Naa12 compensates for Naa10 in mice in the amino-terminal acetylation pathway
- 주제(기타) Biology
- 설명문(일반) [Kweon, Hyae Yon; Lee, Mi-Ni; Seo, Seungwoon; Sonn, Seong-Keun; Jeon, Sejin; Kim, Taesoo; Kim, Hyun-Seok; Oh, Goo Taeg] Ewha Womans Univ, Dept Life Sci, Seoul, South Korea; [Kweon, Hyae Yon; Lee, Mi-Ni; Seo, Seungwoon; Sonn, Seong-Keun; Jeon, Sejin; Kim, Taesoo; Kim, Hyun-Seok; Oh, Goo Taeg] Ewha Womans Univ, Coll Nat Sci, Seoul, South Korea; [Lee, Mi-Ni] Lab Anim Resource Ctr Korea ResearchInst Biosci &, Chungbuk, South Korea; [Dorfel, Max; PaPazyan, Thomas; Crain, Jonathan; Sebold, Alison; Lyons, Scott; Ismail, Ahmed; Lyon, Gholson J.] Cold Spring Harbor Lab, Stanley Inst Cognit Genom, Woodbury, NY 11724 USA; [Gottlieb, Leah; Marmorstein, Ronen] Univ Penn, Dept Chem, Philadelphia, PA 19104 USA; [Gottlieb, Leah; Marmorstein, Ronen] Univ Penn, Perelman Sch Med, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA; [McTiernan, Nina; Ree, Rasmus; Arnesen, Thomas] Univ Bergen, Dept Biomed, Bergen, Norway; [Bolton, David] New York State Inst Basic Res Dev Disabil, Dept Mol Biol, 1050 Forest Hill Rd, Staten Isl, NY 10314 USA; [Garcia, Andrew; Marchi, Elaine; Lyon, Gholson J.] New York State Inst Basic Res Dev Disabil, Dept Human Genet, 1050 Forest Hill Rd, Staten Isl, NY 10314 USA; [Flory, Michael] New York State Inst Basic Res Dev Disabil, Res Design & Anal Serv, 1050 Forest Hill Rd, Staten Isl, NY 10314 USA; [Jeong, Se-Jin] Washington Univ, Sch Med, Ctr Cardiovasc Res, St Louis, MO USA; [Ju, Shinyeong; Lee, Cheolju] Korea Inst Sci & Technol, Ctr Theragnosis, Seoul, South Korea; [Conway, Simon J.] Indiana Univ Sch Med, Herman B Wells Ctr Pediat Res, Indianapolis, IN 46202 USA; [Lee, Cheolju] Kyung Hee Univ, Dept Converging Sci & Technol, KHU KIST, Seoul, South Korea; [Roh, Tae-Young] Pohang Univ Sci & Technol, Dept Life Sci, Pohang, South Korea; [Arnesen, Thomas] Univ Bergen, Dept Biol Sci, Bergen, Norway; [Arnesen, Thomas] Haukeland Hosp, Dept Surg, Bergen, Norway; [Marmorstein, Ronen] Univ Penn, Perelman Sch Med, Dept Biochem & Biophys, Philadelphia, PA 19104 USA; [Lyon, Gholson J.] CUNY, Grad Ctr, Biol PhD Program, New York, NY 10010 USA; [Lyon, Gholson J.] New York State Inst Basic Res Dev Disabil, George A Jervis Clin, 1050 Forest Hill Rd, Staten Isl, NY 10314 USA; [Lee, Mi-Ni] Korea Res Inst Biosci & Biotechnol, Lab Anim Resource Ctr, Chungbuk, South Korea
- 등재 SCIE, SCOPUS
- 발행기관 ELIFE SCIENCES PUBLICATIONS LTD
- 발행년도 2021
- 총서유형 Journal
- URI http://www.dcollection.net/handler/ewha/000000183455
- 본문언어 영어
- Published As http://dx.doi.org/10.7554/eLife.65952
초록/요약
Amino-terminal acetylation is catalyzed by a set of N-terminal acetyltransferases (NATs). The NatA complex (including X-linked Naa10 and Naa15) is the major acetyltransferase, with 40-50% of all mammalian proteins being potential substrates. However, the overall role of amino-terminal acetylation on a whole-organism level is poorly understood, particularly in mammals. Male mice lacking Naa10 show no globally apparent in vivo amino-terminal acetylation impairment and do not exhibit complete embryonic lethality. Rather Naa10 nulls display increased neonatal lethality, and the majority of surviving undersized mutants exhibit a combination of hydrocephaly, cardiac defects, homeotic anterior transformation, piebaldism, and urogenital anomalies. Naa12 is a previously unannotated Naa10-like paralog with NAT activity that genetically compensates for Naa10. Mice deficient for Naa12 have no apparent phenotype, whereas mice deficient for Naa10 and Naa12 display embryonic lethality. The discovery of Naa12 adds to the currently known machinery involved in amino-terminal acetylation in mice.
more