Genome-wide identification of the CONSTANS-LIKE (COL) family and mechanism of fruit senescence regulation by PpCOL8 in sand pear (Pyrus pyrifolia)
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 genes associated with wheat cadmium accumulation remains scarce. In this study, a high-density 660K SNP array was employed for conducting genome-wide association studies (GWASs) 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 locus (QTLs)capable of reliably modulating wheat Cd accumulation phenotypes. Through gene annotation, transcriptomics, and gene molecular features, four candidate genes (TraesCS7B02G000200, TraesCS4A02G035900, TraesCS4A02G040900, TraesCS5D02G564000) were identified as potential constituents of the biological process of wheat Cd accumulation. Furthermore, in this study 6 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 employmentuse in genetic enhancement and marker-assisted selection in the breeding of wheat with low Cd accumulation.
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.