoptosis. Moreover, embryonic trophoblast stem cell lines established from early PARG null embryos are viable only when cultured in medium containing the poly(ADP-ribose) polymerase inhibitor benzamide. Cells lacking PARG also show reduced growth, accumulation of PAR, and increased sensitivity to cytotoxicity induced by N-methyl-N′-nitro-N-nitrosoguanidine and menadione after benzamide withdrawal. These results provide compelling evidence that the failure to degrade PAR has deleterious consequences. Further, they define a role for PARG in embryonic development and a protective role in the response to genotoxic stress.

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Publisher

National Academy of Sciences,National Acad Sciences

Subject

Alleles

/ Animals

/ Apoptosis

/ Biological Sciences

/ Blastocyst

/ Blastocyst - cytology

/ Blastocyst - metabolism