宿主遗传和肠道微生物群协同调节蛋鸡的饲料利用率。

IF 6.3 Q1 AGRICULTURE, DAIRY & ANIMAL SCIENCE Journal of Animal Science and Biotechnology Pub Date : 2024-09-09 DOI:10.1186/s40104-024-01076-7
Wenxin Zhang, Fangren Lan, Qianqian Zhou, Shuang Gu, Xiaochang Li, Chaoliang Wen, Ning Yang, Congjiao Sun
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引用次数: 0

摘要

背景:饲料效率是家禽业的一个重要经济特征。宿主遗传和肠道微生物群都会影响饲料效率。然而,在蛋鸡产蛋后期,肠道微生物群与宿主遗传之间的关联以及它们对饲料效率的综合贡献在很大程度上仍不清楚:方法:总共对 686 只蛋鸡进行了全基因组重测序和肝脏转录组测序。对 705 只蛋鸡的肠道食糜(十二指肠、空肠、回肠和盲肠)和粪便样本进行了 16S rRNA 基因测序。通过整合基因组、转录组和微生物组进行了生物信息分析,以筛选与饲料效率相关的关键遗传变异、基因和肠道微生物群:结果:饲料转化率(FCR)和剩余采食量(RFI)的遗传率分别为 0.28 和 0.48。回肠和粪便微生物群分别占饲料转化率变异的15%和10%,而空肠、盲肠和粪便微生物群分别占RFI变异的20%、11%和10%。通过基于肝脏 eQTL 图谱和 GWAS 总结数据的 SMR 分析,我们进一步确定了影响蛋鸡饲料效率的四个蛋白编码基因:SUCLA2、TNFSF13B、SERTM1 和 MARVELD3。SUCLA2和TNFSF13B基因分别与SNP 1:25664581和SNP rs312433097显著相关。SERTM1与rs730958360和1:33542680呈显著相关,是与粪便中的棒状杆菌丰度相关的潜在致病基因。MARVELD3 与 1:135348198 显著相关,并且与回肠中肠球菌的数量显著相关。具体而言,回肠中肠球菌的丰度越低,粪便中棒状杆菌的丰度越高,饲料效率就越高:这项研究证实,宿主遗传和肠道微生物群都能驱动饲料效率的变化。肠道微生物群的一小部分往往与宿主基因相互作用,共同提高饲料效率。因此,通过支持更高效的类群和选择性育种来针对肠道微生物群和宿主遗传变异,可提高蛋鸡产蛋后期的饲料效率。
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Host genetics and gut microbiota synergistically regulate feed utilization in egg-type chickens.

Background: Feed efficiency is a crucial economic trait in poultry industry. Both host genetics and gut microbiota influence feed efficiency. However, the associations between gut microbiota and host genetics, as well as their combined contributions to feed efficiency in laying hens during the late laying period, remain largely unclear.

Methods: In total, 686 laying hens were used for whole-genome resequencing and liver transcriptome sequencing. 16S rRNA gene sequencing was conducted on gut chyme (duodenum, jejunum, ileum, and cecum) and fecal samples from 705 individuals. Bioinformatic analysis was performed by integrating the genome, transcriptome, and microbiome to screen for key genetic variations, genes, and gut microbiota associated with feed efficiency.

Results: The heritability of feed conversion ratio (FCR) and residual feed intake (RFI) was determined to be 0.28 and 0.48, respectively. The ileal and fecal microbiota accounted for 15% and 10% of the FCR variance, while the jejunal, cecal, and fecal microbiota accounted for 20%, 11%, and 10% of the RFI variance. Through SMR analysis based on summary data from liver eQTL mapping and GWAS, we further identified four protein-coding genes, SUCLA2, TNFSF13B, SERTM1, and MARVELD3, that influence feed efficiency in laying hens. The SUCLA2 and TNFSF13B genes were significantly associated with SNP 1:25664581 and SNP rs312433097, respectively. SERTM1 showed significant associations with rs730958360 and 1:33542680 and is a potential causal gene associated with the abundance of Corynebacteriaceae in feces. MARVELD3 was significantly associated with the 1:135348198 and was significantly correlated with the abundance of Enterococcus in ileum. Specifically, a lower abundance of Enterococcus in ileum and a higher abundance of Corynebacteriaceae in feces were associated with better feed efficiency.

Conclusions: This study confirms that both host genetics and gut microbiota can drive variations in feed efficiency. A small portion of the gut microbiota often interacts with host genes, collectively enhancing feed efficiency. Therefore, targeting both the gut microbiota and host genetic variation by supporting more efficient taxa and selective breeding could improve feed efficiency in laying hens during the late laying period.

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