کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8398894 | 1544406 | 2018 | 35 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
A mitochondrial proteomics view of complex I deficiency in Candida albicans
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیوفیزیک
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چکیده انگلیسی
Fungal mitochondria are critical for fungal pathogenesis. The absence of any of the three fungal specific CI subunits in mitochondria causes an avirulence phenotype of C. albicans in a murine model of invasive disease. As model yeast (Saccharomyces cerevisiae) lacks a CI and is rarely a pathogen of humans, C. albicans is a better choice for establishing a link between mitochondrial CI and pathogenesis. Apart from the general effects of CI mutants on respiration, previous phenotyping of these mutants were quite similar to each other or to CI conservative subunit. By comparison to transcriptional data, the proteomic data obtained in this study indicate that biosynthetic events in each mutant such as cell wall and cell membrane phospholipids and ergosterol are generally decreased in both transcriptomal and translational levels. However, in the case of mitochondrial function, glycolysis/gluconeogenesis, and ROS scavengers, often gene changes are opposite that of proteomic data in mutants. We hypothesize that the loss of energy production in mutants is compensated by increases in protein levels of glycolysis, gluconeogenesis, and anti-ROS scavengers that at least extend mutant survival.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Mitochondrion - Volume 38, January 2018, Pages 48-57
Journal: Mitochondrion - Volume 38, January 2018, Pages 48-57
نویسندگان
Xiaodong She, Pengyi Zhang, Ying Gao, Lulu Zhang, Qiong Wang, Hui Chen, Richard Calderone, Weida Liu, Dongmei Li,