👤 Michael Hiller

High-sugar diets cause human metabolic diseases, yet several bird lineages convergently adapted to feeding on sugar-rich nectar or fruits. We investigated the underlying molecular mechanisms in hummingbirds, parrots, honeyeaters, and sunbirds by generating nine new genomes and 90 tissue-specific transcriptomes. Comparative screens revealed an excess of repeated selection in both protein-coding and regulatory sequences in sugar-feeding birds, suggesting reuse of genetic elements. Sequence or expression changes in sugar-feeders affect genes involved in blood pressure regulation and lipid, amino acid, and carbohydrate metabolism, with experiments showing functional changes in honeyeater hexokinase 3. Show less

We systematically investigate whether losses of human disease-associated genes occurred in other mammals during evolution. We first show that genes lost in any of 62 non-human mammals generally have a lower degree of pleiotropy, and are highly depleted in essential and disease-associated genes. Despite this under-representation, we discovered multiple genes implicated in human disease that are truly lost in non-human mammals. In most cases, traits resembling human disease symptoms are present but not deleterious in gene-loss species, exemplified by losses of genes causing human eye or teeth disorders in poor-vision or enamel-less mammals. We also found widespread losses of Show less

The effect of a 10-week supplementation with polyunsaturated fatty acids [via sunflower oil/DHA-rich algae (SUNA) or linseed oil/DHA-rich algae (LINA) enriched diets] versus saturated fatty acids (SAT) of lactating German Holstein dairy cows in mid-lactation on expression patterns of lipid metabolism-associated genes and gene products in hepatic, longissimus muscle and subcutaneous/perirenal/omental adipose tissue was assessed. Most pronounced transcriptomic responses to dietary PUFA were obtained in hepatic [down-regulated ACACA (FC = 0.83, SUNA; FC = 0.86, LINA), FADS1 (FC = 0.60, SUNA; FC = 0.72, LINA), FADS2 (FC = 0.64, SUNA; FC = 0.79, LINA), FASN (FC = 0.64, SUNA; FC = 0.72, LINA), SCD (FC = 0.37, SUNA; FC = 0.47, LINA) and SREBF1 (FC = 0.79, SUNA, LINA) expression] and omental adipose [up-regulated ACACA (FC = 1.58, SUNA; FC = 1.22, LINA), ADFP (FC = 1.33, SUNA; FC = 1.32, LINA), CEBPA (FC = 1.75, SUNA; FC = 1.40, LINA), FASN (FC = 1.57, SUNA; FC = 1.21, LINA), LPL (FC = 1.50, SUNA; FC = 1.20, LINA), PPARG (FC = 1.36, SUNA; FC = 1.12, LINA), SCD (FC = 1.41, SUNA; FC = 1.17, LINA) and SREBF1 (FC = 1.56, SUNA; FC = 1.18, LINA) expression] tissue. Interestingly, gene/gene product associations were comparatively low in hepatic and omental adipose tissue compared with longissimus muscle, perirenal adipose and subcutaneous adipose tissue, indicating matches only in regard to minor concentrations of SCD product 18:1c9, FADS1 product 20:4n-6 and FADS2 product 18:3n-6 in hepatic tissue, and higher concentrations of ACACA and FASN gene products 12:0 and 14:0 and SCD product 18:2c9,t11 in omental adipose tissue. Whereas all analyzed tissues accumulated dietary PUFA and their ruminally generated biohydrogenation products, tissue-divergent preferences for certain fatty acids were identified. This descriptive study reports tissue-divergent effects of dietary PUFA and outlines the significance of a PUFA intervention with regard to dairy cows' nutritional management. Show less