The Pax5 gene encodes a transcription factor important during B cell development, as well as brain development and spermatogenesis. Mutations in the human PAX5 gene are associated with several lymphomas. These Pax5lacZ mice carry an in-frame insertion of lacZ in exon 2, which disrupts gene expression and serves as a reporter. Homozygotes are postnatal lethal, dying at approximately 3 weeks of age. Mice that are heterozygous for the targeted mutation are viable and fertile. No gene product (mRNA) is detected by RNase protection assay of 12.5 day old embryos, spleen from 2 week old homozygous, and testes from 6 month old homozygous. Homozygotes, while indistinguishable from littermates at birth, exhibit growth delays by 2 weeks of age, weighing approximately 1/3 of the wildtype control weight. Homozygotes on the 129 background exhibit limb-clasping, reduced posterior midbrain regions, anterior expansion of the cerebellar culmen, and abnormal cerebellar foliation. Heterozygotes on the mixed B6;129S2 background, exhibit abnormal cerebellar morphology. On the mixed B6;129S2 background, homozygotes display arrested B cell development at the pro-B cell stage, with an increased number of mature T cells detected in the spleen. Homozygotes are are osteopenic, with increased number of osteoclasts. During backcrossing, the Y chromosome may not have been fixed to the C57BL/6J genetic background.

This Pax5lacZ knockout strain homozygous postnatal lethality, abnormal cerebellar morphology and arrested B cell differentiation. These mice may be suitable for use in studies related to B lymphopoiesis and CNS development.

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