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BackgroundToll-like receptor 2 (TLR2), an important pattern recognition receptor, activates proinflammatory pathways in response to various pathogens. It has been reported in humans and chicken, but not in geese, an important waterfowl species in China. Since some vaccines stimulate robust immune responsesl in chicken but not in geeeses we speculated that their immune systems are different.ResultsIn this study, we cloned the goose TLR2-1 gene using rapid amplification of cDNA ends (RACE)and showed that geese TLR2-1 encoded a 793-amino-acid protein, containing a signal secretion peptide, an extracellular leucine-rich repeat domain, a transmembrane domain and a Toll/interleukin-1 receptor signaling domain deduced from amino acid sequence. TLR2-1 shared 38.4%–93.5% homology with its homologues in other species. Tissue expression of geese TLR2-1 varied markedly, and was higher in kidney, cloacal bursa, skin and brain compared to other organs/tissues. HEK293 cells transfected with plasmids carrying goose TLR2-1 and NF-κB-luciferase responded significantly to stimulation with Mycoplasma fermentans lipopeptide. Furthermore, geese infected with Mycoplasma gallisepticum (MG) and Salmonella enteritidis (SE) showed significant upregulation of TLR2-1 in both in vivo and in vitro.ConclusionGeese TLR2-1 is a functional homologue of TLR2 present in other species and plays an important role in bacterial recognition in geese.

Qingyuan partridge chicken is one of the most well-known Chinese indigenous yellow broilers. In breeding programmes, five traits are usually selected when the chickens are 105 days old, namely body weight (BW), comb height (CH), shank length (SL), shank girth (SG) and feather maturity (FM). The objective of this study was to estimate the genetic parameters of these five traits, especially direct additive genetic correlations, to lay the foundation for balanced selection of Qingyuan partridge chickens. Approximately 9600 records were used for estimation. Variance components for these five traits were estimated using three multitrait models incorporating different effects via Gibbs sampling. Based on model 1 in which the random effects included direct additive genetic effects and residuals, the estimated direct heritabilities for BW, CH, SL, SG and FM were 0.29 ± 0.04, 0.53 ± 0.04, 0.47 ± 0.04, 0.43 ± 0.05 and 0.18 ± 0.03, respectively. The direct genetic correlations ranged from −0.08 to 0.46. When additionally considering maternal additive genetic effects (model 2), the estimates of direct heritabilities and absolute values of direct additive genetic correlations were smaller. The heritabilities were 0.14 ± 0.04, 0.40 ± 0.02, 0.34 ± 0.05, 0.27 ± 0.05 and 0.12 ± 0.03 for BW, CH, SL, SG and FM, respectively. The direct additive genetic correlations ranged from −0.33 to 0.36. More specifically, the direct additive genetic correlations between BW and CH, SL, SG and FM were 0.19 ± 0.13, 0.15 ± 0.15, 0.36 ± 0.15 and − 0.33 ± 0.21, respectively. The genetic correlations of FM with SL, SG and CH were − 0.15 ± 0.15, −0.08 ± 0.17 and 0.18 ± 0.15, respectively. The direct genetic correlations between CH and SG and SL were − 0.02 ± 0.11 and − 0.20 ± 0.11, respectively, and that between SL and SG was 0.19 ± 0.11. The total heritabilities and maternal additive genetic correlations ranged from 0.16 to 0.44 and from −0.13 to 0.61, respectively.The third model also included the maternal permanent environmental effect for BW. The estimates of direct heritability, direct additive genetic correlation, total heritability and maternal additive genetic correlation were only slightly different

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