PATERNAL EFFECTS IN INHERITANCE OF A PATHOGEN RESISTANCE TRAIT IN IPOMOEA PURPUREA

Ellen L Simms; Jim K Triplett

doi:10.1111/j.1558-5646.1996.tb03608.x

PATERNAL EFFECTS IN INHERITANCE OF A PATHOGEN RESISTANCE TRAIT IN IPOMOEA PURPUREA

Evolution. 1996 Dec;50(6):2178-2186. doi: 10.1111/j.1558-5646.1996.tb03608.x.

Authors

Ellen L Simms^{1

2}, Jim K Triplett²

Affiliations

¹ Department of Ecology and Evolution, The University of Chicago, 1101 East 57th Street, Chicago, Illinois, 60637.
² Department of Biology, Box 7325 Reynolda Station, Wake Forest University, Winston-Salem, North Carolina, 27109.

PMID: 28565670
DOI: 10.1111/j.1558-5646.1996.tb03608.x

Abstract

For continuously variable, polygenic characters, the response to selection depends upon the proportion of phenotypic variance that is caused by additive genetic variance, or narrow-sense heritability. Thus, a major goal of quantitative genetics is to partition phenotypic variance for a trait in a way that isolates additive genetic variance from other causes. The variance among paternal half-sib families, which is frequently used to estimate additive variance, is commonly recognized to include additive epistatic effects. However, this variance component can also include non-Mendelian paternal effects. We report here the results from a diallel crossing design used to isolate nonnuclear effects from the paternal nuclear contribution to disease resistance in the common morning glory, Ipomoea purpurea. In particular, we found that genetic variance for resistance to anthracnose, a disease caused by the fungal pathogen Colletotrichum dematium, was determined largely by a nonnuclear, additive paternal effect. We discuss potential mechanisms for this effect as well as some of their evolutionary implications.

Keywords: Gametophytic competition; genomic imprinting; maternal effects; pollen competition; quantitative genetics.