Genetic and dietary interactions of fishy-egg taint in brown-shelled laying hens

Abstract

Fishy-egg tainting has long been a problem associated with feeding canola meal (CM) to brown-shelled laying hens. It is a classical example of nutrigenetics, as both dietary and genetic factors must be present for a hen to lay fishy-tainted eggs. Trimethylamine (TMA), the compound responsible for the fishy smell, is produced by bacterial fermentation of choline in the lower gut. CM contains large amounts of choline in the form of sinapine. Choline must first be hydrolyzed from sinapine before it can be absorbed or converted to TMA. Normally, the malodourous TMA is metabolized to the odourless trimethylamine N-oxide (TMAO) by flavin-containing monooxygenase 3 (FMO3). A mutation in FMO3 (c.984A>T) prevents TMA from being oxidized to TMAO, and subsequently TMA accumulates in the developing egg yolks. Our objective was to determine the inheritance pattern of fishy-egg tainting when hens are fed canola meal, reflecting typical industry conditions. In the first of two trials, hens of a commercial brown-shelled strain were genotyped at FMO3 c.984A>T and fed graded levels of CM (0, 6, 12, or 18%). These hens were bred to produce a second generation of hens, which were also genotyped and fed graded levels of CM (0, 6, 12, 18, or 24%) or choline chloride (0, 0.055, 0.110, 0.165, or 0.220%). Choline chloride, at levels up to 0.220%, does not lead to the production of fishy tainted-eggs. When fed CM, TT hens laid fishy-tainted eggs. Mean yolk TMA concentration was not significantly different between hens of the AA and AT genotypes, with means from both genotypes remaining below the human detection threshold for all of the dietary treatments. Large day-to-day variations in yolk TMA concentration were seen in hens of all three genotypes. We concluded that fishy-egg tainting is recessive when hens are fed CM at levels reflecting typical commercial practices.