The function of the sperm storage tubules is directly correlated with the fertility of laying hens. However, little is known about the molecular mechanisms regulating the fertility traits in chicken. To identify genetic markers associated with reproductive traits, we calculated fertility rate at 61 to 69 wk (51 D) of Jing Hong chickens parent generation as the phenotype and the genotype were detected by the chicken 600K Affymetrix Axiom High Density single nucleotide polymorphisms ( SNP )-array. The genome-wide association study using 190 Jing Hong hens showed that the 20 SNP in chromosomes 3 and 13 were significantly associated with fertility rate. To verify these results, a total of 1900 Jing Hong laying hens from 2 populations (P1 and P2) were further genotyped by polymerase chain reaction–restriction fragments length polymorphisms method. The association analysis results revealed that 12 polymorphisms (AX-75769978, AX-76582632, AX-75730546, AX-75730496, AX-75730588, AX-76530282, AX-76530329, AX-76529310, AX-75769906, AX-75755394, AX-80813697 and AX-76582809) out of 20 showed highly significant effects ( P < 0.0001) on fertility rate in P1, P2 and P1+P2. Six haplotypes (TTAA, TTGG, TTAG, CTAA, CTGG, and CTAG) were inferred based on significant loci (AX-75730546 and AX-76530282) also showed significant association with fertility rate, where haplotype CTAG was shown to be markedly associated with the significantly highest ( P < 0.0001) fertility rate (in P1, 86.42 ± 0.59; P2, 85.98 ± 0.59 and P1+P2, 86.16 ± 0.42) followed by other haplotypes for the irrespective of population studied. Collectively, we report for the first time that 12 SNP in the chromosomes 3 and 13 were significantly associated with fertility rate during the later stage of egg production, which could be used as the potential genetic markers that would be able to facilitate in the selection and improvement of fertility rate through chicken breeding.

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Understanding the genetic mechanism of highland adaptation is of great importance for breeding improvement of Tibetan chickens (TBC). Some studies of TBC have identified some candidate genes and pathways from multiple subgroups, but the related genetic mechanisms remain largely unknown. Different genetic backgrounds and the independent genetic basis of highland adaptation make it difficult to identity the selective region of highland adaptation with all TBC samples. In this study, we conducted preanalysis in a large-scale population to select a TBC subgroup with the purest and highest level of highland-specific lineage for the further analysis. Finally, the 37 samples from a TBC subgroup and 19 Lahsa White chickens were used to represent the highland group for further analysis with 80 samples from five Chinese local lowland breeds as controls. Population structure analysis revealed that highland adaptation significantly affected population stratification in Chinese local chicken breeds. Genome-wide selection signal analysis identified 201 candidate genes associated with highland adaptation of TBC, and these genes were significantly enriched in calcium signaling, vascular smooth muscle contraction and the cellular response to oxidative stress pathways.Additionally, we identified a narrow 1.76 kb region containing an overlapping region between HBZ and an active enhancer, and our identified region showed a highly significant signal. The highland group selected the haplotype with high activity to improve the oxygen-carrying capacity, thus being adapted to

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Background Acute heat stress could induce high mortality and cause huge economic losses in the poultry industry. Although many studies have revealed heat stress-induced injuries of multiple tissues, the main target tissue and molecular mechanism of death under acute heat stress was largely unknown. This study systematically compared the transcriptome data of five main visceral tissues in chickens to reveal the response of multiple tissues to acute heat stress and determine the main target tissue of acute heat stress, further revealing the injuries of main target tissue and their potential mechanism by combing pathological section and qRT-PCR technologies. Results The transcriptome data of five visceral tissues revealed that acute heat stress broadly caused inflammatory response and damaged tissues metabolic homeostasis. Among the five tested visceral tissues, the number of differentially expressed genes in the lung was the highest, and their fold changes were the greatest, indicating that the lung was the main target tissue of acute heat stress. The results of pathological section revealed severe inflammation, emphysema and pulmonary hemorrhage in the lung under acute heat stress. Our study found that some pro-inflammatory genes, including CNTFR, FURIN, CCR6, LIFR and IL20RA, were significantly up-regulated both in the heat-stress and heat-death groups, and their fold changes in the heat-death group were significantly greater than that in the heat-stress group. We also found an anti-inflammatory gene, AvBD9, exhibiting an extremely high expression in the heat-stress group but a low expression in the heat-death group. Conclusions Our study found that acute heat stress caused multiple tissue injuries broadly and the lung was the main target tissue of acute heat stress in chicken. Acute heat stress caused a severe inflammatory response, emphysema, and pulmonary haemorrhage, The severe inflammatory response in the heat-death group was related to the up-regulation of pro-inflammatory genes and down-regulation of anti-inflammatory genes.