دورية أكاديمية
أعرض في EDS

Cap-independent translation promotes C. elegans germ cell apoptosis through Apaf-1/CED-4 in a caspase-dependent mechanism.

التفاصيل البيبلوغرافية
العنوان: Cap-independent translation promotes C. elegans germ cell apoptosis through Apaf-1/CED-4 in a caspase-dependent mechanism.
المؤلفون: Contreras V; Department of Biochemistry and Molecular Biology, Brody School of Medicine at East Carolina University, Greenville, North Carolina, United States of America., Friday AJ, Morrison JK, Hao E, Keiper BD
المصدر: PloS one [PLoS One] 2011; Vol. 6 (9), pp. e24444. Date of Electronic Publication: 2011 Sep 01.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
اللغة: English
بيانات الدورية: Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
أسماء مطبوعة: Original Publication: San Francisco, CA : Public Library of Science
مواضيع طبية MeSH: Apoptosis* , Protein Biosynthesis*, Caenorhabditis elegans/*cytology , Caenorhabditis elegans Proteins/*metabolism , Calcium-Binding Proteins/*metabolism , Caspase 3/*metabolism , Germ Cells/*cytology , RNA Caps/*metabolism, Animals ; Apoptosomes/metabolism ; Apoptotic Protease-Activating Factor 1/metabolism ; Aspartic Acid/metabolism ; Base Sequence ; Binding Sites ; Biocatalysis ; Caenorhabditis elegans/metabolism ; Caspases/metabolism ; Eukaryotic Initiation Factor-4G/metabolism ; Germ Cells/metabolism ; Humans ; Molecular Sequence Data ; Protein Isoforms/metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Recombinant Proteins/metabolism ; Substrate Specificity
مستخلص: Apoptosis is a natural process during animal development for the programmed removal of superfluous cells. During apoptosis general protein synthesis is reduced, but the synthesis of cell death proteins is enhanced. Selective translation has been attributed to modification of the protein synthesis machinery to disrupt cap-dependent mRNA translation and induce a cap-independent mechanism. We have previously shown that disruption of the balance between cap-dependent and cap-independent C. elegans eIF4G isoforms (IFG-1 p170 and p130) by RNA interference promotes apoptosis in developing oocytes. Germ cell apoptosis was accompanied by the appearance of the Apaf-1 homolog, CED-4. Here we show that IFG-1 p170 is a native substrate of the worm executioner caspase, CED-3, just as mammalian eIF4GI is cleaved by caspase-3. Loss of Bcl-2 function (ced-9ts) in worms induced p170 cleavage in vivo, coincident with extensive germ cell apoptosis. Truncation of IFG-1 occurred at a single site that separates the cap-binding and ribosome-associated domains. Site-directed mutagenesis indicated that CED-3 processes IFG-1 at a non-canonical motif, TTTD(456). Coincidentally, the recognition site was located 65 amino acids downstream of the newly mapped IFG-1 p130 start site suggesting that both forms support cap-independent initiation. Genetic evidence confirmed that apoptosis induced by loss of ifg-1 p170 mRNA was caspase (ced-3) and apoptosome (ced-4/Apaf-1) dependent. These findings support a new paradigm in which modal changes in protein synthesis act as a physiological signal to initiate cell death, rather than occur merely as downstream consequences of the apoptotic event.
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المشرفين على المادة: 0 (Apoptosomes)
0 (Apoptotic Protease-Activating Factor 1)
0 (Caenorhabditis elegans Proteins)
0 (Calcium-Binding Proteins)
0 (Ced-4 protein, C elegans)
0 (Ced-9 protein, C elegans)
0 (Eukaryotic Initiation Factor-4G)
0 (Protein Isoforms)
0 (Proto-Oncogene Proteins c-bcl-2)
0 (RNA Caps)
0 (Recombinant Proteins)
30KYC7MIAI (Aspartic Acid)
EC 3.4.22.- (Caspase 3)
EC 3.4.22.- (Caspases)
EC 3.4.22.- (ced-3 protein, C elegans)
تواريخ الأحداث: Date Created: 20110913 Date Completed: 20120105 Latest Revision: 20211020
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC3164730
DOI: 10.1371/journal.pone.0024444
PMID: 21909434
قاعدة البيانات: MEDLINE
الوصف
تدمد:1932-6203
DOI:10.1371/journal.pone.0024444