Intercontinental Population Structure of the Chestnut Blight Fungus, Cryphonectria parasitica

Mycologia ◽  
1996 ◽  
Vol 88 (2) ◽  
pp. 179 ◽  
Author(s):  
Michael G. Milgroom ◽  
Kerong Wang ◽  
Yang Zhou ◽  
Susanne E. Lipari ◽  
Shigeru Kaneko
2013 ◽  
Vol 103 (12) ◽  
pp. 1280-1286 ◽  
Author(s):  
Joshua C. Springer ◽  
Anita L. Davelos Baines ◽  
Dennis W. Fulbright ◽  
Matthew T. Chansler ◽  
Andrew M. Jarosz

Vegetative compatibility (VC) is commonly used to characterize structure and diversity in fungal populations. In the chestnut blight fungus, Cryphonectria parasitica, high VC diversity is hypothesized to be responsible for the failure of hyperparasitic mycoviruses to spread through pathogen populations in North America. To test this hypothesis, we assessed VC diversity at three recovering sites in Michigan where mycoviruses had invaded and compared them with four epidemic population sites where mycoviruses were absent. VC diversity was assessed for samples collected in 1996 and 2009, which allowed us to determine how C. parasitica populations changed with time. Twelve VC types were found in 1996 while 29 were found in 2009; 75% of types overlapped between the sample dates. Sites where mycoviruses were present had unique VC structures with the exception of the recovering population site at County Line where the main VC group was also detected at two epidemic sites. With one exception, epidemic sites contained more VC groups and displayed higher population level diversity than recovering sites. Mating-type analyses of blight populations revealed that two of three recovering populations were significantly skewed for MAT2 suggesting asexual reproduction, while epidemic sites with a long history of blight infection had ratios near 50:50 suggesting sexual reproduction. We propose that selection in the largely asexual C. parasitica populations at two recovering sites favors the most-fit fungal genotype by mycovirus combination and results in reduced diversity relative to the sexually reproducing pathogen populations at epidemic sites.


Genetics ◽  
1992 ◽  
Vol 131 (2) ◽  
pp. 297-306 ◽  
Author(s):  
M G Milgroom ◽  
S E Lipari ◽  
W A Powell

Abstract We analyzed DNA fingerprints in the chestnut blight fungus, Cryphonectria parasitica, for stability, inheritance, linkage and variability in a natural population. DNA fingerprints resulting from hybridization with a dispersed moderately repetitive DNA sequence of C. parasitica in plasmid pMS5.1 hybridized to 6-17 restriction fragments per individual isolate. In a laboratory cross and from progeny from a single perithecium collected from a field population, the presence/absence of 11 fragments in the laboratory cross and 12 fragments in the field progeny set segregated in 1:1 ratios. Two fragments in each progeny set cosegregated; no other linkage was detected among the segregating fragments. Mutations, identified by missing bands, were detected for only one fragment in which 4 of 43 progeny lacked a band present in both parents; no novel fragments were detected in any progeny. All other fragments appeared to be stably inherited. Hybridization patterns did not change during vegetative growth or sporulation. However, fingerprint patterns of single conidial isolates of strains EP155 and EP67 were found to be heterogenous due to mutations that occurred during culturing in the laboratory since these strains were first isolated in 1976-1977. In a population sample of 39 C. parasitica isolates, we found 33 different fingerprint patterns with pMS5.1. Most isolates differed from all other isolates by the presence or absence of several fragments. Six fingerprint patterns each occurred twice. Isolates with identical fingerprints occurred in cankers on the same chestnut stems three times; isolates within the other three pairs were isolated from cankers more than 5 m apart. The null hypothesis of random mating in this population could not be rejected if the six putative clones were removed from the analysis. Thus, a rough estimate of the clonal fraction of this population is 6 in 39 isolates (15.4%).


Mycologia ◽  
1996 ◽  
Vol 88 (2) ◽  
pp. 179-190 ◽  
Author(s):  
Michael G. Milgroom ◽  
Kerong Wang ◽  
Yang Zhou ◽  
Susanne E. Lipari ◽  
Shigeru Kaneko

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

2000 ◽  
Vol 24 (4) ◽  
pp. 196-201 ◽  
Author(s):  
Seth J. Diamond ◽  
Robert H. Giles ◽  
Roy L. Kirkpatrick ◽  
Gary J. Griffin

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.


2008 ◽  
Vol 82 (6) ◽  
pp. 2613-2619 ◽  
Author(s):  
Xuemin Zhang ◽  
Gert C. Segers ◽  
Qihong Sun ◽  
Fuyou Deng ◽  
Donald L. Nuss

ABSTRACT The disruption of one of two dicer genes, dcl-2, of the chestnut blight fungus Cryphonectria parasitica was recently shown to increase susceptibility to mycovirus infection (G. C. Segers, X. Zhang, F. Deng, Q. Sun, and D. L. Nuss, Proc. Natl. Acad. Sci. USA 104:12902-12906, 2007). We now report the accumulation of virus-derived small RNAs (vsRNAs) in hypovirus CHV1-EP713-infected wild-type and dicer gene dcl-1 mutant C. parasitica strains but not in hypovirus-infected dcl-2 mutant and dcl-1 dcl-2 double-mutant strains. The CHV1-EP713 vsRNAs were produced from both the positive and negative viral RNA strands at a ratio of 3:2 in a nonrandom distribution along the viral genome. We also show that C. parasitica responds to hypovirus and mycoreovirus infections with a significant increase (12- to 20-fold) in dcl-2 expression while the expression of dcl-1 is increased only modestly (2-fold). The expression of dcl-2 is further increased (∼35-fold) following infection with a hypovirus CHV1-EP713 mutant that lacks the p29 suppressor of RNA silencing. The combined results demonstrate the biogenesis of mycovirus-derived small RNAs in a fungal host through the action of a specific dicer gene, dcl-2. They also reveal that dcl-2 expression is significantly induced in response to mycovirus infection by a mechanism that appears to be repressed by the hypovirus-encoded p29 suppressor of RNA silencing.


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