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Nature 376, 167-170 (13 July 1995) | doi:10.1038/376167a0; Accepted 16 May 1995
Embryonic lethality and liver degeneration in mice lacking the RelA component
of NF-
B
Amer A. Beg*, William C. Sha*, Roderick T. Bronson†, Sankar Ghosh‡ & David Baltimore§
Abstract
NF-
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 stress1. Indeed, although
developmentally normal, mice deficient in p50 display functional defects in immune
responses2. Here we describe the generation of mice deficient in the
RelA subunit of NF-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 IB
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-B-regulated pathways.
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