• Media type: E-Article
  • Title: A novel knockout mouse for the small EDRK-rich factor 2 (Serf2) showing developmental and other deficits
  • Contributor: Cleverley, Karen; Lee, Weaverly Colleen; Mumford, Paige; Collins, Toby; Rickman, Matthew; Cunningham, Thomas J.; Cleak, James; Mianne, Joffrey; Szoke-Kovacs, Zsombor; Stewart, Michelle; Teboul, Lydia; Maduro, Cheryl; Wells, Sara; Wiseman, Frances K.; Fisher, Elizabeth M. C.
  • imprint: Springer Science and Business Media LLC, 2021
  • Published in: Mammalian Genome
  • Language: English
  • DOI: 10.1007/s00335-021-09864-6
  • ISSN: 0938-8990; 1432-1777
  • Keywords: Genetics
  • Origination:
  • Footnote:
  • Description: <jats:title>Abstract</jats:title><jats:p>The small EDRK-rich factor 2 (SERF2) is a highly conserved protein that modifies amyloid fibre assembly in vitro and promotes protein misfolding. However, the role of SERF2 in regulating age-related proteotoxicity remains largely unexplored due to a lack of in vivo models. Here, we report the generation of <jats:italic>Serf2</jats:italic> knockout mice using an ES cell targeting approach, with <jats:italic>Serf2</jats:italic> knockout alleles being bred onto different defined genetic backgrounds. We highlight phenotyping data from heterozygous <jats:italic>Serf2</jats:italic><jats:sup>+/−</jats:sup> mice, including unexpected male-specific phenotypes in startle response and pre-pulse inhibition. We report embryonic lethality in <jats:italic>Serf2</jats:italic><jats:sup>−/−</jats:sup> null animals when bred onto a C57BL/6 N background. However, homozygous null animals were viable on a mixed genetic background and, remarkably, developed without obvious abnormalities. The <jats:italic>Serf2</jats:italic> knockout mice provide a powerful tool to further investigate the role of SERF2 protein in previously unexplored pathophysiological pathways in the context of a whole organism.</jats:p>