scholarly journals Mutagenesis of Putative Acylation Sites Alters Function, Localization, and Accumulation of a Giα Subunit of the Chestnut Blight Fungus Cryphonectria parasitica

1998 ◽  
Vol 11 (11) ◽  
pp. 1130-1135 ◽  
Author(s):  
Shaojian Gao ◽  
Donald L. Nuss
Keyword(s):  
Immunoblot Analysis ◽  
Cryphonectria Parasitica ◽  
Chestnut Blight ◽  
Biological Processes ◽  
Targeted Disruption ◽  
Gene Encoding ◽  
Chestnut Blight Fungus ◽  
Post Transcriptional Regulation ◽  
Western Immunoblot Analysis

Targeted disruption of cpg-1, a gene encoding the G protein Giα subunit, CPG-1, in the chestnut blight fungus, Cryphonectria parasitica, results in reduced mycelial growth, reduced orange pigmentation, loss of virulence, loss of asexual sporulation, and female infertility. We report the development of a complementation system for cpg-1 null mutants and its use to evaluate the in vivo consequences of mutating conserved putative CPG-1 myristoylation (G2) and palmitoylation (C3) sites. Independent mutations of the two putative acylation sites differentially altered complex fungal biological processes, including virulence, and modified CPG-1 membrane association. Results of combined Northern (RNA) and Western (immunoblot) analysis also indicated a role for lipid modification in post-transcriptional regulation of CPG-1 accumulation.

scholarly journals A Hydrophobin of the Chestnut Blight Fungus, Cryphonectria parasitica, Is Required for Stromal Pustule Eruption

2005 ◽  
Vol 4 (5) ◽  
pp. 931-936 ◽  
Author(s):  
Pam Kazmierczak ◽  
Dae Hyuk Kim ◽  
Massimo Turina ◽  
Neal K. Van Alfen
Keyword(s):  
Liquid Culture ◽  
Essential Role ◽  
Normal Development ◽  
Cryphonectria Parasitica ◽  
Chestnut Blight ◽  
Deletion Mutants ◽  
Fruiting Bodies ◽  
Gene Encoding ◽  
Chestnut Blight Fungus ◽  
Small Hydrophobic

ABSTRACT Hydrophobins are abundant small hydrophobic proteins that are present on the surfaces of many filamentous fungi. The chestnut blight pathogen Cryphonectria parasitica was shown to produce a class II hydrophobin, cryparin. Cryparin is the most abundant protein produced by this fungus when grown in liquid culture. When the fungus is growing on chestnut trees, cryparin is found only in the fungal fruiting body walls. Deletion of the gene encoding cryparin resulted in a culture phenotype typical of hydrophobin deletion mutants of other fungi, i.e., easily wettable (nonhydrophobic) hyphae. When grown on the natural substrate of the fungus, however, cryparin-null mutation strains were unable to normally produce its fungal fruiting bodies. Although the stromal pustules showed normal development initially, they were unable to erupt through the bark of the tree. The hydrophobin cryparin thus plays an essential role in the fitness of this important plant pathogen by facilitating the eruption of the fungal fruiting bodies through the bark of its host tree.

scholarly journals A Host Factor Involved in Hypovirus Symptom Expression in the Chestnut Blight Fungus, Cryphonectria parasitica

2007 ◽  
Vol 82 (2) ◽  
pp. 740-754 ◽  
Author(s):  
M. Iqbal Faruk ◽  
Ana Eusebio-Cope ◽  
Nobuhiro Suzuki
Keyword(s):  
Insertion Site ◽  
Cryphonectria Parasitica ◽  
Inverse Pcr ◽  
Chestnut Blight ◽  
Wild Type ◽  
Targeted Disruption ◽  
Chestnut Blight Fungus ◽  
Virulence Attenuation ◽  
Symptom Modulation ◽  
Sequence Similarities

ABSTRACT The prototype hypovirus CHV1-EP713 causes virulence attenuation and severe suppression of asexual sporulation and pigmentation in its host, the chestnut blight fungus, Cryphonectria parasitica. We identified a factor associated with symptom induction in C. parasitica using a transformation of C. parasitica strain EP155 with a full-length cDNA clone from a mild mutant virus strain, Cys(72). This was accomplished by using mutagenesis of the transformant fungal strain TCys(72)-1 by random integration of plasmid pHygR, conferring hygromycin resistance. The mutant, namA (after nami-gata, meaning wave shaped), showed an irregular fungal morphology with reduced conidiation and pigmentation while retaining similar levels of virulence and virus accumulation relative to TCys(72)-1- or Cys(72)-infected strain EP155. However, the colony morphology of virus-cured namA (VC-namA) was indistinguishable from those of EP155 and virus-cured TCys(72)-1 [VC-TCys(72)-1]. The phenotypic difference between VC-namA and VC-TCys(72)-1 was found only when these strains infected with the wild type or certain mutant CHV1-EP713 strains but not when infected with Mycoreovirus 1. Sequence analysis of inverse-PCR-amplified genomic DNA fragments and cDNA identified the insertion site of the mutagenic plasmid in exon 8 of the nam-1 gene. NAM-1, comprising 1,257 amino acids, shows sequence similarities to counterparts from other filamentous fungi and possesses the CorA domain that is conserved in a class of Mg2+ transporters from prokaryotes and eukaryotes. Complementation assays using the wild-type and mutant alleles and targeted disruption of nam-1 showed that nam-1 with an extension of the pHygR-derived sequence contributed to the altered phenotype in the namA mutant. The molecular mechanism underlying virus-specific fungal symptom modulation in VC-namA is discussed.

Crypt1, an active Ac-like transposon from the chestnut blight fungus, Cryphonectria parasitica

2001 ◽  
Vol 265 (4) ◽  
pp. 730-738 ◽  
Author(s):  
D. Linder-Basso ◽  
R. Foglia ◽  
P. Zhu ◽  
B.I. Hillman
Keyword(s):  
Cryphonectria Parasitica ◽  
Chestnut Blight ◽  
Chestnut Blight Fungus

scholarly journals TCF12 controls oligodendroglial cell proliferation and regulates signaling pathways conserved in gliomas

2021 ◽  
Author(s):  
Sofia Archontidi ◽  
Corentine Marie ◽  
Beata Gyorgy ◽  
Justine Guegan ◽  
Marc Sanson ◽  
...  
Keyword(s):  
Biological Processes ◽  
Oligodendrocyte Differentiation ◽  
Gene Encoding ◽  
Genome Wide ◽  
Diffuse Gliomas ◽  
Mrna And Protein Expression ◽  
Oligodendrocyte Precursor ◽  
Oligodendrocyte Development ◽  
Chromatin Profiling

Diffuse gliomas are primary brain tumors originating from the transformation of glial cells. In particular, oligodendrocyte precursor cells constitute the major tumor-amplifying population in the gliomagenic process. We previously identified the TCF12 gene, encoding a transcription factor of the E protein family, as being recurrently mutated in oligodendrogliomas. In this study, we sought to understand the function of TCF12 in oligodendroglial cells, the glioma lineage of origin. We first describe TCF12 mRNA and protein expression pattern in oligodendroglial development in the mouse brain. Second, by TCF12 genome wide chromatin profiling in oligodendroglial cells, we show that TCF12 binds active promoters of genes involved in proliferation, translation/ribosomes, and pathways involved in oligodendrocyte development and cancer. Finally, we perform OPC-specific Tcf12 inactivation in vivo and demonstrate by immunofluorescence and transcriptomic analyses that TCF12 is transiently required for OPC proliferation but dispensable for oligodendrocyte differentiation. We further show that Tcf12 inactivation results in deregulation of biological processes that are also altered in oligodendrogliomas. Together, our data suggest that TCF12 directly regulates transcriptional programs in oligodendroglia development that are relevant in a glioma context.

scholarly journals Hard Mast Production Before and After the Chestnut Blight

2000 ◽  
Vol 24 (4) ◽  
pp. 196-201 ◽  
Author(s):  
Seth J. Diamond ◽  
Robert H. Giles ◽  
Roy L. Kirkpatrick ◽  
Gary J. Griffin
Keyword(s):  
Carrying Capacity ◽  
Basal Area ◽  
Cryphonectria Parasitica ◽  
Castanea Dentata ◽  
Chestnut Blight ◽  
Wildlife Species ◽  
Chestnut Blight Fungus ◽  
Southern Appalachian ◽  
Before And After ◽  
Mast Production

Abstract We estimated hard mast production of a Southern Appalachian forest for two 10 yr intervals: one before and one, 35 yr after, the chestnut blight fungus (Cryphonectria parasitica) (Murr.) Barr, had killed all mature chestnut trees. The basal area of hard mast-producing trees in the postblight forest was 28% less than in the preblight forest. The estimate of hard mast output was 34% less after the chestnut blight. Postblight production was less than preblight production for 8 of 10 yr. During 5 of these years, postblight production was only 5-27% of preblight production. Annual preblight mast production was relatively stable, whereas annual postblight production fluctuated substantially. Our findings suggest that the loss of mature chestnuts (Castanea dentata) markedly reduced the Southern Appalachian forest's carrying capacity for certain wildlife species. South. J. Appl. For 24(4):196-201.

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