Inheritance of virulence in Fusarium circinatum, the cause of pitch canker in pines

Abstract

Wildtype strains of Fusarium circinatum, the causal agent of pitch canker, were crossed to obtain an F1 generation. Progeny of this cross were tested for virulence by inoculating Pinus radiata seedlings, and were found to induce a wide range of lesion lengths. Two strains from the F1 generation that induced long lesions (= high virulence) were used as parents to produce an F2 generation, followed by a second round of selection for high virulence to obtain an F3 generation. Mean lesion lengths were not significantly different between the three generations (P ≥ 0.196). A parallel set of crosses was performed to select for low virulence by using progeny in the F1 and F2 generations that induced short lesions as parents for F2 and F3 generations, respectively. In this case, both rounds of selection resulted in a significant reduction in mean lesion length, from 33.8 ± 0.8 mm in the F1 generation, to 19.7 ± 0.7 and 12.9 ± 0.7 mm in the F2 and F3 generations, respectively. Thus it is apparent that F. circinatum retains the genetic capacity for avirulence to pines, which could reflect a lack of strong selection for virulence in nature. Progeny of a cross between high and low virulence parents manifested nearly continuous variation in lesion lengths, consistent with virulence being a quantitatively inherited trait. Based on this cross, broad‐sense heritability (H2) was determined to be 0.74, which suggests that virulence is under strong genetic control.