Throughout the eastern United States, several morning glory (Ipomoea) species are alternate hosts to a red rust, Coleosporium ipomoeae. Among these species are Ipomoea coccinea L., Ipomoea hederacea Jacq., and Ipomoea purpurea (L.) Roth, each of which is an annual herbaceous flowering plant that occurs commonly in agricultural fields, field margins, and other disturbed habitat. Outcrossing rates in these species vary: I. hederacea is highly selfing [93% (15)], I. purpurea’s selfing rate has been reported to be between 20% and 70% (15–17), and, although selfing in I. coccinea has not been explicitly quantified, the species is self-fertile (18). None of the species are capable of hybridizing.
Throughout the eastern United States, the rust C. ipomoeae attacks several species of morning glory hosts, including I. hederacea, I. purpurea, and I. coccinea. The pathogen is a heteroecious rust, with pines (especially Pinus taeda) in the southeastern United States as its primary host. In early summer (late May through early June), dikaryotic spores (aeciospores) are formed on pines and subsequently infect the Ipomoea secondary hosts. Infections of Ipomoea produce asexual spores (urediniospores) that reinfect the secondary hosts, with up to 15 asexual generations occurring during the summer. In the fall, asexual spores (teliospores) colonize the primary hosts and subsequently undergo diploidization, meiosis, and fusion to form the dikaryotic hyphae that give rise to the aeciospores in the spring.
Crossing experiments have shown that resistance to individual pathogen inocula (spores collected from the same host species at a particular site) is often determined by genotype at a single genetic locus (19, 20). In addition, these studies provided evidence indicating that loci conferring resistance to a particular pathogen inoculum sometimes differ between populations of the same host species. These results suggest that GFG interactions may frequently be involved in the coevolution of C. ipomoeae and its hosts. In addition, infection by C. ipomoeae reduces fitness substantially in I. purpurea (21, 22), suggesting the potential for the pathogen to drive the evolution of resistance in its hosts.
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