Embryonic lethality and liver degeneration in mice lacking the RelA componenet of NF-kappa B.
Beg, Amer A.; Sha, William C.; Bronson, Roderick T.; Ghosh, Sankar; Baltimore, David
[Letter] Nature. 376(6536):167-170, July 13, 1995.

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NF-kappa B, which consists of two polypeptides, p50 (Mr 50K) and p65/RelA (Mr 65K), is thought to be a key regulator of genes involved in responses to infection, inflammation and stress [1]. Indeed, although developmentally normal, mice deficient in p50 display functional defects in immune responses [2]. Here we describe the generation of mice deficient in the RelA subunit of NF-kappa B. Disruption of the relA locus leads to embryonic lethality at 15-16 days of gestation, concomitant with a massive degeneration of the liver by programmed cell death or apoptosis. Embryonic fibroblasts from RelA-deficient mice are defective in the tumour necrosis factor (TNF)-mediated induction of messenger RNAs for I kappa B alpha and granulocyte/macrophage colony stimulating factor (GM-CSF), although basal levels of these transcripts are unaltered. These results indicate that RelA controls inducible, but not basal, transcription in NF-kappa B-regulated pathways.

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