scholarly journals Nuclear Gene Dosage Effects Upon the Expression of Maize Mitochondrial Genes

Genetics ◽  
2001 ◽  
Vol 157 (4) ◽  
pp. 1711-1721
Author(s):  
Donald L Auger ◽  
Kathleen J Newton ◽  
James A Birchler
Keyword(s):  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Gene Dosage ◽  
Nuclear Gene ◽  
Eukaryotic Cell ◽  
Mitochondrial Genes ◽  
Northern Analysis ◽  
Α Subunit ◽  
Dosage Effects ◽  
A Genome

Abstract Each mitochondrion possesses a genome that encodes some of its own components. The nucleus encodes most of the mitochondrial proteins, including the polymerases and factors that regulate the expression of mitochondrial genes. Little is known about the number or location of these nuclear factors. B-A translocations were used to create dosage series for 14 different chromosome arms in maize plants with normal cytoplasm. The presence of one or more regulatory factors on a chromosome arm was indicated when variation of its dosage resulted in the alteration in the amount of a mitochondrial transcript. We used quantitative Northern analysis to assay the transcript levels of three mitochondrially encoded components of the cytochrome c oxidase complex (cox1, cox2, and cox3). Data for a nuclearly encoded component (cox5b) and for two mitochondrial genes that are unrelated to cytochrome c oxidase, ATP synthase α-subunit and 18S rRNA, were also determined. Two tissues, embryo and endosperm, were compared and most effects were found to be tissue specific. Significantly, the array of dosage effects upon mitochondrial genes was similar to what had been previously found for nuclear genes. These results support the concept that although mitochondrial genes are prokaryotic in origin, their regulation has been extensively integrated into the eukaryotic cell.

scholarly journals PET111, a Saccharomyces cerevisiae Nuclear Gene Required for Translation of the Mitochondrial mRNA Encoding Cytochrome c Oxidase Subunit II

Genetics ◽  
1987 ◽  
Vol 115 (4) ◽  
pp. 637-647
Author(s):  
Candace G Poutre ◽  
Thomas D Fox
Keyword(s):  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Mitochondrial Gene ◽  
Nuclear Gene ◽  
State Level ◽  
Mitochondrial Genes ◽  
Chimeric Proteins ◽  
Wild Type ◽  
Oxidase Subunit ◽  
A Site

ABSTRACT Mutations in the nuclear gene PET111 are recessive and specifically block accumulation of cytochrome c oxidase subunit II (coxII), the product of a mitochondrial gene. However, the coxII mRNA is present in pet111 mutants at a level approximately one-third that of wild type. The simplest explanation for this phenotype is that PET111 is required for translation of the coxII mRNA. The reduced steady-state level of this mRNA is probably a secondary effect, caused by increased degradation of the untranslated transcript. Mitochondrial suppressors of pet111, carried on rho- mtDNAs, bypass the requirement for PET111 in coxII translation. Three suppressors are fusions between the coxII structural gene and other mitochondrial genes, that encode chimeric proteins consisting of the N-terminal portions of other mitochondrially coded proteins fused to the coxII precursor protein. When present together with rho  + mtDNA in a heteroplasmic state, these suppressors allow coxII synthesis in pet111 mutants. Thus in wild type, the PET111 product, or something under its control, probably acts at a site coded in the proximal portion of the gene for coxII to promote translation of the mRNA. PET111 was isolated by molecular cloning and genetically mapped to a position approximately midway between rna1 and SUP8 on chromosome XIII.

scholarly journals A genome-wide copper-sensitized screen identifies novel regulators of mitochondrial cytochrome c oxidase activity

2021 ◽  
Vol 296 ◽  
pp. 100485
Author(s):  
Natalie M. Garza ◽  
Aaron T. Griffin ◽  
Mohammad Zulkifli ◽  
Chenxi Qiu ◽  
Craig D. Kaplan ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Oxidase Activity ◽  
Mitochondrial Cytochrome ◽  
Genome Wide ◽  
A Genome ◽  
Mitochondrial Cytochrome C

Rpm2, the Protein Subunit of Mitochondrial RNase P in Saccharomyces cerevisiae, Also Has a Role in the Translation of Mitochondrially Encoded Subunits of Cytochrome c Oxidase

Genetics ◽  
2001 ◽  
Vol 158 (2) ◽  
pp. 573-585
Author(s):  
Vilius Stribinskis ◽  
Guo-Jian Gao ◽  
Steven R Ellis ◽  
Nancy C Martin
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Protein ◽  
Nuclear Gene ◽  
Rnase P ◽  
Wild Type ◽  
Protein Subunit ◽  
Mitochondrial Translation

Abstract RPM2 is a Saccharomyces cerevisiae nuclear gene that encodes the protein subunit of mitochondrial RNase P and has an unknown function essential for fermentative growth. Cells lacking mitochondrial RNase P cannot respire and accumulate lesions in their mitochondrial DNA. The effects of a new RPM2 allele, rpm2-100, reveal a novel function of RPM2 in mitochondrial biogenesis. Cells with rpm2-100 as their only source of Rpm2p have correctly processed mitochondrial tRNAs but are still respiratory deficient. Mitochondrial mRNA and rRNA levels are reduced in rpm2-100 cells compared to wild type. The general reduction in mRNA is not reflected in a similar reduction in mitochondrial protein synthesis. Incorporation of labeled precursors into mitochondrially encoded Atp6, Atp8, Atp9, and Cytb protein was enhanced in the mutant relative to wild type, while incorporation into Cox1p, Cox2p, Cox3p, and Var1p was reduced. Pulse-chase analysis of mitochondrial translation revealed decreased rates of translation of COX1, COX2, and COX3 mRNAs. This decrease leads to low steady-state levels of Cox1p, Cox2p, and Cox3p, loss of visible spectra of aa3 cytochromes, and low cytochrome c oxidase activity in mutant mitochondria. Thus, RPM2 has a previously unrecognized role in mitochondrial biogenesis, in addition to its role as a subunit of mitochondrial RNase P. Moreover, there is a synthetic lethal interaction between the disruption of this novel respiratory function and the loss of wild-type mtDNA. This synthetic interaction explains why a complete deletion of RPM2 is lethal.

Phylogeny of Dorippoidea (Crustacea : Decapoda : Brachyura) inferred from three mitochondrial genes

2009 ◽  
Vol 23 (3) ◽  
pp. 223 ◽  
Author(s):  
Y. W. Sin ◽  
Joelle C. Y. Lai ◽  
Peter K. L. Ng ◽  
K. H. Chu
Keyword(s):  
Molecular Markers ◽  
Cytochrome C ◽  
16S Rrna ◽  
Cytochrome C Oxidase ◽  
Phylogenetic Relationships ◽  
Phylogenetic Trees ◽  
Mitochondrial Genes ◽  
12S Rrna ◽  
Generic Relationships ◽  
I Gene

The phylogenetic relationships between 10 of 13 genera of crabs from the superfamily Dorippoidea were investigated using mitochondrial 16S rRNA, 12S rRNA and cytochrome c oxidase subunit I gene sequences. The resultant phylogenetic trees based on the three molecular markers support the division of Dorippidae and Ethusidae as monophyletic families within the Dorippoidea. The inferred inter-generic relationships within Dorippidae concur with groupings based on the overall morphology of the carapace and structures of the male first pleopods.

Neither respiration nor cytochrome c oxidase affects mitochondrial morphology in Saccharomyces cerevisiae.

1998 ◽  
Vol 201 (11) ◽  
pp. 1729-1737 ◽  
Author(s):  
C Church ◽  
R O Poyton
Keyword(s):  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Respiratory Chain ◽  
Glucose Repression ◽  
Nuclear Gene ◽  
Yeast Cells ◽  
Mitochondrial Proteins ◽  
Mitochondrial Morphology ◽  
Per Se ◽  
Mitochondrial Reticulum

Previous studies have reported that mitochondrial morphology and volume in yeast cells are linked to cellular respiratory capacity. These studies revealed that mitochondrial morphology in glucose-repressed or anaerobically grown cells, which lack or have reduced levels of respiration, is different from that in fully respiring cells. Although both oxygen deprivation and glucose repression decrease the levels of respiratory chain proteins, they decrease the expression of many non-mitochondrial proteins as well, making it difficult to determine whether it is a defect in respiration or something else that effects mitochondrial morphology. To determine whether mitochondrial morphology is dependent on respiration per se, we used a strain with a null mutation in PET100, a nuclear gene that is specifically required for the assembly of cytochrome c oxidase. Although this strain lacks respiration, the mitochondrial morphology and volumes are both comparable to those found in its respiration-proficient parent. These findings indicate that respiration is not involved in the establishment or maintenance of yeast mitochondrial morphology, and that the previously observed effects of oxygen availability and glucose repression on mitochondrial morphology are not exerted through the respiratory chain. By applying the principle of symmorphosis to these findings, we conclude that the shape and size of the mitochondrial reticulum found in respiring yeast cells is maintained for reasons other than respiration.

Identification of mitochondrial genes in Trypanosoma brucei and homology to cytochrome c oxidase II in two different reading frames

1985 ◽  
Vol 15 (2) ◽  
pp. 159-170 ◽  
Author(s):  
Mark Payne ◽  
Victoria Rothwell ◽  
Douglas P. Jasmer ◽  
Jean E. Feagin ◽  
Kenneth Stuart
Keyword(s):  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Trypanosoma Brucei ◽  
Mitochondrial Genes ◽  
Reading Frames
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