Epigenetic protection of vertebrate lymphoid progenitor cells by Dnmt1 Norimasa Iwanami, Kohei Takeshita, Divine-Fondzenyuy Lawir, Isao Suetake, Shoji Tajima, Katarzyna Sikora, Inês Trancoso, Connor P. O’Meara, Iliana Siamishi, Yousuke Takahama, Makoto Furutani-Seiki, Hisato Kondoh, Yasushige Yonezawa, Michael Schorpp, Thomas Boehm 

Erscheinungsform: einbändiges Werk
Autor/Urheber:
  • Iwanami, Norimasa
Beteiligte:
  • Takeshita, Kohei
  • Lawir, Divine Fondzenyuy
  • Suetake, Isao
  • Tajima, Shoji
  • Sikora, Katarzyna
  • Trancoso, Inês
  • O’Meara, Connor P.
  • Siamishi, Iliana
  • Takahama, Yousuke
  • Furutani-Seiki, Makoto
  • Kondoh, Hisato
  • Yonezawa, Yasushige
  • Schorpp, Michael
  • Boehm, Thomas
Umfang: 1 Online-Ressource (38 Seiten) Illustrationen, Diagramme
Identifikatoren/​Sonstige Nummern: 1758958189 [PPN]
Inhalt:
  • Abstract: DNA methylation is a universal epigenetic mechanism involved in regulation of gene expression and genome stability. The DNA maintenance methylase DNMT1 ensures that DNA methylation patterns are faithfully transmitted to daughter cells during cell division. Because loss of DNMT1 is lethal, a pan-organismic analysis of DNMT1 function is lacking. We identified new recessive dnmt1 alleles in medaka and zebrafish and, guided by the structures of mutant proteins, generated a recessive variant of mouse Dnmt1. Each of the three missense mutations studied here distorts the catalytic pocket and reduces enzymatic activity. Because all three DNMT1 mutant animals are viable, it was possible to examine their phenotypes throughout life. The consequences of genome-wide hypomethylation of DNA of somatic tissues in the Dnmt1 mutants are surprisingly mild but consistently affect the development of the lymphoid lineage. Our findings indicate that developing lymphocytes in vertebrates are sensitive to perturbations of DNA maintenance methylation
URL: https://nbn-resolving.de/urn:nbn:de:bsz:25-freidok-1757869
Weiter im Partnersystem: https://swb.bsz-bw.de/DB=2.1/PPNSET?PPN=1758958189
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