背景:精子储存能力(SSC)决定了母鸡的生育力持续时间,是生产中不可忽视的重要繁殖性状。目前,母鸡SSC的遗传机制尚不清楚。因此,探索SSC的遗传基础,我们通过RNA-seq和Ribo-seq分析了不同SSC的母鸡在授精后不同时间的子宫-阴道连接处(UVJ)。
结果:我们的结果表明,589、596和527个差异表达基因(DEGs),730、783和324个差异翻译基因(DTG),5日检测到804、625和467个差异翻译效率基因(DTEGs),第十,在授精后的第15天,分别。在转录水平上,我们发现,授精后不同时间SSC的差异主要体现在细胞间信息的传递,细胞间粘附复合物的组成,离子通道的调节,细胞生理活动的调节,细胞的组成,和细胞膜的组成。在翻译效率(TE)级别中,SSC的差异主要与细胞内的生理代谢活动有关,细胞器膜的组成,氧化的生理活动,细胞组件,和细胞生长过程。根据路径分析,SSC与神经活性配体-受体相互作用有关,组氨酸代谢,以及转录水平的PPAR信号通路和谷胱甘肽代谢,氧化磷酸化,钙信号通路,细胞粘附分子,半乳糖代谢,和Wnt信号通路在TE水平。我们在转录水平筛选了影响SSC的候选基因(COL4A4,MUC6,MCHR2,TACR1,AVPR1A,COL1A1,HK2,RB1,VIPR2,HMGCS2)和TE水平(COL4A4,MUC6,CYCS,NDUFA13,CYTB,RRM2,CAMK4,HRH2,LCT,GCK,GALT).其中,COL4A4和MUC6是转录不同的关键候选基因,翻译,翻译效率。
结论:我们的研究首次使用RNA-seq和Ribo-seq的联合分析来研究SSC并揭示与SSC相关的生理过程。筛选影响SSC的关键候选基因,为分析SSC的分子调控机制提供了理论依据。
BACKGROUND: Sperm storage capacity (SSC) determines the duration of fertility in hens and is an important reproduction trait that cannot be ignored in production. Currently, the genetic mechanism of SSC is still unclear in hens. Therefore, to explore the genetic basis of SSC, we analyzed the uterus-vagina junction (UVJ) of hens with different SSC at different times after insemination by RNA-seq and Ribo-seq.
RESULTS: Our results showed that 589, 596, and 527 differentially expressed genes (DEGs), 730, 783, and 324 differentially translated genes (DTGs), and 804, 625, and 467 differential translation efficiency genes (DTEGs) were detected on the 5th, 10th, and 15th days after insemination, respectively. In transcription levels, we found that the differences of SSC at different times after insemination were mainly reflected in the transmission of information between cells, the composition of intercellular adhesion complexes, the regulation of ion channels, the regulation of cellular physiological activities, the composition of cells, and the composition of cell membranes. In translation efficiency (TE) levels, the differences of SSC were mainly related to the physiological and metabolic activities in the cell, the composition of the organelle membrane, the physiological activities of oxidation, cell components, and cell growth processes. According to pathway analysis, SSC was related to neuroactive ligand-receptor interaction, histidine metabolism, and PPAR signaling pathway at the transcriptional level and glutathione metabolism, oxidative phosphorylation, calcium signaling pathway, cell adhesion molecules, galactose metabolism, and Wnt signaling pathway at the TE level. We screened candidate genes affecting SSC at transcriptional levels (COL4A4, MUC6, MCHR2, TACR1, AVPR1A, COL1A1, HK2, RB1, VIPR2, HMGCS2) and TE levels(COL4A4, MUC6, CYCS, NDUFA13, CYTB, RRM2, CAMK4, HRH2, LCT, GCK, GALT). Among them, COL4A4 and MUC6 were the key candidate genes differing in transcription, translation, and translation efficiency.
CONCLUSIONS: Our study used the combined analysis of RNA-seq and Ribo-seq for the first time to investigate the SSC and reveal the physiological processes associated with SSC. The key candidate genes affecting SSC were screened, and the theoretical basis was provided for the analysis of the molecular regulation mechanism of SSC.