کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5508729 1400396 2017 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Sirtuin 5 protects mitochondria from fragmentation and degradation during starvation
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
Sirtuin 5 protects mitochondria from fragmentation and degradation during starvation
چکیده انگلیسی


- Deletion of Sirt5 increases the levels of MiD51 and Fis1.
- Ablation of Sirt5 induces mitochondrial DRP1 accumulation and mitochondrial fission.
- Deletion of Sirt5 blocks the starvation-induced mitochondrial elongation.
- Sirt5 modulates mitophagy during starvation.

During starvation, intra-mitochondrial sirtuins, NAD+ sensitive deacylating enzymes that modulate metabolic homeostasis and survival, directly adjust mitochondrial function to nutrient availability; concomitantly, mitochondria elongate to escape autophagic degradation. However, whether sirtuins also impinge on mitochondrial dynamics is still uncharacterized. Here we show that the mitochondrial Sirtuin 5 (Sirt5) is essential for starvation induced mitochondrial elongation. Deletion of Sirt5 in mouse embryonic fibroblasts increased levels of mitochondrial dynamics of 51 kDa protein and mitochondrial fission protein 1, leading to mitochondrial accumulation of the pro-fission dynamin related protein 1 and to mitochondrial fragmentation. During starvation, Sirt5 deletion blunted mitochondrial elongation, resulting in increased mitophagy. Our results indicate that starvation induced mitochondrial elongation and evasion from autophagic degradation requires the energy sensor Sirt5.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1864, Issue 1, January 2017, Pages 169-176
نویسندگان
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