Abstract
Quail eggs comprise a significant and favourable part of table eggs in certain countries. Some quail eggs, however, present fishy off-flavor which directly influences their quality. It is reported that flavin-containing monooxygenase 3 (FMO3) is associated with fish-odour trait in human and animal products. FMO3 is responsible for the degradation of trimethylamine (TMA) in vivo. Loss-of-function mutations in FMO3 gene can result in defective TMA N-oxygenation, giving rise to disorder known as “fish-odour syndrome” in human, as well as the fishy off-flavor in cow milk and chicken eggs. In order to reveal the genetic factor of fishy taint in quail eggs, we cloned the cDNA sequence of quail FMO3 gene, investigated FMO3 mRNA expression level in various tissues, detected SNPs in the coding region of the gene and conducted association analysis between a mutation and the TMA content in quail egg yolks. The 1888 bp cDNA sequence of quail FMO3 gene encoding 532 amino acids was obtained and characterized. The phylogenetic analysis revealed quail FMO3 had a closer relationship with chicken FMO3. The FMO3 mRNA was highly expressed in liver and kidney of quail. Nine SNPs were detected in the coding sequence of quail FMO3 gene, including a nonsense mutation (Q319X) which was significantly associated with the elevated TMA content in quail egg yolks. Genotype TT at Q319X mutation loci was sensitive to choline. With addition of choline in the feed, the quails with homozygote TT at the Q319X mutation loci laid fish-odour eggs, indicating an interaction between genotype and diet. The results indicated that Q319X mutation was associated with the fishy off-flavor in quail eggs. Identification of the unfavorable allele T of quail FMO3 gene can be applied in future quail breeding to eliminate fishy off-flavor trait in quail eggs.
Highlights
Flavin-containing monooxygenases (FMOs, EC 1.14.13.8) are responsible for the oxidation of numerous xenobiotics containing a nucleophilic nitrogen, sulfur, phosphorous, or selenium heteroatom [1,2]
The individuals with disabled flavin-containing monooxygenase 3 (FMO3) cannot oxidize TMA to trimethylamine Noxide (TMAO) in the liver, and that will result in massive amounts of TMA excreted in urine, sweat and breath and present a body odour like the rotting fish, which is called trimethylaminuria (TMAU) or fish-odour syndrome [10,11]
We described the variation in the quail FMO3 gene coding sequence and found a nonsense mutation (Q319X) in exon 7 was highly associated with the elevated TMA content in quail egg yolks, which could be used as an important marker to eliminate the fishy taint in quail eggs in future quail molecular breeding
Summary
Flavin-containing monooxygenases (FMOs, EC 1.14.13.8) are responsible for the oxidation of numerous xenobiotics containing a nucleophilic nitrogen, sulfur, phosphorous, or selenium heteroatom [1,2]. The individuals with disabled FMO3 cannot oxidize TMA to TMAO in the liver, and that will result in massive amounts of TMA excreted in urine, sweat and breath and present a body odour like the rotting fish, which is called trimethylaminuria (TMAU) or fish-odour syndrome [10,11] This metabolic disorder disease is inherited in a recessive manner. Since the first P153L mutation in human FMO3 gene was verified to be associated with TMAU [12], more than 30 distinct causative mutations in human FMO3 gene have been identified in subsequent studies [13,14,15,16] Some animal products such as cow milk and chicken eggs present fishy off-flavor or fish-odour due to the elevated levels of TMA in them [17,18]. We described the variation in the quail FMO3 gene coding sequence and found a nonsense mutation (Q319X) in exon 7 was highly associated with the elevated TMA content in quail egg yolks, which could be used as an important marker to eliminate the fishy taint in quail eggs in future quail molecular breeding
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