Geese, descendants of migratory birds, have preserved the distinct reproductive and lipid metabolism traits of their wild ancestors. Therefore, compared to other poultry, geese have lower egg production ability and greater susceptibility to fatty liver. Recent research underscores the impact of lipid metabolism disorders on female reproductive health. In this context, we observed reproductive disorders (RD) and lipid metabolism anomalies in certain geese populations. This study systematically elucidated the differences between RD and normal geese at various levels, including genomics, transcriptomics, bile acid metabolomics, and microbiomics, revealing the crucial role of microorganisms. Our study provides a thorough examination of the ovarian anatomical, histological, and transcriptomic profiles between normal and RD geese. Genomic analyses pinpoint mutations in genes associated with bile acid metabolism, highlighting their potential role in RD pathogenesis. The genomic discoveries are substantiated by precise bile acid assays and ileum transcriptome analyses, which expose a significant disruption in bile acid absorption, activation of FXR, and an increase in serum chenodeoxycholic acid (CDCA) concentrations within RD geese. Notably, 16S rRNA sequencing uncovers significantly greater beta diversity in the ileum microbiota of RD geese than in the normal group. Both Wilcoxon rank sum test and LEfSe analyses highlighted a marked increase in Romboutsia abundance in RD geese. Experimental cultivation of microbiota with CDCA supplementation confirms the impact of CDCA on Romboutsia lituseburensis proliferation. Gavage experiments with R. lituseburensis elucidate its involvement in primary follicle reduction via immune-mediated pathways. Collectively, our multifaceted analysis unravels the intricate involvement of Romboutsia in goose RD, offering insights from genetic, physiological, and microbial dimensions. Our findings not only deepen understanding of the etiology of RD in geese but also suggest potential avenues for therapeutic interventions targeting bile acid metabolism and modulation of specific microbiota components.
Cadmium (Cd) contamination in wheat farmland is increasing at an alarming rate, posing threats to food security and public health. Breeding and utilizing wheat varieties characterized by low Cd accumulation levels constitute an effective strategy in the battle against wheat Cd contamination. The adoption of molecular marker-assisted approaches can greatly expedite the selection and enhancement of wheat varieties with low Cd accumulation. Nonetheless, research concerning the genes associated with wheat cadmium accumulation remains scarce. In this study, a high-density 660K SNP array was employed for conducting a genome-wide association study (GWAS) on the grain Cd concentration (GCdC), bioconcentration factor (BCF) and translocation factor (TF) in 175 wheat germplasms. The findings revealed 401 significant SNPs identified across three diverse environments. Linkage disequilibrium analysis revealed 30 core quantitative trait loci (QTLs) capable of reliably modulating wheat Cd accumulation phenotypes. Through gene annotation, transcriptomics, and gene molecular features, four candidate genes (TraesCS7B02G000200, TraesCS4A02G035900, TraesCS4A02G040900, and TraesCS5D02G564000) were identified as potential constituents in the biological process of wheat Cd accumulation. Furthermore, six wheat germplasms exhibiting low grain Cd accumulation were isolated, and two kompetitive allele specific PCR (KASP) markers conducive to breeding selection were developed. These findings provide valuable genetic resources for cultivating wheat with low Cd accumulation and establish a foundation for understanding the molecular mechanisms underlying low Cd accumulation in wheat. The candidate genes and KASP markers elucidated in this research have potential for effective use in genetic enhancement and marker-assisted selection in the breeding of wheat with low Cd accumulation.
Genome-wide identification of the CONSTANS-LIKE (COL) family and mechanism of fruit senescence regulation by PpCOL8 in sand pear (Pyrus pyrifolia)
Brucella spp., an intracellular bacterium, uses its type IV secretion system (T4SS) to regulate host signaling pathways and promote intracellular survival, but the molecular mechanism of this process remains largely unknown. Here we found that increasing the abundance of acetylated protein in host cells promotes the intracellular survival of Brucella. Moreover, our results demonstrated that the Brucella effector protein BspF can impact protein acetylation modification in host cells by interacting with other intracellular proteases. We conducted LC-MS/MS to characterize the protein acetylation mediated by BspF. We identified that SNAP29 K103 was acetylated, and that acetylated SNAP29 inhibited its interaction with STX17, thereby regulating the autophagy and providing an environment for the intracellular survival of Brucella. Furthermore, our results provide the first report of a bacterial effector using acetylation to affect the SNAP29-STX17-VAMP8 complex, and inhibit the host's defense system. Our results suggest a vital role of SNAP29 acetylation in autophagy of host cells under intracellular infection, by specifically regulating the assemble of SNARE.