scholarly journals The C-terminal region of subunit 4 (subunit b) is essential for assembly of the F0 portion of yeast mitochondrial ATP synthase

1992 ◽  
Vol 205 (1) ◽  
pp. 163-172 ◽  
Author(s):  
Marie-Francoise PAUL ◽  
Bernard GUERIN ◽  
Jean VELOURS
Keyword(s):  
Atp Synthase ◽  
Terminal Region ◽  
Mitochondrial Atp Synthase ◽  
Subunit B

scholarly journals Characterisation of a highly diverged mitochondrial ATP synthase peripheral stalk subunit b in Trypanosoma brucei

2021 ◽  
Author(s):  
Caroline E. Dewar ◽  
Silke Oeljeklaus ◽  
Bettina Warscheid ◽  
André Schneider
Keyword(s):  
Cell Cycle ◽  
Membrane Potential ◽  
Trypanosoma Brucei ◽  
Atp Synthase ◽  
Mitochondrial Protein ◽  
Normal Growth ◽  
Native Page ◽  
Peripheral Stalk ◽  
Mitochondrial Atp Synthase ◽  
Subunit B

The mitochondrial F1Fo ATP synthase of Trypanosoma brucei has been studied in detail. Whereas its F1 moiety is relatively highly conserved in structure and composition, the same is not the case for the Fo part and the peripheral stalk. A core subunit of the latter, the normally conserved subunit b, could not be identified in trypanosomes suggesting that it might be absent. Here we have identified a 17 kDa mitochondrial protein of the inner membrane that is essential for normal growth, efficient oxidative phosphorylation and membrane potential maintenance. Pulldown experiments and native PAGE analysis indicate that the protein is associated with the F1Fo ATP synthase. Its ablation reduces the levels of Fo subunits, but not those of F1, and disturbs the cell cycle. HHpred analysis showed that the protein has structural similarities to subunit b of other species, indicating that the Fo part of the trypanosomal ATP synthase does contain a highly diverged subunit b. Thus, the Fo part of the trypanosomal ATPase synthase may be more widely conserved than initially thought.

scholarly journals The ATP Synthase Deficiency in Human Diseases

Life ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 325
Author(s):  
Chiara Galber ◽  
Stefania Carissimi ◽  
Alessandra Baracca ◽  
Valentina Giorgio
Keyword(s):  
Oxidative Phosphorylation ◽  
Atp Synthase ◽  
Mitochondrial Protein ◽  
High Energy ◽  
Neurocognitive Disorders ◽  
Human Diseases ◽  
Age Related ◽  
Muscle Tissues ◽  
Mitochondrial Atp Synthase ◽  
Genes Encoding

Human diseases range from gene-associated to gene-non-associated disorders, including age-related diseases, neurodegenerative, neuromuscular, cardiovascular, diabetic diseases, neurocognitive disorders and cancer. Mitochondria participate to the cascades of pathogenic events leading to the onset and progression of these diseases independently of their association to mutations of genes encoding mitochondrial protein. Under physiological conditions, the mitochondrial ATP synthase provides the most energy of the cell via the oxidative phosphorylation. Alterations of oxidative phosphorylation mainly affect the tissues characterized by a high-energy metabolism, such as nervous, cardiac and skeletal muscle tissues. In this review, we focus on human diseases caused by altered expressions of ATP synthase genes of both mitochondrial and nuclear origin. Moreover, we describe the contribution of ATP synthase to the pathophysiological mechanisms of other human diseases such as cardiovascular, neurodegenerative diseases or neurocognitive disorders.

scholarly journals Lysine methylation of mitochondrial ATP synthase subunit c stored in tissues of dogs with hereditary ceroid lipofuscinosis

1994 ◽  
Vol 269 (13) ◽  
pp. 9906-9911
Author(s):  
M.L. Katz ◽  
J.S. Christianson ◽  
N.E. Norbury ◽  
C.L. Gao ◽  
A.N. Siakotos ◽  
...  
Keyword(s):  
Atp Synthase ◽  
Lysine Methylation ◽  
Subunit C ◽  
Ceroid Lipofuscinosis ◽  
Mitochondrial Atp Synthase
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