PubMed HealthSearch

Biomedical subjects

Yuqing Liu

Publications and source records attributed to Yuqing Liu.

4 recordsLinked to original sources

Natural variation in BRN1 enhances nitrogen sensitivity to improve rice nitrogen use efficiency.

Green Revolution rice varieties deliver high yields but require excessive nitrogen (N) fertilizer and show diminished N responsiveness, severely reducing nitrogen-use efficiency (NUE). To dissect the molecular basis of low N sensitivity in modern cultivars, we conducted a genome-wide association study (GWAS) for biomass response to N (BRN), a trait tightly linked to N sensitivity, using a diverse rice germplasm panel. We identified BRN1 as a key regulator of N-dependent biomass accumulation that regulates NLP3, a master transcription factor governing nitrate signaling. Under elevated N supply, the strigolactone signaling repressor D53 accumulates substantially and interacts with BRN1 to repress NLP3 transcription, thereby reducing rice N response. Notably, the high-response BRN1H allele encodes a more stable protein that alleviates D53-mediated suppression. Introgression of this allele into modern cultivars significantly enhanced N sensitivity and grain yield under both low and high N conditions. Our findings establish a D53-BRN1-NLP3 regulatory module controlling rice NUE, providing a target for rice breeding to sustain high productivity with improved resource sustainability.

Oryza

OsCLSY4 modulates epigenomic patterns and grain size in rice.

De novo DNA methylation, orchestrated by the RNA-directed DNA methylation (RdDM) pathway, is essential for gene regulation and transposon silencing. While CLASSY (CLSY) proteins facilitate RNA POLYMERASE IV (Pol IV) recruitment to initiate the RdDM pathway in plants, their roles in crops are incompletely explored. Here, we report OsCLSY4 as the dominant regulator within the OsCLSY family, driving Pol IV-mediated epigenomic patterns and influencing diverse agricultural traits. Epigenomics analyses reveal that OsCLSY4 controls over 95% of Pol IV-dependent 24-nucleotide small interfering RNA (24-nt siRNA) clusters and more than 70% of Pol IV-dependent hypomethylated CHH differentially methylated regions (DMRs), predominantly at miniature inverted-repeat transposable elements (MITEs). Loss of OsCLSY4 leads to dysregulation of MADS22 and GA20ox1 in a DNA methylation-dependent manner. SunTag-mediated targeted demethylation confirms that reduced DNA methylation in promoter regions leads to MADS22 activation and GA20ox1 repression to influence grain size, linking epigenetic changes to phenotypic outcomes of osclsy4. Moreover, OsCLSY4 governs tissue-specific methylation patterns in panicle and seedling. Mechanistically, OsCLSY4 is the predominantly expressed OsCLSY family member and interacts with Pol IV. Collectively, our findings position OsCLSY4 as a central hub for Pol IV-mediated epigenomic regulation in rice and suggest its potential utility in epigenetic breeding strategies.

Oryza

ABCD-type phage cocktail targeting distinct LPS receptor sites demonstrates superior efficacy against multidrug-resistant Salmonella.

The narrow host range of phages poses a limitation in addressing multidrug-resistant bacteria, whereas phage cocktail therapy, targeting multiple bacterial receptors, broadens the phage host spectrum. This study establishes a comprehensive Salmonella phages repository through nationwide surveillance in China, isolating 242 phages classified into 29 genera, with genome sizes ranging from 5.4 to 350.3 Kb. Based on LPS specificity, phages were categorized into four types A-D. Here, we developed an ABCD-Type phage cocktail targeting four distinct LPS recognition sites, demonstrating superior efficacy versus single phages or phage cocktail with different receptors (CCR-Type). In vitro, ABCD-Type phage cocktail treatment sustained bactericidal activity > 36 h versus CCR's 8 h, effectively controlling Salmonella in lettuce, milk, and Galleria mellonella infection models. Moreover, ABCD-Type phage cocktail effectively cleared Salmonella biofilms and showed promising results in the treatment of animal infections, significantly reducing bacterial loads in infected chicks and improving their survival rates. Resistant mutants predominantly harbored mutations in the btuB gene and LPS biosynthesis genes. These mutants showed increased antibiotic sensitivity and attenuated virulence. Collectively, these findings underscore the therapeutic potential of Salmonella phages, specifically ABCD-Type phage cocktail formulations which contain the phages PJNS014, PJNS023, PJNS036, and PJNS038, for controlling Salmonella infections. This work provides a foundation for developing advanced phage-based therapeutics.

Salmonella Phages

The R203M and D377Y mutations of the nucleocapsid protein promote SARS-CoV-2 infectivity by impairing RIG-I-mediated antiviral signaling.

The viral protein mutations can modify virus-host interactions during virus evolution, and thus alter the extent of infection or pathogenicity. Studies indicate that nucleocapsid (N) protein of SARS-CoV-2 participates in viral genome assembly, intracellular signal regulation and immune interference. However, its biological function in viral evolution is not well understood. SARS-CoV-2 N protein mutations were analyzed in Delta, Omicron, and original strains. Two mutations with a methionine (M) residue at site 203 and a tyrosine (Y) residue at site 377 of the N protein were found in Delta strain but not in Omicron and original strains, and promoted SARS-CoV-2 infection therein. Those mutations, R203M and D377Y, enhanced the inhibitory impact of N protein on the impairment of RIG-I-mediated antiviral signaling, such as IRF3 phosphorylation and IFN-β activation. The viral RNA-binding activity of N protein was promoted by these mutations, effectively attenuating the recognition and interaction of RIG-I with viral RNA compared to the original or other variants. The R203M/D377Y mutations thus enhanced the suppressive activity of the N protein on RIG-I-mediated interferon induction both in vitro and in vivo, which in turn promoted viral replication. This study helps to understand the variability of SARS-CoV-2 in regulating host immunity.

SARS-CoV-2