Requirement of the RNA-editing enzyme ADAR2 for normal physiology in mice

Marion Horsch; Peter H. Seeburg; Thure Adler; Juan Antonio Aguilar-Pimentel; Lore Becker; Julia Calzada-Wack; Lilian Garrett; Alexander Götz; Wolfgang Hans; Miyoko Higuchi; Sabine M. Hölter; Beatrix Naton; Cornelia Prehn; Oliver Puk; Ildikó Rácz; Birgit Rathkolb; Jan Rozman; Anja Schrewe; Jerzy Adamski; Dirk H. Busch; Irene Esposito; Jochen Graw; Boris Ivandic; Martin Klingenspor; Thomas Klopstock; Martin Mempel; Markus Ollert; Holger Schulz; Eckhard Wolf; Wolfgang Wurst; Andreas Zimmer; Valérie Gailus-Durner; Helmut Fuchs; Martin Hrabě De Angelis; Johannes Beckersa

doi:10.1074/jbc.M110.200881

Requirement of the RNA-editing enzyme ADAR2 for normal physiology in mice

Marion Horsch, Peter H. Seeburg, Thure Adler, Juan Antonio Aguilar-Pimentel, Lore Becker, Julia Calzada-Wack, Lilian Garrett, Alexander Götz, Wolfgang Hans, Miyoko Higuchi, Sabine M. Hölter, Beatrix Naton, Cornelia Prehn, Oliver Puk, Ildikó Rácz, Birgit Rathkolb, Jan Rozman, Anja Schrewe, Jerzy Adamski, Dirk H. BuschIrene Esposito, Jochen Graw, Boris Ivandic, Martin Klingenspor, Thomas Klopstock, Martin Mempel, Markus Ollert, Holger Schulz, Eckhard Wolf, Wolfgang Wurst, Andreas Zimmer, Valérie Gailus-Durner, Helmut Fuchs, Martin Hrabě De Angelis, Johannes Beckersa

Lehrstuhl für Molekulare Ernährungsmedizin

Publikation: Beitrag in Fachzeitschrift › Artikel › Begutachtung

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Abstract

ADAR2, an RNA editing enzyme that converts specific adenosines to inosines in certain pre-mRNAs, often leading to amino acid substitutions in the encoded proteins, is mainly expressed in brain. Of all ADAR2-mediated edits, a single one in the pre-mRNA of the AMPA receptor subunit GluA2 is essential for survival. Hence, early postnatal death of mice lacking ADAR2 is averted when the critical edit is engineered into both GluA2 encoding Gria2 alleles. Adar2 ^-/-/Gria2^R/R mice display normal appearance and life span, but the general phenotypic effects of global lack of ADAR2 have remained unexplored. Here we have employed the Adar2^-/-/Gria2^R/R mouse line, and Gria2^R/R mice as controls, to study the phenotypic consequences of loss of all ADAR2-mediated edits except the critical one in GluA2. Our extended phenotypic analysis covering ∼320 parameters identified significant changes related to absence of ADAR2 in behavior, hearing ability, allergy parameters and transcript profiles of brain.

Originalsprache	Englisch
Seiten (von - bis)	18614-18622
Seitenumfang	9
Fachzeitschrift	Journal of Biological Chemistry
Jahrgang	286
Ausgabenummer	21
DOIs	https://doi.org/10.1074/jbc.M110.200881
Publikationsstatus	Veröffentlicht - 27 Mai 2011

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Horsch, M., Seeburg, P. H., Adler, T., Aguilar-Pimentel, J. A., Becker, L., Calzada-Wack, J., Garrett, L., Götz, A., Hans, W., Higuchi, M., Hölter, S. M., Naton, B., Prehn, C., Puk, O., Rácz, I., Rathkolb, B., Rozman, J., Schrewe, A., Adamski, J., ... Beckersa, J. (2011). Requirement of the RNA-editing enzyme ADAR2 for normal physiology in mice. Journal of Biological Chemistry, 286(21), 18614-18622. https://doi.org/10.1074/jbc.M110.200881

@article{603996dd99954cd5b22e832793ea4856,

title = "Requirement of the RNA-editing enzyme ADAR2 for normal physiology in mice",

abstract = "ADAR2, an RNA editing enzyme that converts specific adenosines to inosines in certain pre-mRNAs, often leading to amino acid substitutions in the encoded proteins, is mainly expressed in brain. Of all ADAR2-mediated edits, a single one in the pre-mRNA of the AMPA receptor subunit GluA2 is essential for survival. Hence, early postnatal death of mice lacking ADAR2 is averted when the critical edit is engineered into both GluA2 encoding Gria2 alleles. Adar2 -/-/Gria2R/R mice display normal appearance and life span, but the general phenotypic effects of global lack of ADAR2 have remained unexplored. Here we have employed the Adar2-/-/Gria2R/R mouse line, and Gria2R/R mice as controls, to study the phenotypic consequences of loss of all ADAR2-mediated edits except the critical one in GluA2. Our extended phenotypic analysis covering ∼320 parameters identified significant changes related to absence of ADAR2 in behavior, hearing ability, allergy parameters and transcript profiles of brain.",

author = "Marion Horsch and Seeburg, {Peter H.} and Thure Adler and Aguilar-Pimentel, {Juan Antonio} and Lore Becker and Julia Calzada-Wack and Lilian Garrett and Alexander G{\"o}tz and Wolfgang Hans and Miyoko Higuchi and H{\"o}lter, {Sabine M.} and Beatrix Naton and Cornelia Prehn and Oliver Puk and Ildik{\'o} R{\'a}cz and Birgit Rathkolb and Jan Rozman and Anja Schrewe and Jerzy Adamski and Busch, {Dirk H.} and Irene Esposito and Jochen Graw and Boris Ivandic and Martin Klingenspor and Thomas Klopstock and Martin Mempel and Markus Ollert and Holger Schulz and Eckhard Wolf and Wolfgang Wurst and Andreas Zimmer and Val{\'e}rie Gailus-Durner and Helmut Fuchs and {De Angelis}, {Martin Hrab{\v e}} and Johannes Beckersa",

year = "2011",

month = may,

day = "27",

doi = "10.1074/jbc.M110.200881",

language = "English",

volume = "286",

pages = "18614--18622",

journal = "Journal of Biological Chemistry",

issn = "0021-9258",

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Horsch, M, Seeburg, PH, Adler, T, Aguilar-Pimentel, JA, Becker, L, Calzada-Wack, J, Garrett, L, Götz, A, Hans, W, Higuchi, M, Hölter, SM, Naton, B, Prehn, C, Puk, O, Rácz, I, Rathkolb, B, Rozman, J, Schrewe, A, Adamski, J, Busch, DH, Esposito, I, Graw, J, Ivandic, B, Klingenspor, M, Klopstock, T, Mempel, M, Ollert, M, Schulz, H, Wolf, E, Wurst, W, Zimmer, A, Gailus-Durner, V, Fuchs, H, De Angelis, MH & Beckersa, J 2011, 'Requirement of the RNA-editing enzyme ADAR2 for normal physiology in mice', Journal of Biological Chemistry, Jg. 286, Nr. 21, S. 18614-18622. https://doi.org/10.1074/jbc.M110.200881

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T1 - Requirement of the RNA-editing enzyme ADAR2 for normal physiology in mice

AU - Horsch, Marion

AU - Seeburg, Peter H.

AU - Adler, Thure

AU - Aguilar-Pimentel, Juan Antonio

AU - Becker, Lore

AU - Calzada-Wack, Julia

AU - Garrett, Lilian

AU - Götz, Alexander

AU - Hans, Wolfgang

AU - Higuchi, Miyoko

AU - Hölter, Sabine M.

AU - Naton, Beatrix

AU - Prehn, Cornelia

AU - Puk, Oliver

AU - Rácz, Ildikó

AU - Rathkolb, Birgit

AU - Rozman, Jan

AU - Schrewe, Anja

AU - Adamski, Jerzy

AU - Busch, Dirk H.

AU - Esposito, Irene

AU - Graw, Jochen

AU - Ivandic, Boris

AU - Klingenspor, Martin

AU - Klopstock, Thomas

AU - Mempel, Martin

AU - Ollert, Markus

AU - Schulz, Holger

AU - Wolf, Eckhard

AU - Wurst, Wolfgang

AU - Zimmer, Andreas

AU - Gailus-Durner, Valérie

AU - Fuchs, Helmut

AU - De Angelis, Martin Hrabě

AU - Beckersa, Johannes

PY - 2011/5/27

Y1 - 2011/5/27

N2 - ADAR2, an RNA editing enzyme that converts specific adenosines to inosines in certain pre-mRNAs, often leading to amino acid substitutions in the encoded proteins, is mainly expressed in brain. Of all ADAR2-mediated edits, a single one in the pre-mRNA of the AMPA receptor subunit GluA2 is essential for survival. Hence, early postnatal death of mice lacking ADAR2 is averted when the critical edit is engineered into both GluA2 encoding Gria2 alleles. Adar2 -/-/Gria2R/R mice display normal appearance and life span, but the general phenotypic effects of global lack of ADAR2 have remained unexplored. Here we have employed the Adar2-/-/Gria2R/R mouse line, and Gria2R/R mice as controls, to study the phenotypic consequences of loss of all ADAR2-mediated edits except the critical one in GluA2. Our extended phenotypic analysis covering ∼320 parameters identified significant changes related to absence of ADAR2 in behavior, hearing ability, allergy parameters and transcript profiles of brain.

AB - ADAR2, an RNA editing enzyme that converts specific adenosines to inosines in certain pre-mRNAs, often leading to amino acid substitutions in the encoded proteins, is mainly expressed in brain. Of all ADAR2-mediated edits, a single one in the pre-mRNA of the AMPA receptor subunit GluA2 is essential for survival. Hence, early postnatal death of mice lacking ADAR2 is averted when the critical edit is engineered into both GluA2 encoding Gria2 alleles. Adar2 -/-/Gria2R/R mice display normal appearance and life span, but the general phenotypic effects of global lack of ADAR2 have remained unexplored. Here we have employed the Adar2-/-/Gria2R/R mouse line, and Gria2R/R mice as controls, to study the phenotypic consequences of loss of all ADAR2-mediated edits except the critical one in GluA2. Our extended phenotypic analysis covering ∼320 parameters identified significant changes related to absence of ADAR2 in behavior, hearing ability, allergy parameters and transcript profiles of brain.

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U2 - 10.1074/jbc.M110.200881

DO - 10.1074/jbc.M110.200881

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AN - SCOPUS:79956313243

SN - 0021-9258

VL - 286

SP - 18614

EP - 18622

JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

IS - 21

ER -

Requirement of the RNA-editing enzyme ADAR2 for normal physiology in mice

Abstract

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