The objective of the current study was to investigate the effect of dietary β-alanine supplementation on growth performance, meat quality, antioxidant ability, carnosine content, and gene expression of carnosine-related enzymes in broiler chicks. We randomly assigned 540 1-day-old Arbor Acres broilers to 5 dietary treatments supplemented with 0 (control group), 250, 500, 1,000, or 2,000 mg/kg of β-alanine (mg β-alanine per kg feed). Each treatment included 6 replicates of 18 birds. The feeding trial lasted for 42 d. Dietary β-alanine supplementation linearly and quadratically increased the average daily gain (ADG) during the starting period (d 1 to 21, P = 0.02 and P = 0.002). The feed conversion ratio (FCR) decreased quadratically in response to dietary β-alanine supplementation during the starting and entire periods (P < 0.001 and P = 0.003, respectively). For the entire period, the predicted best FCR would be achieved when β-alanine was fed at a level of 1,100 mg/kg from quadratic regression. The concentrations of carnosine and β-alanine in breast muscle increased quadratically with dietary β-alanine supplementation (d 42, P < 0.001 and P = 0.001, respectively). The predicted dietary β-alanine level for highest breast carnosine content was 1,196 mg/kg. Dietary supplementation with β-alanine reduced the taurine concentrations in plasma (d 42, linear and quadratic, P < 0.001). Breast muscle yield increased linearly and quadratically in response to dietary β-alanine addition (d 21, P = 0.017 and P = 0.007). Dietary supplementation with β-alanine quadratically reduced the shear force (P = 0.003), whereas a*45 min and a*24 h values increased quadratically in response to dietary β-alanine supplementation (d 42, P = 0.020 and P = 0.021, respectively). Dietary β-alanine addition quadratically enhanced the expression of carnosine synthase and taurine transporter mRNAs (P < 0.05). Overall, dietary β-alanine supplementation improved growth performance and carnosine content, ameliorated antioxidant capacity and meat quality, and upregulated the gene expression of carnosine synthesis-related enzymes in broiler chicks.

To investigate the genetic mechanism of Al-tolerance in soybean, a recombinant inbred line population (RIL) with 184 F(2:7:11) lines derived from the cross of Kefeng No.1 x Nannong 1138-2 (Al-tolerant x Al-sensitive) were tested in pot experiment with sand culture medium in net room in Nanjing. Four traits, i.e. plant height, number of leaves, shoot dry weight and root dry weight at seedling stage, were evaluated and used to calculate the average membership index (FAi) as the indicator of Al-tolerance. The composite interval mapping (CIM) under WinQTL Cartographer v. 2.5 detected five QTLs (i.e. qFAi-1, qFAi-2, qFAi-3, qFAi-4 and qFAi-5), explaining 5.20%-9.07% of the total phenotypic variation individually. While with the multiple interval mapping (MIM) of the same software, five QTLs (qFAi-1, qFAi-5, qFAi-6, qFAi-7, and qFAi-8) explaining 5.7%-24.60% of the total phenotypic variation individually were mapped. Here qFAi-1 and qFAi-5 were detected by both CIM and MIM with the locations in a same flanking marker region, GMKF046-GMKF080 on B1 and satt278-sat_95 on L, respectively. While qFAi-2 under CIM and qFAi-6 under MIM both on D1b2 were located in neighboring regions with their confidence intervals overlapped and might be the same locus. Segregation analysis under major gene plus polygene inheritance model showed that Al-tolerance was controlled by two major genes (h(2) (mg) = 33.05%) plus polygenes (h(2) (pg) = 52.73%). Both QTL mapping and segregation analysis confirmed two QTLs responsible for Al-tolerance with relatively low heritability, and there might be a third QTL, confounded with the polygenes in segregation analysis.

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