Genetic dissection of fusiform rust and pitch canker disease traits in loblolly pine

Abstract

Loblolly pine (Pinus taeda L.) exhibits genetic resistance to fusiform rust disease (incited by the biotrophic fungus, Cronartium quercuum f. sp. fusiforme) and pitch canker disease (incited by the necrotrophic fungus, Fusarium circinatum). In this study, a total of 14,015 loblolly pine cuttings from 1,065 clones were screened in controlled greenhouse conditions to identify phenotypes of clones, families, and parents that guide a genetic dissection of disease traits associated with pitch canker and fusiform rust. A total of 23,373 phenotypic data points were collected for lesion length (pitch canker) and gall score, gall length, and gall width (fusiform rust). We verified heritable fusiform rust and pitch canker traits and calculated parental, clonal, and full-sib family rankings for both diseases. Genetic correlations revealed that traits associated with fusiform rust are genetically distinct from one another, and that the genetic mechanisms underlying pitch canker and fusiform rust resistance are independent. The disease phenotyping described here is a critical step towards identifying specific loci and alleles associated with fusiform rust and pitch canker resistance.

Mapping Fusiform Rust Resistance Genes within a Complex Mating Design of Loblolly Pine

“…We also analyzed gall length on susceptible genotypes, in which larger galls indicate greater severity of the disease, whereas smaller galls may reflect a certain degree of tolerance; a possible indicator of partial resistance [16,35,36]. No SNPs were shared between gall score and length datasets, which reinforces the observed lack of genetic correlation between the traits using quantitative genetic methods [16].…”

“…Phenotypic data from the 69 full-sib families of CCLONES were obtained from a previous study [16], where inocula were derived from aeciospores from a single gall (one gall inoculum), as well as with a mixture of aeciospores collected from 10 different galls (10 gall inoculum). The data consisted of results obtained six months after inoculation for both tests.…”

“…Gall score was recorded at the ramet level: 1 for ramets with at least one gall or 0 for ramets with no galls, and then the gall score was calculated for each genotype as the proportion of galled ramets. Gall length (mm) was measured as a continuous trait on all galled ramets [16]. The initial measurements [16] had misclassified families that were discovered after genotypic data became available.…”

“…Gall length (mm) was measured as a continuous trait on all galled ramets [16]. The initial measurements [16] had misclassified families that were discovered after genotypic data became available. Therefore, a DNA marker-corrected pedigree structure of CCLONES was utilized for the current study [21].…”

“…Instead, phenotypes and genotypes can be associated to identify SNPs that explain variance in (i.e., co-segregate with) host resistance to the inoculum. We reasoned that the presence of parents 17 (known Fr1/fr1) and 32 (known Fr8/fr8) in the CCLONES population [16], coupled with the reported avirulence of both one gall and 10 gall inocula to Fr1 [9], would create useful internal checks for validating the approach, and for the possible discovery of additional Fr genes within the population.…”