Abstract Detail



Reproductive Processes

Harkness, Alexander [1], Brandvain, Yaniv [2], Goldberg, Emma [1].

Self-incompatibility haplotypes can diversify through sequential mutation and gene conversion.

The origin of novel complex regulatory mechanisms is a central problem in evolutionary biology. The RNase-based system of self-pollen rejection in the Solanacese is a prime example of this problem. In this case, an S-haplotype consists of a poison RNase expressed in the style tightly linked to multiple SLF paralogs which act as antidotes expressed in pollen. The SLF that detoxifies a given RNase is not found on that haplotype and thus self pollen is rejected, while pollen from other S-haplotypes can be accepted. Clearly, there is no benefit to a stylar poison without an antidote, and there is similarly no benefit to an SLF antidote without a toxin. How then can a new incompatibility allele spread? Here we develop a population genetic model of the evolution of a novel S-haplotype. We show that a novel RNase poison is initially favored because it reduces the fitness of haplotypes lacking the antidote to it, and a new equilibrium of RNases is achieved. We then show the conditions allowing the SLF variant that detoxifies this RNase to spread through the population by gene conversion before S-haplotypes lacking this antidote are lost. Our results show that a parsimonious model including only gene conversion and known incompatibility relations is sufficient to explain the possibility of diversification of S-locus haplotypes, though additional factors probably determine the rate of RNase diversification in nature.


1 - University of Minnesota, Ecology, Evolution, and Behavior, 1479 Gortner Ave, 140 Gortner Lab, St. Paul, MN, 55108, United States
2 - University of Minnesota, Plant and Microbial Biology, 1479 Gortner Ave, 140 Gortner Lab, St. Paul, MN, 55108, United States

Keywords:
Self-incompatibility
Breeding system
Solanaceae.

Presentation Type: Poster
Number: PRP009
Abstract ID:435
Candidate for Awards:None


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