Science Topics: Forest Genetics
White Pine Blister Rust in Western North America
A disease native to Asia, white pine blister rust was introduced separately into both eastern and western North America early in the 20th century. In both cases, the vector was seedlings of native eastern white pine imported from European nurseries, where they had become infected. Blister rust had first appeared in Europe in the mid-nineteenth century, and within three decades had spread across the continent wherever the popular eastern white pine had been planted.
In western North America, the rust spread in serial jumps from a nursery near Vancouver, British Columbia, south through the Cascades and Sierra Nevada, and east to the northern Rocky Mountains. All native white pine are susceptible. Economic impact has been most acute on the two large commercial species, western white pine and sugar pine, but ecological damage has been equally severe on high elevation species such as whitebark and limber pines in many places. More recently, an outbreak was recorded in the Sacramento Mountains of New Mexico on southwestern white pine. Infection is not always uniform; it often forms a mosaic pattern over the landscape, where patches of intense infection give way to areas of lighter or no infection.
Infected seedlings and saplings are almost always killed directly but trees of all ages and sizes are vulnerable. In larger trees, mortality is often indirect; when trees become weakened from heavy infection in their crowns, they more easily succumb to drought or attack by bark beetles. Where hazard is high, over 95% of mature trees in a stand can be killed over time. [learn more]
Blister rust alternates between white pines (subgenus strobus, section strobus), and currants and gooseberries in the genus Ribes. Five different spore stages are necessary to complete the life cycle; two are on pine, and three on Ribes. [learn more]
In both alternate hosts, infection takes place through open stomata on leaves. On pines, a basidiospore sends a germ tube through a stomate, and develops a bulbous substomatal vessicle. From this, a primary infection hypha extends into mesophyll tissue, where a mass of mycelium grows into a "pseudosclerotium'' like structure. At this point, a macroscopic symptom of the disease is expressed as a yellow spot. Soon, mycelium penetrates into the vascular cylindar, grows down the phloem to the base of the needle, and establishes in living bark tissues of the shoot. The visible incipient symptom is a pink/orange discoloration of the shoot. This is followed about a year later by pycnia, spore structures that bear pycniospores (spermatia), that function as gametes. A year later, aecia and aeciospores are formed in the same locus (see Life Cycle) [learn more]
Research at IFG has four main objectives:
- Understand the mechanisms and inheritance of resistance
- Major gene resistance (MGR) - A hypersensitive reaction in needle tissues conditioned by a dominant gene.
- Slow rustin resistance (SRR) - SRR is a composite term for several independent mechanisms of partial resistance, which individually or collectively reduce the rate of infection and mortality.
- Ontogenetic resistance (OGR) - OGR is a kind of resistance that increases with age. The inheritance and age of onset are unknown, but it is genetype specific.
- Understand the genetic structure of rust populations, including virulence
- Develop gene deployment strategies for durable resistance
- Chromosomal mapping and cloning resistance genes