scholarly journals Genetic Specificity in the White Pine-Blister Rust Pathosystem

2002 ◽  
Vol 92 (3) ◽  
pp. 278-280 ◽  
Author(s):  
Bohun B. Kinloch ◽  
Gayle E. Dupper

Four of eight white pine species native to western North America surveyed for resistance to white pine blister rust by artificial inoculation showed classical hypersensitive reactions (HR) at frequencies ranging from very low to moderate. Mendelian segregation, indicating a single dominant allele for resistance (Cr3), was observed in southwestern white pine (Pinus strobiformis), as it was previously in sugar pine (P. lambertiana, Cr1) and western white pine (P. monticola, Cr2). HR was present at a relatively high frequency (19%) in one of five bulk seed lot sources of limber pine (P. flexilis), and was also presumed to be conditioned by a single gene locus, by analogy with the other three species. HR was not found in whitebark pine (P. albcaulis), Mexican white pine (P. ayacahuite), foxtail pine (P. balfouriana), or Great Basin bristlecone pine (P. longaeva), but population and sample sizes in these species may have been below the level of detection of alleles in low frequency. When challenged by (haploid) inocula from specific locations known to harbor virulence to Cr1 or Cr2, genotypes carrying these alleles and Cr3 reacted differentially, such that inoculum virulent to Cr1 was avirulent to Cr2, and inoculum virulent to Cr2 was avirulent to Cr1. Neither of these two inocula was capable of neutralizing Cr3. Although blister rust traditionally is considered an exotic disease in North America, these results, typical of classic gene-for-gene interactions, suggest that genetic memory of similar encounters in past epochs has been retained in this pathosystem.

1999 ◽  
Vol 89 (3) ◽  
pp. 192-196 ◽  
Author(s):  
Bohun B. Kinloch ◽  
Gayle E. Dupper

Tests for Mendelian segregation of virulence and avirulence in Cronartium ribicola, causal agent of white pine blister rust, to a major gene (R) for resistance in sugar pine were made using haploid basidiospore progenies from single diploid telia as inoculum on resistant genotypes. The telia were sampled from a small deme in the Siskyou Mountains of northern California, where a few mature sugar pines known to be Rr genotypes had become infected after withstanding the chronic blister rust epidemic for several decades and where intermediate frequencies of virulence in the ambient basidiospore population were subsequently measured. Infection type on inoculated seedlings with R was qualitative: all progenies of 81 single telia tested over 3 different years were either virulent (compatible) or avirulent (inducing hypersensitive necrosis), never a mixture of both reactions. The complete absence of heterozygotes in the telia population is strong evidence that virulence is not controlled by a nuclear gene. The data are consistent with earlier tests showing that basidiospore inoculum derived from aeciospores isolated from infected Rr trees produced mostly (>90%) virulent reactions on R— seedlings. The evidence indicates that transmission of virulence is uniparental via the cytoplasm of aeciospores. Exchange of spermatia between haploid thalli does not appear to be involved.


Plant Disease ◽  
2004 ◽  
Vol 88 (3) ◽  
pp. 311-311 ◽  
Author(s):  
J. T. Blodgett ◽  
K. F. Sullivan

White pine blister rust caused by Cronartium ribicola was introduced into North America in the early 20th century and is spreading throughout the range of five-needle pines. In northern Colorado, this pathogen was first observed in 1998 on limber pine (Pinus flexilis) (1). It has not been reported on Rocky Mountain or Great Basin bristlecone pine (Pinus aristata and P. longaeva, respectively) in nature. However, Rocky Mountain bristlecone pine is susceptible to the disease when artificially inoculated (2). In October 2003, a Rocky Mountain bristlecone pine was found infected with C. ribicola in the Great Sand Dunes National Monument, Alamosa County, Colorado. Seven branch cankers were observed on the tree. Cankers ranged in length from 15 to 41 cm and were estimated to be approximately 5 to 7 years old. Distinct C. ribicola branch symptoms were observed, including flagging, spindle-shaped swellings, and 6 mm long aecial scars. A branch was deposited at the Colorado State Herbarium. Microscopic examination of spores within remnant aecial blisters revealed aeciospores characteristic of C. ribicola (yellow-orange, ellipsoid, verrucose, and 19 × 25 μm). Cankers were only observed on one bristlecone pine. However, most limber pines in the area were infected with C. ribicola, including a limber pine less than 1 m from the infected bristlecone pine. To our knowledge, this is the first report that shows Rocky Mountain bristlecone pine can become infected naturally, and the pathogen is further south in Colorado on limber pine than previously reported. These observations suggest the need for a more complete investigation of this disease on bristlecone pines. References: (1) D. W. Johnson and W. R. Jacobi. Plant Dis. 84:595, 2000. (2) B. R. Stephan, Allg. Forst Z. 28:695, 1985.


2008 ◽  
Vol 98 (4) ◽  
pp. 413-420 ◽  
Author(s):  
B. A. Richardson ◽  
N. B. Klopfenstein ◽  
P. J. Zambino ◽  
G. I. McDonald ◽  
B. W. Geils ◽  
...  

Cronartium ribicola, the causal agent of white pine blister rust, has been devastating to five-needled white pines in North America since its introduction nearly a century ago. However, dynamic and complex interactions occur among C. ribicola, five-needled white pines, and the environment. To examine potential evolutionary influences on genetic structure and diversity of C. ribicola in western United States, population genetic analyses of C. ribicola were conducted using amplified fragment length polymorphism (AFLP) molecular markers. The fungus was sampled at six sites. Collections for two of the six sites were from separate plantings of resistant-selected western white pine and sugar pine. Heterozygosity based on polymorphic loci among populations ranged from 0.28 to 0.40, with resistant-selected plantations at the extremes. Genetic differentiation was also highest between these two populations. Principal coordinates analysis and Bayesian assignment placed most isolates that are putative carriers of virulence to major-gene resistance into a discernable cluster, while other isolates showed no clustering by site or host species. These results indicate that C. ribicola in western North America is not genetically uniform, despite its presumed single site of introduction and relatively brief residence. Moreover, major-gene resistance appears to have imposed strong selection on the rust, resulting in reduced genetic diversity. In contrast, no evidence of selection was observed in C. ribicola from hosts that exhibit only multigenic resistance.


1977 ◽  
Vol 55 (9) ◽  
pp. 1148-1155 ◽  
Author(s):  
Bohun B. Kinloch Jr. ◽  
Julia L. Littlefield

Resistance to white pine blister rust in sugar pine is simply inherited and can be identified by distinct needle spot morphs. After artificial inoculation at 2 years of age, seedlings from selfed and full-sib families developed either 'fleck' spots, characterized by a pale, yellow margin with a necrotic fleck in the center, or they developed typical yellow or red spots (or both). Seedlings segregated for needle spot reaction in monohybrid ratios with fleck dominant. Mycelium in secondary needle tissues of fleck spots, in contrast to yellow and red spots, was relatively sparse and confined by dense tannin deposits. Bark infection and mortality was heavy on seedlings with yellow and red spots. On seedlings with fleck spots, no bark symptoms developed from secondary needle infection but small, abortive cankers did develop on some of these seedlings as a result of primary needle infection. These atypical cankers did not sporulate or spread extensively, and had healed by the 2nd year after inoculation. The gene responsible for the fleck reaction thus elicits a hypersensitive response in secondary needles and, apparently, in bark tissues as well.


2001 ◽  
Vol 2 (1) ◽  
pp. 10 ◽  
Author(s):  
Otis C. Maloy

White pine blister rust is probably the most destructive disease of five-needle (white) pines in North America. The rust fungus cannot spread from pine to pine but requires an alternate host, Ribes species, to complete the disease cycle. Several management tools might enable the reestablishment of western white pine stands. Accepted for publication 20 September 2001. Published 24 September 2001.


Science ◽  
1970 ◽  
Vol 167 (3915) ◽  
pp. 193-195 ◽  
Author(s):  
B. B. Kinloch ◽  
G. K. Parks ◽  
C. W. Fowler

2007 ◽  
Vol 85 (3) ◽  
pp. 299-306 ◽  
Author(s):  
Bryce A. Richardson ◽  
Paul J. Zambino ◽  
Ned B. Klopfenstein ◽  
Geral I. McDonald ◽  
Lori M. Carris

The white-pine blister rust fungus, Cronartium ribicola Fisch. in Rabenh., continues to spread in North America, utilizing various aecial (primary) and telial (alternate) hosts, some of which have only recently been discovered. This introduced pathogen has been characterized as having low genetic diversity in North America, yet it has demonstrated a capacity to invade diverse environments. The recent discovery of this rust fungus on the telial host Pedicularis racemosa Dougl. ex Benth., raises questions of whether this host association represents a recent acquisition by C. ribicola or a long-standing host association that was overlooked. Here we explore two questions: (i) is host specialization detectable at a local scale and (ii) is the capacity to infect Pedicularis racemosa local or widespread? Genetic analysis of C. ribicola isolates from different aecial and telial hosts provided no evidence for genetic differentiation and showed similar levels of expected heterozygosity within a geographic population. An inoculation test showed that diverse C. ribicola sources from across North America had the capacity to infect Pedicularis racemosa. These results support a hypothesis that ability to infect Pedicularis racemosa is common in C. ribicola from North America. Utilization of Pedicularis racemosa by C. ribicola may be dependent on the co-occurrence of this host, inoculum, and favorable environments.


2010 ◽  
Vol 40 (3-4) ◽  
pp. 382-401 ◽  
Author(s):  
M.-S. Kim ◽  
N. B. Klopfenstein ◽  
Y. Ota ◽  
S. K. Lee ◽  
K.-S. Woo ◽  
...  

Author(s):  
Maria Newcomb ◽  
Diana Six

White pine blister rust is a disease caused by an introduced fungal pathogen (Cronartium ribicola). The disease system is a complex cross-Kingdom interaction between three groups of organisms (white pines, Ribes, and a fungal pathogen). The pathogen alternates between white pine hosts (subgenus Strobus) where it persists as a perennial and often lethal infection, and currant and goosebeny hosts (members of the genus Ribes) where it infects the deciduous leaves and results in relatively minor impacts. In many areas of North America white pines are severely threatened by the disease, which is often recognized as the most devastating disease of conifers (Klinkowski 1970). Since the early 1900s when the pathogen first arrived in North America, forest managers have been challenged by the difficulties of blister rust control and predictions of damage and spread. Recent control efforts have focused on developing rust-resistant white pines (Maloy 1997). Advances in molecular techniques have led to a rapid increase in our understanding of pathogen virulence and plant disease resistance. Thus thorough research on white pine blister rust will encompass a combination of investigations of small parts of the system, including molecular descriptions of individual members and controlled-environment studies of simplified interactions, and ecological investigations of infection patterns in real-world forest conditions (where all the parts are interacting simultaneously). This study is a field investigation of white pine blister rust in the Greater Yellowstone Area (GYA).


2000 ◽  
Vol 10 (3) ◽  
pp. 515-517 ◽  
Author(s):  
Kim E. Hummer

The center of diversity for white pine blister rust (WPBR) (Cronartium ribicola J.C. Fischer) most likely stretches from central Siberia east of the Ural Mountains to Asia, possibly bounded by the Himalayas to the south. The alternate hosts for WPBR, Asian five-needled pines (Pinus L.) and Ribes L. native to that region have developed WPBR resistance. Because the dispersal of C. ribicola to Europe and North America occurred within the last several hundred years, the North American five-needled white pines, Pinus subsections, Strobus and Parya, had no previous selection pressure to develop resistance. Establishment of WPBR in North American resulted when plants were transported both ways across the Atlantic Ocean. In 1705, Lord Weymouth had white pine (P. strobis L.), also called weymouth pine in Europe, seed and seedlings brought to England. These trees were planted throughout eastern Europe. In the mid-1800s, WPBR outbreaks were reported in Ribes and then in white pines in eastern Europe. The pathogen may have been brought to Europe on an infected pine from Russia. In the late 1800s American nurserymen, unaware of the European rust incidence, imported many infected white pine seedlings from France and Germany for reforestation efforts. By 1914, rust-infected white pine nursery stock was imported into Connecticut, Indiana, Massachusetts, Minnesota, New Hampshire, Ohio, Pennsylvania, Vermont, and Wisconsin, and in the Canadian provinces of Ontario, Quebec, and British Columbia. The range of WPBR is established in eastern North America and the Pacific Northwest. New infection sites in Nevada, South Dakota, New Mexico and Colorado have been observed during the 1990s.


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