Developmental silencing and independency from E2F of apoptotic gene expression in postmitotic tissues
Copyright policy )Developmental silencing and independency from E2F of apoptotic gene expression in postmitotic tissues
The involvement of caspases in postmitotic cell death is controversial. Here we report that adult brain and heart are devoid of many key pro‐apoptotic proteins due to a progressive postnatal silencing event involving a reduction of their transcript levels. E2F has been shown to control cell cycle progression and to be transcriptional activator of apoptotic genes. However, our data demonstrate that apoptotic gene expression in heart, brain and liver, as well as cardiac and neuronal apoptotic gene silencing during development, are E2F‐independent events. Therefore, the genes regulating caspase‐dependent cell death are expressed in embryonic organs in an E2F‐independent manner and a developmental‐related silencing event represses these genes in postmitotic adult tissues.
Male, Mitosis, Apoptosis, Development, Mice, E2F, Animals, Humans, Myocytes, Cardiac, Gene Silencing, RNA, Messenger, Cells, Cultured, Mice, Knockout, Gene Expression Profiling, Myocardium, Brain, Gene Expression Regulation, Developmental, Heart, Embryo, Mammalian, Caspase, E2F Transcription Factors, Rats, Animals, Newborn, Caspases
Male, Mitosis, Apoptosis, Development, Mice, E2F, Animals, Humans, Myocytes, Cardiac, Gene Silencing, RNA, Messenger, Cells, Cultured, Mice, Knockout, Gene Expression Profiling, Myocardium, Brain, Gene Expression Regulation, Developmental, Heart, Embryo, Mammalian, Caspase, E2F Transcription Factors, Rats, Animals, Newborn, Caspases
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