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Amino-terminal phosphorylation of c-Jun regulates stress-induced apoptosis and cellular proliferation.

Abstract：

:c-Jun is a major component of the heterodimeric transcription factor AP-1 and is essential for embryonic development, as fetuses lacking Jun die at mid-gestation with impaired hepatogenesis and primary Jun-/- fibroblasts have a severe proliferation defect and undergo premature senescence in vitro. c-Jun and AP-1 activities are regulated by c-Jun N-terminal phosphorylation (JNP) at serines 63 and 73 through Jun N-terminal kinases(JNKs). JNP is thought to be required for the anti-apoptotic function of c-Jun during hepatogenesis, as mice lacking the JNK kinase SEK1 exhibit liver defects similar to those seen in Jun-/- fetuses. To investigate the physiological relevance of JNP, we replaced endogenous Jun by a mutant Jun allele with serines 63 and 73 mutated to alanines (Jun(tm1wag); hereafter referred to as JunAA). Here we show that primary JunAA fibroblasts have proliferation- and stress-induced apoptotic defects, accompanied by reduced AP-1 activity. JunAA mice are viable and fertile, smaller than controls and resistant to epileptic seizures and neuronal apoptosis induced by the excitatory amino acid kainate. Primary mutant neurons are also protected from apoptosis and exhibit unaltered JNK activity. Our results provide evidence that JNP is dispensable for mouse development, and identify c-Jun as the essential substrate of JNK signalling during kainate-induced neuronal apoptosis.

journal_name

Nat Genet

journal_title

Nature genetics

authors

Behrens A,Sibilia M,Wagner EF

doi

10.1038/6854

keywords:

subject

Has Abstract

pub_date

1999-03-01 00:00:00

pages

326-9

issue

3

eissn

1061-4036

issn

1546-1718

journal_volume

21

pub_type

杂志文章

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