scholarly journals First Report of White Pine Blister Rust in Nevada

Plant Disease ◽  
2000 ◽  
Vol 84 (5) ◽  
pp. 594-594 ◽  
Author(s):  
J. P. Smith ◽  
J. T. Hoffman ◽  
K. F. Sullivan ◽  
E. P. Van Arsdel ◽  
D. Vogler
Keyword(s):  
Sierra Nevada ◽  
Great Basin ◽  
Lake Tahoe ◽  
White Pine Blister Rust ◽  
White Pine ◽  
Infection Age ◽  
Blister Rust ◽  
Infection Dynamics ◽  
Stem Cankers ◽  
Region Ii

White pine blister rust, caused by Cronartium ribicola Fisch., was found in 1997 infecting white pines (genus Pinus, subgenus Strobus) at two locations in the Carson Range of western Nevada. Rust incidence, infection age, damage to trees, rust phenology, and host distribution were evaluated at one of these locations and a nearby location in California in 1998. At the first location (39.3°N, 119.9°W), C. ribicola was found infecting 24 of 49 whitebark pines (P. albicaulis Engelm.) near Mt. Rose Summit on Highway 27 at 2,710 m elevation, ≈6 km northeast of Incline Village, Washoe County, NV. Among infected trees, 33% had only branch cankers, 54% had live stem cankers, and 12% had stem cankers that had killed portions of trees distal to cankers. No trees had died from infection. At the second location (39.1°N, 119.9°W), we found only 6 of 50 (12%) infected western white pines (P. monticola Dougl.) near Genoa Peak (≈2,750 m elevation), 3 km east of Lake Tahoe, Douglas County, NV; however, stem cankers occurred on 4 of the 6 infected trees. In September 1998, whitebark pines at Mt. Rose and Tahoe Meadows (2,550 m elevation, 1.5 km southwest of Mt. Rose Summit) were examined, and the following was observed: (i) aeciospore production was at its peak, indicating that sporulation can occur exceptionally late in the season in this region; (ii) signs of blister rust infection were absent on the telial hosts of C. ribicola (Ribes cereum, R. montigenum, and R. nevadense) at both locations; (iii) ≈80% of the cankers occurred on host wood produced in 1978 and 1979; and (iv) the oldest cankers originated on wood produced in 1968 and the youngest on wood produced in 1980. In October 1998, infected western white pines were examined at a location (2,650 m elevation) ≈30 km north of Lake Tahoe on Babbitt Peak, Sierra County, CA (39.6°N, 120.1°W). At this location, no trees had died from infection, fresh aeciospores were abundant on live cankers, R. montigenum and R. cereum were present but did not show signs of infection, and 19 of 20 cankers examined were on wood produced between 1978 and 1980. White pine blister rust was not found at any of 10 other locations examined throughout Nevada from 1995 to 1997. This is believed to be the first documented report of C. ribicola infecting white pines in Nevada and the easternmost extension of blister rust in the Sierra Nevada Region. These observations suggest that our understanding of blister rust spread and infection dynamics east of the Sierra Nevada crest is incomplete and that future surveys and research in this region must address, among other issues, timing of aeciospore production on pine, and the possibility of blister rust spread into the Great Basin.

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
Keyword(s):  
North America ◽  
Great Basin ◽  
Single Gene ◽  
Low Frequency ◽  
White Pine Blister Rust ◽  
White Pine ◽  
Mendelian Segregation ◽  
Blister Rust ◽  
Sugar Pine ◽  
Bristlecone Pine

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.

scholarly journals Pruning Western White Pine in British Columbia to Reduce White Pine Blister Rust Losses: 10-Year Results

1998 ◽  
Vol 13 (2) ◽  
pp. 60-63 ◽  
Author(s):  
R. S. Hunt
Keyword(s):  
Early Age ◽  
White Pine Blister Rust ◽  
White Pine ◽  
Blister Rust ◽  
Western White Pine ◽  
Pine Stands ◽  
Number Of Stems ◽  
Ribes Spp ◽  
Stem Cankers ◽  
Spore Movement

Abstract Survey lines were located in areas that had been pruned to control blister rust (Cronartium ribicola) 10 yr previously and adjacent control (unpruned) areas in 10 stands of western white pine. Stands were classified as densely stocked, moderately stocked, or open. Cankers were tallied and their position noted. The success of pruning varied from stand to stand. Since the stands had not been pruned at an early age, there was only a 4 and 5% reduction in threatening cankers and stem cankers respectively, as few new cankers were initiated. Stands with the greatest increase in cankering had Ribes spp., were open grown, or possessed a high component of small white pine. Repruning these specific stands may be worthwhile, but in general, entering stands again to do either pruning or scribing would produce few additional healthy trees. Doing both treatments, however, may significantly enhance the number of healthy stems. To optimize the benefits of pruning, stands should be entered early and pruning should continue until a sufficient number of stems are pruned to a height of 3 m to ensure full stocking. Other species may be impediments to spore movement within stands, and thus they should not be pruned. Dense stands initially had less rust than open stands and could be entered later, but once spaced, they also need to be pruned to 3 m to minimize rust infection. West. J. Appl. For: 13(2):60-63.

scholarly journals Whitebark and Foxtail Pine in Yosemite, Sequoia, and Kings Canyon National Parks: Initial Assessment of Stand Structure and Condition

Forests ◽  
2019 ◽  
Vol 10 (1) ◽  
pp. 35 ◽  
Author(s):  
Jonathan C.B. Nesmith ◽  
Micah Wright ◽  
Erik S. Jules ◽  
Shawn T. McKinney
Keyword(s):  
Sierra Nevada ◽  
National Parks ◽  
Mountain Pine Beetle ◽  
Whitebark Pine ◽  
White Pine Blister Rust ◽  
White Pine ◽  
Blister Rust ◽  
Mountain Pine ◽  
Pine Beetle ◽  
Foxtail Pine

The Inventory & Monitoring Division of the U.S. National Park Service conducts long-term monitoring to provide park managers information on the status and trends in biological and environmental attributes including white pines. White pines are foundational species in many subalpine ecosystems and are currently experiencing population declines. Here we present results on the status of whitebark and foxtail pine in the southern Sierra Nevada of California, an area understudied relative to other parts of their ranges. We selected random plot locations in Yosemite, Sequoia, and Kings Canyon national parks using an equal probability spatially-balanced approach. Tree- and plot-level data were collected on forest structure, composition, demography, cone production, crown mortality, and incidence of white pine blister rust and mountain pine beetle. We measured 7899 whitebark pine, 1112 foxtail pine, and 6085 other trees from 2012–2017. All factors for both species were spatially highly variable. Whitebark pine occurred in nearly-pure krummholz stands at or near treeline and as a minor component of mixed species forests. Ovulate cones were observed on 25% of whitebark pine and 69% of foxtail pine. Whitebark pine seedlings were recorded in 58% of plots, and foxtail pine seedlings in only 21% of plots. Crown mortality (8% in whitebark, 6% in foxtail) was low and significantly higher in 2017 compared to previous years. Less than 1% of whitebark and zero foxtail pine were infected with white pine blister rust and <1% of whitebark and foxtail pine displayed symptoms of mountain pine beetle attack. High elevation white pines in the southern Sierra Nevada are healthy compared to other portions of their range where population declines are significant and well documented. However, increasing white pine blister rust and mountain pine beetle occurrence, coupled with climate change projections, portend future declines for these species, underscoring the need for broad-scale collaborative monitoring.

A protein associated with frost hardiness of western white pine is up-regulated by infection in the white pine blister rust pathosystem

1998 ◽  
Vol 28 (3) ◽  
pp. 412-417 ◽  
Author(s):  
Abul KM Ekramoddoullah ◽  
Joanne J Davidson ◽  
Doug W Taylor
Keyword(s):  
Frost Hardiness ◽  
White Pine Blister Rust ◽  
Pinus Monticola ◽  
White Pine ◽  
Blister Rust ◽  
Pine Seedlings ◽  
Western White Pine ◽  
Pine Trees ◽  
High Level ◽  
Stem Cankers

A 19-kDa protein, Pin m III, was recently shown to be associated with overwintering and frost hardiness of western white pine (Pinus monticola Dougl. ex D. Don) seedlings. Here, we report that this protein is up-regulated by the fungus Cronartium ribicola Fisch, the causal agent of white pine blister rust in western white pine trees. Between 1991 and 1994, bark samples of mature western white pine trees (resistant with no stem cankers and susceptible with stem cankers) were collected in winter, spring, and fall. Proteins were extracted and analyzed by Western immunoblot utilizing specific rabbit polyclonal anti-Pin l I (a homologue of Pin m III) antibodies. During all collection dates, but particularly in the spring, susceptible trees had more Pin m III than resistant trees. In July 1995, 43 previously inoculated 7-year-old white pine seedlings were also analyzed. In all susceptible seedlings (cankered) tested, cankered tissue had high levels of Pin m III, and samples collected from the outside edge of the canker margin had low levels of Pin m III; this protein was also detected in some healthy bark of cankered trees. Since the level of Pin m III in healthy white pine trees is normally lowest in summer months, the high level Pin m III in summer samples of infected tissues is a consequence of the fungal infection.

scholarly journals First Report of White Pine Blister Rust on Rocky Mountain Bristlecone Pine

Plant Disease ◽  
2004 ◽  
Vol 88 (3) ◽  
pp. 311-311 ◽  
Author(s):  
J. T. Blodgett ◽  
K. F. Sullivan
Keyword(s):  
Great Basin ◽  
Sand Dunes ◽  
Rocky Mountain ◽  
White Pine Blister Rust ◽  
White Pine ◽  
First Report ◽  
Limber Pine ◽  
Blister Rust ◽  
Bristlecone Pine ◽  
Pinus Aristata

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.

Cronartium ribicola. [Descriptions of Fungi and Bacteria].

1971 ◽  
Author(s):  
G. F. Laundon
Keyword(s):  
Geographical Distribution ◽  
Turn Of The Century ◽  
Cronartium Ribicola ◽  
White Pine Blister Rust ◽  
White Pine ◽  
Black Currant ◽  
Blister Rust ◽  
Pine Seedlings ◽  
Almost All ◽  
Stem Cankers

Abstract A description is provided for Cronartium ribicola. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Pycnia and aecia on numerous members of Pinus sect. Strobus (= sect. Cembra) (white pines) especially P. albicaulis, P. lambertiana, P. monticola and P. strobus; uredia and telia on almost all Ribes and Grossularia species, the cultivated black currant being particularly susceptible. DISEASE: White pine blister rust, currant rust. Causes stem cankers on pines and leaf lesions on currants. GEOGRAPHICAL DISTRIBUTION: Asia, Europe and N. America (CMI Map 6, ed. 3). TRANSMISSION: Overwinters almost exclusively on pines from which aeciospores may be blown hundreds of kilometres (7: 813) to infect Ribes leaves through stomata (Spaulding, 1922). In contrast, basidiospores (38: 393) travel only a few hundred metres to infect pine needles through stomata (Patton & Johnson, 1970), from where the mycelium grows into the stem to form cankers. The importation of large quantities of white pine seedlings from Europe at the turn of the century carried the disease to N. America (Spaulding, 1922; 1929).

Distribution and frequency of a gene for resistance to white pine blister rust in natural populations of sugar pine

1992 ◽  
Vol 70 (7) ◽  
pp. 1319-1323 ◽  
Author(s):  
Bohun B. Kinloch Jr.
Keyword(s):  
Sierra Nevada ◽  
Genetic Resistance ◽  
Natural Populations ◽  
Close Relative ◽  
Cronartium Ribicola ◽  
White Pine Blister Rust ◽  
White Pine ◽  
Blister Rust ◽  
Single Leaf ◽  
Sugar Pine

The gametic frequency of a dominant allele (R) for resistance to white pine blister rust, a disease caused by an introduced pathogen (Cronartium ribicola), in natural populations of sugar pine was estimated by the kind of leaf symptom expressed after artificial inoculation of wind-pollinated seedlings from susceptible seed–parent genotypes (rr). Gene frequency increased clinally from near 0 in the southern Cascade Range to 0.08 in the southern Sierra Nevada, but it was not correlated with any major climatic gradient. Because R expresses a typical hypersensitivity response to pathogenesis, it has probably always functioned in disease resistance. A candidate pathogen for this function is C. occidentale, cause of pinyon blister rust, and a close relative of C. ribicola. Increase in allele frequency was positively associated with the proximity of sugar pine to single-leaf pinyon pine populations. Although sugar pine is not presently a natural host of pinyon rust, R may be a relict gene that protected sugar pine from this endemic pathogen in recent geologic epochs, when both pines are known to have been more intimately associated. Key words: Cronartium ribicola, genetic resistance, Pinus lambertiana, population genetics.

scholarly journals Origin and Distribution of Cr2, a Gene for Resistance to White Pine Blister Rust in Natural Populations of Western White Pine

2003 ◽  
Vol 93 (6) ◽  
pp. 691-694 ◽  
Author(s):  
Bohun B. Kinloch ◽  
Richard A. Sniezko ◽  
Gayle E. Dupper
Keyword(s):  
Sierra Nevada ◽  
Natural Populations ◽  
The United States ◽  
Hypersensitive Reaction ◽  
White Pine Blister Rust ◽  
Pinus Monticola ◽  
White Pine ◽  
Blister Rust ◽  
Sugar Pine ◽  
Western White Pine

The distribution and frequency of the Cr2 gene for resistance to white pine blister rust (Cronartium ribicola) in western white pine (Pinus monticola) was surveyed in natural populations of the host by inoculation of open-pollinated seedlings from 687 individual seed parents from throughout most of the species' range. Because Cr2 is dominant and results in a conspicuous hypersensitive reaction (HR) in pine needles, the phenotype can readily be detected in offspring of susceptible seed parents fertilized by unknown Cr2 donors in the ambient pollen cloud. Gametic frequencies of Cr2 were thus determined as the proportion of total challenged seedlings that were pollen receptors exhibiting the Cr2 phenotype. Zygotic frequencies, the proportion of seed parents with progeny that segregated in Mendelian ratios for the Cr2 phenotype to the total number of parents, were a complementary, though less precise, measure. Cr2 frequency was rare overall, ranging from 0.004 to 0.008 in the Sierra Nevada to about 0.001 in the central Cascade Range; it was undetectable further north in the Cascades, as well as in the Rocky Mountains and Coast Mountains of the United States and Canada. The diminishing frequency of Cr2 from the southern and central Sierra Nevada northward mirrors that of Cr1 in sugar pine (P. lambertiana) and points to this region as the origin of both genes. We rationalize that this coincidence may have resulted from protection that these genes may have conferred on both species to an endemic pine stem rust congeneric with C. ribicola (C. occidentale) in recent geologic epochs.

Initial tree mortality and insect and pathogen response to fire and thinning restoration treatments in an old-growth mixed-conifer forest of the Sierra Nevada, California

2008 ◽  
Vol 38 (12) ◽  
pp. 3011-3020 ◽  
Author(s):  
Patricia E. Maloney ◽  
Thomas F. Smith ◽  
Camille E. Jensen ◽  
Jim Innes ◽  
David M. Rizzo ◽  
...  
Keyword(s):  
Sierra Nevada ◽  
Forest Restoration ◽  
Tree Mortality ◽  
Large Diameter ◽  
Heterobasidion Annosum ◽  
White Pine Blister Rust ◽  
Mixed Conifer ◽  
White Pine ◽  
Dwarf Mistletoe ◽  
Blister Rust

Fire and thinning restoration treatments in fire-suppressed forests often damage or stress leave trees, altering pathogen and insect affects. We compared types of insect- and pathogen-mediated mortality on mixed-conifer trees 3 years after treatment. The number of bark beetle attacked trees was greater in burn treatments compared with no-burn treatments, and in some cases, larger pine trees were preferentially attacked. Restoration treatments are not expected to change the trajectory of spread and intensification of dwarf mistletoe. Thinning treatments may have provided a sanitation effect in which large leave trees have lower levels of dwarf mistletoe. Although thinning treatments are known to exacerbate root disease, <12% of cut stumps were infected with root pathogens ( Armillaria gallica and Heterobasidion annosum ). Treatments increased Ribes (alternate host for white pine blister rust) frequency and abundance, which may have very localized impacts on white pine blister rust dynamics. In some instances, fire, insects, and pathogens appear to conflict with forest restoration goals by reducing the percentage of pine and producing proportionally higher rates of tree mortality in large-diameter size classes. To better understand the long-term effects of restoration treatments on pathogens and insects, continued monitoring over the course of varying climatic conditions will be needed.

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