First Author | Kitamoto T | Year | 2005 |
Journal | Biochem Biophys Res Commun | Volume | 331 |
Issue | 4 | Pages | 1154-62 |
PubMed ID | 15882997 | Mgi Jnum | J:98284 |
Mgi Id | MGI:3577798 | Doi | 10.1016/j.bbrc.2005.03.241 |
Citation | Kitamoto T, et al. (2005) Functional redundancy of the Notch gene family during mouse embryogenesis: Analysis of Notch gene expression in Notch3-deficient mice. Biochem Biophys Res Commun 331(4):1154-62 |
abstractText | The Notch3 gene, a member of the Notch gene family, is expressed in a wide variety of tissues during development. We generated and analyzed Notch3-deficient mice to assess the in vivo role of the Notch3 gene. Consistent with previous observation of Krebs et al. [Characterization of Notch3-deficient mice: normal embryonic development and absence of genetic interactions with a Notch1 mutation, Genesis 37 (3) (2003) 139-143], the Notch3(-/-) mice were viable, fertile, and developed normally despite abundant expression of Notch3 in various embryonic tissues. We examined the details of Notch1, 2, and 4 expressions in the Notch3(-/-) embryos compared with those in wild-type embryos. As a result, we found that a deficiency in Notch3 did not affect the expression of Notch1, 2, and 4, and that either Notch1 or Notch2, or sometimes both, was always expressed in all Notch3-expressing tissues examined. These results support the idea that other Notch genes functionally compensate for Notch3 during embryonic development. We also surveyed the adult tissues of Notch3(-/-) mice and found significantly fewer thymocytes in 10-week-old mice. Therefore, the thymus might be a target tissue affected by Notch3 deficiency. |