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Möller, M.

Publications and source records attributed to Möller, M..

3 recordsLinked to original sources

Learning the payoffs and costs of actions

A set of sub-cortical nuclei called basal ganglia is critical for learning the values of actions. The basal ganglia include two pathways, which have been associated with approach and avoid behavior respectively, and are differentially modulated by dopamine projections from the midbrain. According to the influential opponent actor learning model, these pathways represent learned estimates of the positive and negative consequences (payoffs and costs) of actions. The level of dopamine release controls to what extent payoffs and costs enter the overall evaluation of actions. How the knowledge about payoff and cost is acquired is still an open question, even though many theories describe learning from feedback in the basal ganglia. We examine whether a set of plasticity rules proposed to model reinforcement learning in the pathways of the basal ganglia is suitable to extract payoffs and costs from a reward prediction error signal. First, we determine the result of such learning, both analytically and via simulations, for different reward schedules that feature payoffs and costs. Then, we combine the plasticity rules with a decision rule to examine the emerging effect of dopaminergic modulation on the willingness to work for reward. We find that the plasticity rules are suitable to infer the mean payoffs and costs of actions, if those occur at different moments in time. Successful learning requires differential effects of positive and negative reward prediction errors on the two pathways, and a weak decay of synaptic weights over trials. We also confirm that dopaminergic modulation produces effects on the willingness to work for reward similar to those observed in classical experiments.\n\nAuthor summaryThe basal ganglia are structures underneath the surface of the vertebrate brain, associated with error driven learning. Much is known about the anatomical and biological features of the basal ganglia; scientists now try to understand the algorithms implemented by these structures. Numerous models aspire to capture the learning functionality, but many of them only cover some specific aspect of the algorithm. Instead of further adding to that pool of partial models, we unify two existing ones - one which captures what the basal ganglia learns, and one that describes the learning mechanism itself. The first model suggests that the basal ganglia keeps track of both positive and negative consequences of frequent opportunities, and weighs these by the motivational state in decisions. It explains how payoff and cost are represented, but not how those representations arise. The other model consists of biologically plausible plasticity rules, which describe how learning takes place, but not how the brain makes use of what is learned. We show that the two theories are compatible. Together, they form a model of learning and decision making that integrates the motivational state as well as the learned payoffs and costs of opportunities.

neuroscience

Extraordinary genome instability and widespread chromosome rearrangements during vegetative growth

The haploid genome of the pathogenic fungus Zymoseptoria tritici is contained on \"core\" and \"accessory\" chromosomes. While 13 core chromosomes are found in all strains, as many as eight accessory chromosomes show presence/absence variation and rearrangements among field isolates. We investigated chromosome stability using experimental evolution, karyotyping and genome sequencing. We report extremely high and variable rates of accessory chromosome loss during mitotic propagation in vitro and in planta. Spontaneous chromosome loss was observed in 2 to >50 % of cells during four weeks of incubation. Similar rates of chromosome loss in the closely related Z. ardabiliae suggest that this extreme chromosome dynamic is a conserved phenomenon in the genus. Elevating the incubation temperature greatly increases instability of accessory and even core chromosomes, causing severe rearrangements involving telomere fusion and chromosome breakage. Chromosome losses do not impact the fitness of Z. tritici in vitro, but some lead to increased virulence suggesting an adaptive role of this extraordinary chromosome instability.

genomics

An Unexpectedly Complex Architecture for Skin Pigmentation in Africans

Fewer than 15 genes have been directly associated with skin pigmentation variation in humans, leading to its characterization as a relatively simple trait. However, by assembling a global survey of quantitative skin pigmentation phenotypes, we demonstrate that pigmentation is more complex than previously assumed with genetic architecture varying by latitude. We investigate polygenicity in the Khoe and the San, populations indigenous to southern Africa, who have considerably lighter skin than equatorial Africans. We demonstrate that skin pigmentation is highly heritable, but that known pigmentation loci explain only a small fraction of the variance. Rather, baseline skin pigmentation is a complex, polygenic trait in the KhoeSan. Despite this, we identify canonical and non-canonical skin pigmentation loci, including near SLC24A5, TYRP1, SMARCA2/VLDLR, and SNX13 using a genome-wide association approach complemented by targeted resequencing. By considering diverse, under-studied African populations, we show how the architecture of skin pigmentation can vary across humans subject to different local evolutionary pressures.\n\nHighlightsO_LISkin pigmentation in Africans is far more polygenic than light skin pigmentation in Eurasians.\nC_LIO_LIKhoeSan[§] populations, which diverged early in human prehistory from other populations, have lightened skin pigmentation compared to equatorial Africans.\nC_LIO_LISkin color is highly heritable in the KhoeSan, but pigmentation variability is not well explained by previously discovered pigmentation genes.\nC_LIO_LIWe perform the first GWAS for pigmentation in African KhoeSan populations and identify canonical pigmentation loci near TYRP1 and in SLC24A5, as well as novel associations surrounding SMARCA2 and other genes.\nC_LI

genetics