Mutations inactivating mitochondrial genes in Chlamydomonas reinhardtii

2001 ◽  
Vol 29 (4) ◽  
pp. 442-446 ◽  
Author(s):  
C. Remacle ◽  
F. Duby ◽  
P. Cardol ◽  
R. F. Matagne
Keyword(s):  
Chlamydomonas Reinhardtii ◽  
Complex I ◽  
Molecular Level ◽  
Mitochondrial Genes ◽  
Mitochondrial Genetics ◽  
Mitochondrial Mutations ◽  
Mutant Strains ◽  
Genes Encoding ◽  
Photosynthetic Organism ◽  
Recombinational Analysis

Chlamydomonas reinhardtii is now becoming a useful model for the study of mitochondrial genetics in a photosynthetic organism. The small (15.8 kb) mitochondrial genome C. reinhardtii has been sequenced completely and all the genes have been identified. Several mutants inactivated in mitochondrial genes encoding components of the respiratory complexes I, III and IV have been characterized at the molecular level. Assembly of complex I in several mutant strains and mapping of mitochondrial mutations by recombinational analysis are also described.

Polymorphisms in mitochondrial genes encoding complex I subunits are maternal factors of voluntary alcohol consumption in the rat

2009 ◽  
Vol 19 (7) ◽  
pp. 528-537 ◽  
Author(s):  
Amalia Sapag ◽  
Ginez González-Martínez ◽  
Lorena Lobos-González ◽  
Gonzalo Encina ◽  
Lutske Tampier ◽  
...  
Keyword(s):  
Alcohol Consumption ◽  
Complex I ◽  
Mitochondrial Genes ◽  
Maternal Factors ◽  
Genes Encoding

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.

scholarly journals act Operon Control of Developmental Gene Expression in Myxococcus xanthus

2002 ◽  
Vol 184 (4) ◽  
pp. 1172-1179 ◽  
Author(s):  
Thomas M. A. Gronewold ◽  
Dale Kaiser
Keyword(s):  
Fruiting Body ◽  
Myxococcus Xanthus ◽  
The Other ◽  
Loss Of Function ◽  
Wild Type ◽  
Developmental Gene ◽  
Developmental Gene Expression ◽  
Mutant Strains ◽  
Genes Encoding ◽  
Signal Production

ABSTRACT Cell-bound C-signal guides the building of a fruiting body and triggers the differentiation of myxospores. Earlier work has shown that transcription of the csgA gene, which encodes the C-signal, is directed by four genes of the act operon. To see how expression of the genes encoding components of the aggregation and sporulation processes depends on C-signaling, mutants with loss-of-function mutations in each of the act genes were investigated. These mutations were found to have no effect on genes that are normally expressed up to 3 h into development and are C-signal independent. Neither the time of first expression nor the rate of expression increase was changed in actA, actB, actC, or actD mutant strains. Also, there was no effect on A-signal production, which normally starts before 3 h. By contrast, the null act mutants have striking defects in C-signal production. These mutations changed the expression of four gene reporters that are related to aggregation and sporulation and are expressed at 6 h or later in development. The actA and actB null mutations substantially decreased the expression of all these reporters. The other act null mutations caused either premature expression to wild-type levels (actC) or delayed expression (actD), which ultimately rose to wild-type levels. The pattern of effects on these reporters shows how the C-signal differentially regulates the steps that together build a fruiting body and differentiate spores within it.

scholarly journals Proteome dynamics and early salt stress response of the photosynthetic organism Chlamydomonas reinhardtii

BMC Genomics ◽  
2012 ◽  
Vol 13 (1) ◽  
pp. 215 ◽  
Author(s):  
Guido Mastrobuoni ◽  
Susann Irgang ◽  
Matthias Pietzke ◽  
Heike E Aßmus ◽  
Markus Wenzel ◽  
...  
Keyword(s):  
Salt Stress ◽  
Stress Response ◽  
Chlamydomonas Reinhardtii ◽  
Salt Stress Response ◽  
Photosynthetic Organism

scholarly journals Bradyrhizobium japonicum NnrR, a Denitrification Regulator, Expands the FixLJ-FixK2 Regulatory Cascade

2003 ◽  
Vol 185 (13) ◽  
pp. 3978-3982 ◽  
Author(s):  
Socorro Mesa ◽  
Eulogio J. Bedmar ◽  
Astrid Chanfon ◽  
Hauke Hennecke ◽  
Hans-Martin Fischer
Keyword(s):  
Bradyrhizobium Japonicum ◽  
Control Level ◽  
Nitric Oxide Reductase ◽  
Regulatory Cascade ◽  
Additional Control ◽  
Mutant Strains ◽  
Genes Encoding ◽  
Maximal Induction ◽  
Nitrate And Nitrite ◽  
Denitrification Genes

ABSTRACT In Bradyrhizobium japonicum, a gene named nnrR was identified which encodes a protein with high similarity to FNR/CRP-type transcriptional regulators. Mutant strains carrying an nnrR null mutation were unable to grow anaerobically in the presence of nitrate or nitrite, and they lacked both nitrate and nitrite reductase activities. Anaerobic activation of an nnrR′-′lacZ fusion required FixLJ and FixK2. In turn, N oxide-mediated induction of nir and nor genes encoding nitrite and nitric oxide reductase, respectively, depended on NnrR. Thus, NnrR expands the FixLJ-FixK2 regulatory cascade by an additional control level which integrates the N oxide signal required for maximal induction of the denitrification genes.

scholarly journals PERIPHERAL BLOOD MITOCHONDRIAL DNA ALTERATION DURING SYSTEMIC LUPUS NEPHRITIS

2021 ◽  
Vol 10 (19) ◽  
pp. 416-421
Author(s):  
Ruchi Upadhyay ◽  
Ratika Srivastava
Keyword(s):  
Mitochondrial Dna ◽  
Lupus Nephritis ◽  
Lupus Erythematosus ◽  
Peripheral Blood ◽  
Normal Subjects ◽  
Mitochondrial Genes ◽  
Systemic Lupus ◽  
Mt Dna ◽  
Mitochondrial Dna Copy Number ◽  
Genes Encoding

The investigation of mitochondrial DNA (Mt-DNA) alterations could impart light on the involvement of mitochondria in the pathophysiology of Systemic Lupus Erythematosus. The purpose of this study is to examine the peripheral blood mitochondrial DNA copy number variation in Lupus Nephritis patients and also to find out it’s correlation with amount of protein present in urine. The significant correlation could aid in the inspection of mitochondrial involvement, particularly in Lupus Nephritis. Two mitochondrial genes encoding MT-CYT and MT-TL1 were measured quantitatively by qRT-PCR in whole blood of 17 SLE patients and 15 healthy subjects with similar gender (female: male ratio) and age group. The amount of mitochondrial genes MT-CYT and MT-TL1 was 1.69 and 1.26 fold higher respectively in patients. The significantly higher amount of protein detected in lupus nephritis patients (129.4±116.4 mg/dl) in comparison to normal subjects (25.3 ±10.7 mg/dl). No significant correlation was established between Mt-DNA quantity and proteinuria. Alteration in mitochondrial genes reflects the possibilities of altered mitophagy or mitochondrial biosynthesis during SLE. These findings are required to be further validated by studying mitophagy and biogenesis during SLE in details.

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