This course explores the concept of clonal reproduction not being an evolutionary dead end. The learning outcomes include understanding the importance of genotypic-clonal diversity, exploring somatic genetic variation among ramets, and analyzing the role of somatic mutations in adaptation. The course covers topics such as genet vs. ramet terminology, fixed SNPs, genealogy reconstruction, and modes of allele frequency distribution in seagrass data. The teaching method involves a lecture format with discussions on empirical data and challenges in evolutionary pathways. The intended audience includes individuals interested in evolutionary biology, genetic diversity, and adaptation mechanisms in modular species.
Clonal Reproduction Is Not an Evolutionary Dead End
Overview
Syllabus
Intro
Clonal reproduction is not an evolutionary dead end
Clonal reproduction and modularity very widespread life history
Important terminology- genet vs. ramet (J.F. Harper 1977)
A role for genotypic - clonal diversity, replaces species level diversity in species- poor systems
Yet there are millenia-old clones in corals or seagrasses that dominate entire locations
A long-standing ecological riddle
Substantial somatic genetic variation among ramets of the same genet
What to we mean with a fixed SNP?
Genealogy and tree root can be reconstructed
How do we know that this is really a single clone = Benet?
How do these data compare to recent full genome oak studies?
Evolving microbial culture, orange genotype sweeps to fixation
Unitary vs. modular species
Somatic mutations always enterramets as mosaic genetic variation
Proliferating cell population in plants - apical meristem, their genotype determines entire plant
Seagrass data:pronounced modes in allele frequency distribution
Modes of low frequency variants reflect subfixation in stratified meristematic tissue
Evidence for somatic genetic drift: low-frequency variants to rise to fixation consistent with ramet topology
Quick summary
Perspective: can the somatic genetic variation contribute to adaptation?
Challenge #1: mutations need to be partially dominant to be visible to selection in diploids in
Evolutionary pathways with and without sex
But empirical data show appreciable and often similarly rapid adaptation under sexual vs. asexual propagation
What is the evidence that somatic mutations may confer phenotypic variation?
What is the evidence that somatic genetic variation may confer phenotypic variation?
challenge #3: causal polymorphisms difficult to detect since genetic hitchhiking is pervasive (-entire genome linkage group)
Cancer evolutionary biology is facing the same analogous issue what are the casual driver mutations?
Some methods from detecting adaptive dynamics from cancer can be applied to detecting positive selection in modular species
How does the somatically generated variation compare to variation owing to recombination?
Clone members - ramets and concepts of individuality revisited
Taught by
EvoEcoSeminars
