Distinct Morphological and Behavioural Alterations in ENU-Induced Heterozygous Mutant Mice.

(transient receptor potential cation channel, subfamily C, member 7; 862 amino acids) knockout mice are described showing no clear phenotypic alterations, therefore, the functional relevance of the gene remains unclear. A complementary approach for the functional analysis of a given gene is the examination of individuals harbouring a mutant allele of the gene. In the phenotype-driven Munich ENU mouse mutagenesis project, a high number of phenotypic parameters was used for establishing novel mouse models on the genetic background of C3H inbred mice.

Novel mouse mutants with primary cellular immunodeficiencies generated by genome-wide mutagenesis.

Background: Primary cellular immunodeficiencies are a group of genetic disorders in which 1 or more components of the cellular immune system are lacking or dysfunctional.

Objective: We sought to identify novel mouse mutants that display primary cellular immunodeficiencies.

Methods: Genome-wide N-ethyl-N-nitrosourea mutagenesis was performed in mice, followed by a phenotype screen of immunologic blood parameters.