Bohun B. Kinloch

White Pine Blister Rust in North America: Past and Prognosis

ABSTRACT After a full century in North America, the blister rust epidemic has yet to stabilize, continuing to spread into warmer and drier areas previously considered climatically inhospitable. The disease apparently has no environmental limits wherever white pines and Ribes spp. cohabit and will eventually become pandemic. Although much timber value has been lost, more severe long-term damage is disruption caused to ecosystems by altered patterns of natural succession. During the last half of the century just past, development of genetic resistance superceded other direct control measures-mainly Ribes spp. eradication and antibiotics-which proved ineffective and/or unfeasible in large areas of the white pine range, especially in the West. Several mechanisms of complete (major gene) and partial resistance are common to at least several white pine species. Although North American populations of rust have low genetic variability overall, rust genotypes with specific virulence to major resistance genes exist in some local demes at high frequencies. The challenge will be to package and deploy resistance genes in ways that will dampen sudden increases in rust races of wide virulence. New introductions of blister rust from its gene center in Asia remain the gravest threat to genetic improvement programs.

A major gene for resistance to white pine blister rust in Western white pine from the Western cascade range.

ABSTRACT A dominant gene for resistance to white pine blister was indicated by Mendelian segregation in full-sib families of western white pine parent trees selected for phenotypic resistance in six heavily infected stands in the Western Cascades of Oregon and Washington. Seedlings were artificially inoculated three times between 1959 and 1964 and observed for development of stem infection. Segregation at this locus (Cr2) occurred in only two of the six parent populations sampled: one a natural stand, Champion Mine (CM), and the other a plantation of unknown seed origin. At CM, reduced penetrance of this gene was expressed by altered Mendelian ratios (mostly less-than-expected resistant phenotypes) in families of specific combinations of certain parents, indicating the presence of modifier genes with effects that ranged from mild to almost complete suppression of Cr2. Between 1968 and 1994, an apparent shift in virulence at CM caused all of the resistant selections to become infected and die. Recent inoculations of many of the same or related families from these parents, made from grafted ramets in a seed orchard, showed that Cr2 conditions a classical hypersensitive reaction (HR) in needle tissues, the primary infection courts. In the latter tests, seedlings were challenged with wild-type and four other sources of inoculum at and near CM that were also suspected of having wider virulence than wild type. No seedlings segregating for HR that were inoculated with wild type subsequently developed stem symptoms, but the other inocula induced both susceptible and HR needle spots on Cr2- genotypes, and many of these seedlings did develop stem infections. This implied that spore genotypes with specific virulence to Cr2 are carried in these inocula.

Genetic specificity in the white pine-blister rust pathosystem

ABSTRACT 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.

Evidence of Cytoplasmic Inheritance of Virulence in Cronartium ribicola to Major Gene Resistance in Sugar Pine.

ABSTRACT 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.