scholarly journals Immunological studies of ribosomal mutants in the fungus Podospora anserina.

1983 ◽  
Vol 258 (12) ◽  
pp. 7618-7622
Author(s):  
M Crouzet ◽  
J Bégueret
Keyword(s):  
Podospora Anserina

scholarly journals HET-E and HET-D Belong to a New Subfamily of WD40 Proteins Involved in Vegetative Incompatibility Specificity in the Fungus Podospora anserina

Genetics ◽  
2002 ◽  
Vol 161 (1) ◽  
pp. 71-81
Author(s):  
Eric Espagne ◽  
Pascale Balhadère ◽  
Marie-Louise Penin ◽  
Christian Barreau ◽  
Béatrice Turcq
Keyword(s):  
Genetic Difference ◽  
Podospora Anserina ◽  
Wild Type ◽  
Incompatible Interaction ◽  
Vegetative Incompatibility ◽  
Repeat Domain ◽  
Upper Face ◽  
E1a Gene ◽  
Type Strains ◽  
Wd40 Repeats

Abstract Vegetative incompatibility, which is very common in filamentous fungi, prevents a viable heterokaryotic cell from being formed by the fusion of filaments from two different wild-type strains. Such incompatibility is always the consequence of at least one genetic difference in specific genes (het genes). In Podospora anserina, alleles of the het-e and het-d loci control heterokaryon viability through genetic interactions with alleles of the unlinked het-c locus. The het-d2Y gene was isolated and shown to have strong similarity with the previously described het-e1A gene. Like the HET-E protein, the HET-D putative protein displayed a GTP-binding domain and seemed to require a minimal number of 11 WD40 repeats to be active in incompatibility. Apart from incompatibility specificity, no other function could be identified by disrupting the het-d gene. Sequence comparison of different het-e alleles suggested that het-e specificity is determined by the sequence of the WD40 repeat domain. In particular, the amino acids present on the upper face of the predicted β-propeller structure defined by this domain may confer the incompatible interaction specificity.

scholarly journals Cytosolic Ribosomal Mutations That Abolish Accumulation of Circular Intron in the Mitochondria Without Preventing Senescence of Podospora anserina

Genetics ◽  
1997 ◽  
Vol 145 (3) ◽  
pp. 697-705 ◽  
Author(s):  
Philippe Silar ◽  
France Koll ◽  
Michèle Rossignol
Keyword(s):  
Mitochondrial Dna ◽  
Ribosomal Proteins ◽  
Podospora Anserina ◽  
Cox1 Gene ◽  
Accuracy Control ◽  
Additional Function ◽  
Mutant Proteins ◽  
Double Stranded Dna ◽  
Dna Modifications

The filamentous fungus Podospora anserina presents a degeneration syndrome called Senescence associated with mitochondrial DNA modifications. We show that mutations affecting the two different and interacting cytosolic ribosomal proteins (S7 and S19) systematically and specifically prevent the accumulation of senDNAα (a circular double-stranded DNA plasmid derived from the first intron of the mitochondrial cox1 gene or intron α) without abolishing Senescence nor affecting the accumulation of other usually observed mitochondrial DNA rearrangements. One of the mutant proteins is homologous to the Escherichia coli S4 and Saccharomyces cerevisiae S13 ribosomal proteins, known to be involved in accuracy control of cytosolic translation. The lack of accumulation of senDNAα seems to result from a nontrivial ribosomal alteration unrelated to accuracy control, indicating that S7 and S19 proteins have an additional function. The results strongly suggest that modified expression of nucleus-encoded proteins contributes to Senescence in P. anserina. These data do not fit well with some current models, which propose that intron α plays the role of the cytoplasmic and infectious Determinant of Senescence that was defined in early studies.

scholarly journals Identification of Six Loci in Which Mutations Partially Restore Peroxisome Biogenesis and/or Alleviate the Metabolic Defect of pex2 Mutants in Podospora

Genetics ◽  
2002 ◽  
Vol 161 (3) ◽  
pp. 1089-1099
Author(s):  
Gwenaël Ruprich-Robert ◽  
Véronique Berteaux-Lecellier ◽  
Denise Zickler ◽  
Arlette Panvier-Adoutte ◽  
Marguerite Picard
Keyword(s):  
Sole Carbon Source ◽  
Large Scale ◽  
Podospora Anserina ◽  
Developmental Defect ◽  
Dominant Allele ◽  
Peroxisome Biogenesis ◽  
Metabolic Defects ◽  
Metabolic Defect ◽  
Mutant Strains ◽  
Large Scale Screening

Abstract Peroxins (PEX) are proteins required for peroxisome biogenesis. Mutations in PEX genes cause lethal diseases in humans, metabolic defects in yeasts, and developmental disfunctions in plants and filamentous fungi. Here we describe the first large-scale screening for suppressors of a pex mutation. In Podospora anserina, pex2 mutants exhibit a metabolic defect [inability to grow on medium containing oleic acid (OA medium) as sole carbon source] and a developmental defect (inability to differentiate asci in homozygous crosses). Sixty-three mutations able to restore growth of pex2 mutants on OA medium have been analyzed. They fall in six loci (suo1 to suo6) and act as dominant, allele-nonspecific suppressors. Most suo mutations have pleiotropic effects in a pex2+ background: formation of unripe ascospores (all loci except suo5 and suo6), impaired growth on OA medium (all loci except suo4 and suo6), or sexual defects (suo4). Using immunofluorescence and GFP staining, we show that peroxisome biogenesis is partially restored along with a low level of ascus differentiation in pex2 mutant strains carrying either the suo5 or the suo6 mutations. The data are discussed with respect to β-oxidation of fatty acids, peroxisome biogenesis, and cell differentiation.

scholarly journals Identification of the Genes Encoding the Cytosolic Translation Release Factors from Podospora anserina and Analysis of Their Role During the Life Cycle

Genetics ◽  
1998 ◽  
Vol 149 (4) ◽  
pp. 1763-1775 ◽  
Author(s):  
Bénédicte Gagny ◽  
Philippe Silar
Keyword(s):  
Life Span ◽  
Translation Termination ◽  
Podospora Anserina ◽  
Terminal Region ◽  
Terminal Portion ◽  
Nonsense Mutations ◽  
Translation Fidelity ◽  
Reproductive Impairment ◽  
Genes Encoding ◽  
Nonsense Suppressor

Abstract In an attempt to decipher their role in the life history and senescence process of the filamentous fungus Podospora anserina, we have cloned the su1 and su2 genes, previously identified as implicated in cytosolic translation fidelity. We show that these genes are the equivalents of the SUP35 and SUP45 genes of Saccharomyces cerevisiae, which encode the cytosolic translation termination factors eRF3 and eRF1, respectively. Mutations in these genes that suppress nonsense mutations may lead to drastic mycelium morphology changes and sexual impairment but have little effect on life span. Deletion of su1, coding for the P. anserina eRF3, is lethal. Diminution of its expression leads to a nonsense suppressor phenotype whereas its overexpression leads to an antisuppressor phenotype. P. anserina eRF3 presents an N-terminal region structurally related to the yeast eRF3 one. Deletion of the N-terminal region of P. anserina eRF3 does not cause any vegetative alteration; especially life span is not changed. However, it promotes a reproductive impairment. Contrary to what happens in S. cerevisiae, deletion of the N terminus of the protein promotes a nonsense suppressor phenotype. Genetic analysis suggests that this domain of eRF3 acts in P. anserina as a cis-activator of the C-terminal portion and is required for proper reproduction.

scholarly journals Mitochondrial Group II Introns, Cytochrome c Oxidase, and Senescence in Podospora anserina

1999 ◽  
Vol 19 (6) ◽  
pp. 4093-4100 ◽  
Author(s):  
Odile Begel ◽  
Jocelyne Boulay ◽  
Beatrice Albert ◽  
Eric Dufour ◽  
Annie Sainsard-Chanet
Keyword(s):  
Life Span ◽  
Integration Site ◽  
Group Ii Intron ◽  
Podospora Anserina ◽  
Wild Type ◽  
First Intron ◽  
Limited Life ◽  
Related Group ◽  
Group Ii ◽  
Mitochondrial Chromosome

ABSTRACT Podospora anserina is a filamentous fungus with a limited life span. It expresses a degenerative syndrome called senescence, which is always associated with the accumulation of circular molecules (senDNAs) containing specific regions of the mitochondrial chromosome. A mobile group II intron (α) has been thought to play a prominent role in this syndrome. Intron α is the first intron of the cytochrome c oxidase subunit I gene (COX1). Mitochondrial mutants that escape the senescence process are missing this intron, as well as the first exon of theCOX1 gene. We describe here the first mutant of P. anserina that has the α sequence precisely deleted and whose cytochrome c oxidase activity is identical to that of wild-type cells. The integration site of the intron is slightly modified, and this change prevents efficient homing of intron α. We show here that this mutant displays a senescence syndrome similar to that of the wild type and that its life span is increased about twofold. The introduction of a related group II intron into the mitochondrial genome of the mutant does not restore the wild-type life span. These data clearly demonstrate that intron α is not the specific senescence factor but rather an accelerator or amplifier of the senescence process. They emphasize the role that intron α plays in the instability of the mitochondrial chromosome and the link between this instability and longevity. Our results strongly support the idea that in Podospora, “immortality” can be acquired not by the absence of intron α but rather by the lack of active cytochromec oxidase.

Sign in / Sign up

Export Citation Format

Share Document