The Genomic Basis of Life-History Adaptation

The Flatt group investigates the genomic basis of adaptation, using the fruit fly Drosophila melanogaster as a model system. The phenotypic components of Darwinian fitness, so-called life history traits (e.g., growth, size, fecundity, survival and lifespan), are fundamentally important for adaptation because they represent the direct targets of selection. However, despite their importance, still little is known about the genetic basis of evolutionary changes in fitness-related traits.

The research questions we ask include:

  • Which genes and polymorphisms underlie life-history adaptations?
  • What are the genes that underlie the evolution of body size, reproduction, and lifespan?
  • Why do reproduction and survival trade off?
  • What is the genomic basis of adaptation along clinal (e.g., latitudinal) gradients?
  • Why are flies in the cold, i.e. at high latitude, bigger and longer-lived?
  • What is the role of chromosomal inversions and super-genes in shaping adaptation? 
  • What are the mechanisms underlying life-history plasticity?

To address these major questions we combine the tools of population genetics and genomics, developmental genetics, physiology, experimental evolution and artificial selection, and apply them to natural and laboratory populations of Drosophila melanogaster.

  • What molecular polymorphisms underpin life-history adaptations?

    Over the past few years, we have been using two complementary approaches to identify naturally occurring polymorphisms that underlie evolutionary changes in life history: to generate "catalogs" of candidate variants we have applied whole-genome Pool-sequencing to (1) North American populations clinally differentiated for life history and (2) a >30-year-long artificial selection experiment for longevity. Both approaches are "designed" to maximize among-population life-history differentiation and thus to increase our ability to map life-history variants via sequencing. In a second step, we have begun to perform experiments to examine the life-history effects of some of these mechanisms. Based on our genomic analyses, we have prioritized three candidate mechanisms for experiments: (1) for the cline, we have identified clinal SNPs in several genes involved in insulin signaling, a pathway known to regulate life-history physiology; (2) a clinal chromosomal inversion polymorphism to which 80% of the most strongly clinal SNPs map; and (3), in the selection experiment we have found strong enrichment of immunity genes among our top candidates. We are currently working on functional experiments to characterize these and other candidate mechanisms.

  • How do life-history trade-offs work?

    Trade-offs between life-history traits, for example between fecundity and lifespan are ubiquitous, but little is known about their underlying mechanisms. Recent work suggests that reproduction and life span might be linked by molecular signals produced by reproductive tissues. In the nematode C. elegans, life span is extended if worms lack proliferating germ cells in the presence of an intact somatic gonad. This suggests that the gonad is the source of signals which physiologically modulate organismal aging. Our previous work has shown that such gonadal signals are also present in D. melanogaster, suggesting that the regulation of lifespan by the reproductive system is evolutionarily conserved. Ablation of germline stem cells in the fly extends lifespan and modulates components insulin signaling in peripheral tissues, a conserved pathway important in regulating growth, metabolism, reproduction, and aging. Thus, as of yet unidentified endocrine signals from the germline might converge onto IIS to regulate aging. Our current work focuses on understanding the physiological and transcriptomic mechanisms that mediate the trade-off between reproduction and life span.

Thomas Flatt

Professor

Office PER 01 DECANAT/PAVILLON - 0.366b
+41 26 300 8833

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Department of Biology

Chemin du Musée 10 
CH-1700 Fribourg 
Switzerland