Biochemical, genetic and molecular characterization of new respiratory-deficient mutants inChlamydomonas reinhardtii

Autor: Colleaux, Laurence, Dorthu, M, Remy, R, Michel-Wolwertz, R, Colleaux, C, Breyer, D, Beckers, C, Englebert, S, Duyckaerts, C, Sluse, F, Matagne, R
Přispěvatelé: Marseille medical genetics - Centre de génétique médicale de Marseille (MMG), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National de la Santé et de la Recherche Médicale (INSERM)-Aix Marseille Université (AMU)
Rok vydání: 1992
Předmět:
MESH: Chlamydomonas reinhardtii
Mitochondrial DNA
MESH: Mutation
Restriction Mapping
Mutant
Antimycin A
Tetrazolium Salts
Chlamydomonas reinhardtii
Plant Science
MESH: Phenotype
medicine.disease_cause
DNA
Mitochondrial
MESH: Apoproteins
Oxygen Consumption
MESH: Colorimetry
MESH: Blotting
Southern
Genetics
medicine
MESH: Cytochrome b Group
Animals
Cytochrome c oxidase
MESH: Animals
MESH: Oxygen Consumption
MESH: Restriction Mapping
Mutation
Oxidase test
biology
Cytochrome b
Chlamydomonas
MESH: DNA
Mitochondrial
MESH: Tetrazolium Salts
General Medicine
MESH: Cytochromes b
Cytochromes b
Cytochrome b Group
biology.organism_classification
Molecular biology
Blotting
Southern
Phenotype
[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human genetics
Biochemistry
biology.protein
Colorimetry
MESH: Antimycin A
Apoproteins
Agronomy and Crop Science
Zdroj: Plant Molecular Biology
Plant Molecular Biology, Springer Verlag (Germany), 1992, 18 (4), pp.759-72
ISSN: 1573-5028
0167-4412
DOI: 10.1007/bf00020017
Popis: International audience; Eight respiratory-deficient mutants of Chlamydomonas reinhardtii have been isolated after mutagenic treatment with acriflavine or ethidium bromide. They are characterized by their inability to grow or their very reduced growth under heterotrophic conditions. One mutation (Class III) is of nuclear origin whereas the seven remaining mutants (Classes I and II) display a predominantly paternal mt- inheritance, typical of mutations residing in the mitochondrial DNA. Biochemical analysis has shown that all mutants are deficient in the cyanide-sensitive cytochrome pathway of the respiration whereas the alternative pathway is still functional. Measurements of complexes II + III (antimycin-sensitive succinate-cytochrome c oxido-reductase) and complex IV (cytochrome c oxidase) activities allowed to conclude that six mutations have to be localized in the mitochondrial apocytochrome b (COB) gene, one in the mitochondrial cytochrome oxidase subunit I (COI) gene and one in a nuclear gene encoding a component of the cytochrome oxidase complex. By using specific probes, we have moreover demonstrated that five mutants (Class II mutants) contain mitochondrial DNA molecules deleted in the terminal end containing the COB gene and the telomeric region; they also possess dimeric molecules resulting from end-to-end junctions of deleted monomers. The two other mitochondrial mutants (Class I) have no detectable gross alteration. Class I and Class II mutants can also be distinguished by the pattern of transmission of the mutation in crosses. An in vivo staining test has been developed to identify rapidly the mutants impaired in cyanide-sensitive respiration.
Databáze: OpenAIRE
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