作者: Laurie Jo Kurihara , Ekaterina Semenova , John M. Levorse , Shirley M. Tilghman
DOI: 10.1128/MCB.20.7.2498-2504.2000
关键词:
摘要: Mice homozygous for the s(1Acrg) deletion at Ednrb locus arrest embryonic day 8.5. To determine molecular basis of this defect, we initiated positional cloning minimal region. The mouse Uch-L3 (ubiquitin C-terminal hydrolase L3) gene was mapped within Because transcripts were present in structures relevant to phenotype, created a targeted mutation address its role during development and possible contribution phenotype. Uch-L3(Delta3-7) viable, with no obvious developmental or histological abnormalities. Although high levels RNA detected testes thymus, homozygotes fertile, defect intrathymic T-cell differentiation detected. We conclude that phenotype is either complex multigenic due loss another propose may be functionally redundant homologue Uch-L1.