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The Translational Regulators GCN-1 and ABCF-3 Act Together to Promote Apoptosis in


Apoptosis, also referred to as programmed cell death, is a crucial cellular process that eliminates unwanted cells during animal development and tissue homeostasis. Abnormal regulation of apoptosis can cause developmental defects and a variety of other human disorders, including cancer, neurodegenerative diseases and autoimmune diseases. Therefore, it is important to identify regulatory mechanisms that control apoptosis. Previous studies have demonstrated that the transcriptional induction of apoptotic genes can be crucial to initiating an apoptotic program. Less is known about translational controls of apoptosis. Here we report that the evolutionarily conserved C. elegans translational regulators GCN-1 and ABCF-3 promote apoptosis generally and act independently of the anti-apoptotic BCL-2 homolog CED-9. GCN-1 and ABCF-3 physically interact and maintain the phosphorylation level of eukaryotic initiation factor 2α, suggesting that GCN-1 and ABCF-3 act together to regulate the initiation of translation. We propose that the translational regulators GCN-1 and ABCF-3 maternally contribute to the proper execution of the apoptotic program.


Vyšlo v časopise: The Translational Regulators GCN-1 and ABCF-3 Act Together to Promote Apoptosis in. PLoS Genet 10(8): e32767. doi:10.1371/journal.pgen.1004512
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.pgen.1004512

Souhrn

Apoptosis, also referred to as programmed cell death, is a crucial cellular process that eliminates unwanted cells during animal development and tissue homeostasis. Abnormal regulation of apoptosis can cause developmental defects and a variety of other human disorders, including cancer, neurodegenerative diseases and autoimmune diseases. Therefore, it is important to identify regulatory mechanisms that control apoptosis. Previous studies have demonstrated that the transcriptional induction of apoptotic genes can be crucial to initiating an apoptotic program. Less is known about translational controls of apoptosis. Here we report that the evolutionarily conserved C. elegans translational regulators GCN-1 and ABCF-3 promote apoptosis generally and act independently of the anti-apoptotic BCL-2 homolog CED-9. GCN-1 and ABCF-3 physically interact and maintain the phosphorylation level of eukaryotic initiation factor 2α, suggesting that GCN-1 and ABCF-3 act together to regulate the initiation of translation. We propose that the translational regulators GCN-1 and ABCF-3 maternally contribute to the proper execution of the apoptotic program.


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