scholarly journals Downregulation of DJ-1 Fails to Protect Mitochondrial Complex I Subunit NDUFS3 in the Testes and Contributes to the Asthenozoospermia

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Yupeng Wang ◽  
Yi Sun ◽  
Xin Zhao ◽  
Renpei Yuan ◽  
Hui Jiang ◽  
...  
Keyword(s):  
Male Infertility ◽  
Complex I ◽  
Mitochondrial Protein ◽  
Protein Product ◽  
Mitochondrial Activity ◽  
Mitochondrial Complex ◽  
Specific Mechanism ◽  
Nicotinamide Adenine Dinucleotide Dehydrogenase ◽  
Complex I Activity ◽  
Mitochondria Complex I

Asthenozoospermia (AS), an important cause of male infertility, is characterized by reduced sperm motility. Among the aetiologies of AS, inflammation seems to be the main cause. DJ-1, a conserved protein product of thePARK7gene, is associated with male infertility and plays a role in oxidative stress and inflammation. Although our previous studies showed that a reduction in DJ-1 was accompanied by mitochondrial dysfunction in the sperm of patients with AS, the specific mechanism underlying this association remained unclear. In this study, we found that compared to the patients without AS, the expression of mitochondrial protein nicotinamide adenine dinucleotide dehydrogenase (ubiquinone) Fe-S protein 3 (NDUFS3) was also significantly decreased in the sperm of patients with AS. Similarly, decreased expression of DJ-1 and NDUFS3 and reduced mitochondria complex I activity were evident in a rat model of AS. Moreover, we showed that the interaction between DJ-1 and NDUFS3 in rat testes was weakened by ORN treatment. These results suggest that the impaired mitochondrial activity could be due to the broken interaction between DJ-1 and NDUFS3 and that downregulation of DJ-1 in sperm and testes contributes to AS pathogenesis.

Mutants of Chlamydomonas reinhardtii Deficient in Mitochondrial Complex I: Characterization of Two Mutations Affecting the nd1 Coding Sequence

Genetics ◽  
2001 ◽  
Vol 158 (3) ◽  
pp. 1051-1060
Author(s):  
Claire Remacle ◽  
Denis Baurain ◽  
Pierre Cardol ◽  
René F Matagne
Keyword(s):  
Mitochondrial Genome ◽  
Chlamydomonas Reinhardtii ◽  
Complex I ◽  
Slow Growth ◽  
Nadh:Ubiquinone Oxidoreductase ◽  
Sequencing Analysis ◽  
Mitochondrial Complex ◽  
Genetical Analysis ◽  
Complex I Activity

Abstract The mitochondrial rotenone-sensitive NADH:ubiquinone oxidoreductase (complex I) comprises more than 30 subunits, the majority of which are encoded by the nucleus. In Chlamydomonas reinhardtii, only five components of complex I are coded for by mitochondrial genes. Three mutants deprived of complex I activity and displaying slow growth in the dark were isolated after mutagenic treatment with acriflavine. A genetical analysis demonstrated that two mutations (dum20 and dum25) affect the mitochondrial genome whereas the third mutation (dn26) is of nuclear origin. Recombinational analyses showed that dum20 and dum25 are closely linked on the genetic map of the mitochondrial genome and could affect the nd1 gene. A sequencing analysis confirmed this conclusion: dum20 is a deletion of one T at codon 243 of nd1; dum25 corresponds to a 6-bp deletion that eliminates two amino acids located in a very conserved hydrophilic segment of the protein.

CFM6 is an Essential CRM Protein Required for the Splicing of nad5 Transcript in Arabidopsis Mitochondria

2021 ◽  
Author(s):  
Wei-Chih Lin ◽  
Ya-Huei Chen ◽  
Shin-Yuan Gu ◽  
Hwei-Ling Shen ◽  
Kai-Chau Huang ◽  
...  
Keyword(s):  
Complex I ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
High Accumulation ◽  
Stunted Growth ◽  
Growth Defects ◽  
Group I ◽  
Or Genes ◽  
Complex I Activity ◽  
Intron 4

Abstract Plant CRM domain-containing proteins are capable of binding RNA to facilitate the splicing of group I or II introns in chloroplasts, but their functions in mitochondria are less clear. In the present study, Arabidopsis thaliana CFM6, a protein with a single CRM domain, was expressed in most plant tissues, particularly in flower tissues, and restricted to mitochondria. Mutation of CFM6 causes severe growth defects, including stunted growth, curled leaves, delayed embryogenesis, and pollen development. CFM6 functions specifically in the splicing of group II intron 4 of nad5, which encodes a subunit of mitochondrial complex I, as evidenced by the loss of nad5 intron 4 splicing and high accumulation of its pretranscripts in cfm6 mutants. The phenotypic and splicing defects of cfm6 were rescued in transgenic plants overexpressing 35S::CFM6-YFP. Splicing failure in cfm6 also led to the loss of complex I activity and to its improper assembly. Moreover, dysfunction of complex I induced the expression of proteins or genes involved in alternative respiratory pathways in cfm6. Collectively, CFM6, a previously uncharacterized CRM domain-containing protein, is specifically involved in the cis-splicing of nad5 intron 4 and plays a pivotal role in mitochondrial complex I biogenesis and normal plant growth.

scholarly journals Mitochondrial Deoxyguanosine Kinase Regulates NAD+ Biogenesis Independent of Mitochondria Complex I Activity

2020 ◽  
Vol 10 ◽  
Author(s):  
Lei Sang ◽  
Ying-Jie He ◽  
Jiaxin Kang ◽  
Hongyi Ye ◽  
Weiyu Bai ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Cancer Progression ◽  
Complex I ◽  
Ectopic Expression ◽  
Dependent Manner ◽  
Potential Therapeutic Target ◽  
Protein Levels ◽  
Deoxyguanosine Kinase ◽  
Complex I Activity ◽  
Mitochondria Complex I

Overexpression of DGUOK promotes mitochondria oxidative phosphorylation and lung adenocarcinoma progression. However, the role and mechanism of DGUOK in regulation of mitochondria function and lung cancer progression still poorly understood. Here we demonstrated that DGUOK regulated NAD+ biogenesis. Depletion of the DGUOK significantly decreased NAD+ level. Furthermore, knockout of the DGUOK considerably reduced expression of the NMNAT2, a key molecule controlling NAD+ synthesis, at both mRNA and protein levels. Ectopic expression of the NMNAT2 abrogated the effect of knockdown of DGUOK on NAD+. Notably, this regulation is independent of DGUOK -mediated mitochondria complex I activity. We also showed that NMNAT2 was highly expressed in lung adenocarcinoma and negatively correlated with the patient overall survival. Our study suggested that DGUOK regulates NAD+ in a NMNAT2 dependent manner and DGUOK-NMNAT2-NAD+ axis could be a potential therapeutic target in lung adenocarcinoma.

Synthesis and Mitochondrial Complex I Activity of Annonaceous Trans and Cis Solamins Precursors

2004 ◽  
Vol 1 (4) ◽  
pp. 316-322 ◽  
Author(s):  
Julie Defretin ◽  
Christophe Gleye ◽  
Diego Cortes ◽  
Xavier Franck ◽  
Reynald Hocquemiller ◽  
...  
Keyword(s):  
Complex I ◽  
Mitochondrial Complex I ◽  
Mitochondrial Complex ◽  
Complex I Activity
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