scholarly journals Molecular Epidemiology of White Pine Blister Rust: Recombination and Spatial Distribution

2005 ◽  
Vol 95 (7) ◽  
pp. 793-799 ◽  
Author(s):  
R. C. Hamelin ◽  
M. Allaire ◽  
M.-J. Bergeron ◽  
M.-C. Nicole ◽  
N. Lecours

Multilocus haplotypes (MLHs) were derived for the spermogonial (monokaryotic haploid) stage of Cronartium ribicola, the causal agent of white pine blister rust. Six random amplified polymorphic DNA loci and three single-strand conformational polymorphism markers were analyzed for 246 rust samples collected from two heavily infected white pine plantations. All cankers sampled were spatially located within the plantations. The hypothesis that spores are not locally disseminated was supported by the absence of any spatial clustering in the distribution of the MLHs. A large number of MLHs was found at both sites and the haplotypic diversity was close to the maximum (one) in both populations. All measures of recombination were not different from expectations under a scenario of sexual recombination. Genetic differentiation between the two sites was very low (θ = 0.023), yet it was significantly different from zero (P < 0.01). This analysis is in agreement with a scenario of extensive sexual recombination followed by some long-distance dispersal.

1959 ◽  
Vol 40 (6) ◽  
pp. 305-309 ◽  
Author(s):  
Merle G. Lloyd ◽  
Clyde A. O'Dell ◽  
H. J. Wells

Silver-iodide particles were used to simulate the movement of white-pine blister-rust spores on a white-pine plantation in northern Idaho where long-distance spread of the disease is suspected. It was hypothesized that cold drainage winds were carrying spores down to a relatively warm lake where convective currents carried the spores aloft. The spores were then distributed over the plantation when a favorable upper-air flow prevailed. Silver-iodide particles were released at the suspected source of infection and traced into the plantation.


1998 ◽  
Vol 88 (11) ◽  
pp. 1187-1191 ◽  
Author(s):  
Richard C. Hamelin ◽  
Mathieu Dusabenyagasani ◽  
Khalid Et-touil

The fine-level genetic structure of the white pine blister rust agent, Cronartium ribicola, was investigated by sampling multiple monokaryotic spermogonia directly on cankers in four eastern Canadian white pine (Pinus strobus) plantations and assessing genetic variability, using random amplified polymorphic DNA (RAPD) markers. Ninety-eight percent of the cankers surveyed contained a single DNA haplotype, suggesting spermogonia within cankers are the result of clonal reproduction. A single canker contained two haplotypes that were divided between the upper and lower parts of the canker, suggesting it represented two confluent cankers. In contrast, genotypic diversity was high among cankers. Thirty-seven haplotypes were found among forty-three cankers sampled, and an analysis of molecular variance indicated that 93% (P < 0.001) of the total genetic diversity was attributable to sampling of different cankers, strongly suggesting that multiple infections do not take place in the white pine blister rust pathosystem, i.e., a canker is the result of infection by a single genotype. This result is in contrast with the high level of genetic diversity previously reported among dikaryotic aecidia within cankers and is consistent with the hypothesis that variability in the aecidial stage is the result of outcrossing between resident spermogonia and alien spermatia. The genetic structure of the spermogonial stage, which is the vegetative extension of infection by basidiospores and, therefore, the indirect result of meiosis, was consistent with random mating; the observed genotypic diversity was not significantly different (P > 0.05) from the genotypic diversity expected under the assumption of panmixis. The results indicate that monokaryotic cankers can be genotyped by sampling a single unopened spermogonia per canker.


Plant Disease ◽  
2011 ◽  
Vol 95 (4) ◽  
pp. 494-494 ◽  
Author(s):  
M. L. Fairweather ◽  
B. W. Geils

White pine blister rust, caused by Cronartium ribicola J.C. Fisch., was found on southwestern white pine (Pinus flexilis James var. reflexa Engelm., synonym P. strobiformis Engelm.) near Hawley Lake, Arizona (Apache County, White Mountains, 34.024°N, 109.776°W, elevation 2,357 m) in April 2009. Although white pines in the Southwest (Arizona and New Mexico) have been repeatedly surveyed for blister rust since its discovery in the Sacramento Mountains of southern New Mexico in 1990 (1,2), this was the first confirmation of C. ribicola in Arizona. Numerous blister rust cankers were sporulating on 15- to 30-year-old white pines growing in a mixed conifer stand adjacent to a meadow with orange gooseberry bushes (Ribes pinetorum Greene), a common telial host in New Mexico. Most of the observed cankers were producing their first aecia on 5-year-old branch interwhorl segments (i.e., formed in 2004). The two oldest cankers apparently originated on stemwood formed about 14 and 21 years before (1995 and 1988). Neither uredinia nor telia were seen on expanding gooseberry leaves in late April, but these rust structures were found later in the season. Voucher specimens deposited in the Forest Pathology Herbarium-Fort Collins (FPF) were determined by host taxa and macro- and microscopic morphology as C. ribicola–white pine with typical cankers, aecia, and aeciospores (1). Six collections of aeciospores from single, unopened aecia provided rDNA sequences (ITS1-5.8S-ITS2, primers ITS1F and ITS4) with two different repeat types (GenBank Accession Nos. HM156043 and HM156044 [J. W. Hanna conducted analysis with methods described in 3]). A BLASTn search with these sequences showed 100 and 99% similarities, respectively, with sequences of C. ribicola, including accessions L76496, L76498, and L76499 from California (4). Additional reconnaissance of white pines on the Fort Apache Indian Reservation and neighboring Apache-Sitgreaves National Forests was conducted from May through September 2009. Although the blister rust infestation was distributed over more than 100 km2 of forest type, infected trees were restricted to mesic and wet canyon bottoms (climatically high-hazard sites) and were not found on dry sites–even where aecial and telial hosts occurred together. Recent dispersal within the White Mountains was suggested by a presence of infected gooseberry plants on several sites where infected white pines were not yet evident. Geils et al. (1) concluded that the initial infestation in New Mexico had originated by long-distance, aerial transport from California to the Sacramento Mountains in 1969. Since then, numerous additional infestations in the Southwest have been discovered; but we do not know which of these (including Arizona) resulted by dispersal from California or New Mexico. Although rust may eventually infest many host populations in the Southwest and disease may kill most trees in some locations, differences in site hazard and spread provide managers with numerous opportunities to maintain white pines and Ribes spp. References: (1) B. Geils et al. For. Pathol. 40:147, 2010. (2) F. Hawksworth. Plant Dis. 74:938, 1990. (3) M.-S. Kim et al. For. Pathol. 36:145, 2006. (4) D. Vogler and T. Bruns. Mycologia 90:244, 1998.


2011 ◽  
Author(s):  
Amanda Crump ◽  
William R. Jacobi ◽  
Kelly S. Burns ◽  
Brian E. Howell

2008 ◽  
Author(s):  
Kelly S. Burns ◽  
Anna W. Schoettle ◽  
William R. Jacobi ◽  
Mary F. Mahalovich

2013 ◽  
Vol 44 (1) ◽  
pp. 21-38 ◽  
Author(s):  
H. S. J. Kearns ◽  
W. R. Jacobi ◽  
R. M. Reich ◽  
R. L. Flynn ◽  
K. S. Burns ◽  
...  

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