Subterranean Fishes of the World

4270

2019

AIM 2019

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Animals live in dynamic habitats. To cope, they have evolved phenotypic plasticity: the ability to change a trait depending on external conditions. Phenotypic plasticity of the digestive system is advantageous in environments with fluctuating food sources, allowing animals to alter enzyme production or the surface area of the intestinal epithelium to maximize nutrient assimilation during times of food abundance, and conserve energy when food is scarce. Astyanax mexicanus is an ideal model to investigate the evolution and genetic basis of phenotypic plasticity; cave populations have adapted to seasonal cycles of nutrient deprivation and abundance compared to river counterparts that have more regular access to food. Both populations can be maintained in the lab under controlled conditions, allowing dissection of genotype-phenotype interactions. We found that on the same diet, Tinaja cavefish have a longer gastrointestinal (GI) tract and more proliferation in the intestinal epithelium compared to surface fish. Under starved conditions, the Tinaja gut decreases proliferation and length, while the surface gut maintains proliferation and eventually atrophies. Combined, these findings suggest that the Tinaja gut is more responsive to changes in nutrients. To investigate the genetic basis of the observed differences, we carried out a quantitative trait loci (QTL) analysis, measuring the length of the GI tract in 219 surface/Tinaja F2 hybrids that were individual housed and consumed 6mg of food per day. We generated a linkage map using 1792 single nucleotide polymorphisms identified using genotype-bysequencing (GBS). Our analysis revealed a QTL associated with the length of the hindgut. We identified 10 genes within the QTL interval that have fixed differences between Tinaja cavefish and Rio Choy surface fish based on sequencing data from wild populations. The most promising candidate for influencing hindgut length is Kruppel-like transcription factor 5 (KLF5). KLF5 controls proliferation of the intestinal epithelium in mice and has a known role in colon cancer. Our findings establish a link between evolution and stem cell biology and may lead to a better understanding of the genetic and molecular basis of phenotypic plasticity.

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