Chinese Academy of Agricultural Sciences Showcase

Avian Pathogenic Escherichia coli (APEC) produces major economic losses in the poultry industry and may endanger human health. The pathogenic mechanisms of APEC are still not fully understood. The fdhD gene in E. coli is essential for the function of formate dehydrogenases (FDHs), which are key enzymes in various biological processes in bacteria, but little is known about the fdhD in APEC pathogenicity. In this study, the LsrR quorum-sensing regulator expresses the gene fdhD and binds to the region between -96 to -66 of the fdhD promoter. The two motifs 6 bp and 9 bp of the fdhD promoter are crucial for the LsrR binding. The results showed that the inactivation of fdhD in APEC94 (a strain was isolated from diseased poultry) did not affect the growth and motility of APEC94 but led to decreased biofilm formation (P < 0.01), and reduced serum resistance (P < 0.05), alters antibiotic susceptibility. Similarly, the deletion of fdhD declined the adhesion (P < 0.05) and invasion (P < 0.01) of APEC94 towards host cells, reducing APEC94 colonization in blood, lungs, liver, spleen, and intestine (P < 0.05) in mice, and the mortality rate of mutant APEC94∆fdhD and APEC94 was 12.5% and 87.5% in a mice infection model respectively. Furthermore, the fdhD positively affects the expression of fimbrial, flagellar, and virulence genes in APEC. Moreover, the transcription level of the inflammatory cytokines IL-2, IL-4, IL-6, IL-10, TNF-α, and INF-ƴ (P < 0.05) was significantly decreased in mutant APEC94ΔfdhD compared with the wild-type strain. Thus, fdhD is a global regulator that activates the transcription of several genes. The present results suggest that fdhD plays an important role in pathogenicity, making it a good target for managing infection with APEC

Embryonic adipogenesis remains one of the least understood aspects of adipose biology in mammals due to time sensitivity, limited tissue volume, and ethical concerns. Here, we uniquely applied single-cell multi-omics sequencing to the developing adipose tissues of a representative mammalian species, characterized by genetically determined, significant fat deposition in the tail during embryogenesis, with a specific focus on adipogenic patterns and crucial regulatory factors. Our dataset spans all stages of adipogenesis (E50 to E80), revealing three major cellular origins of fat deposition: progenitor and stem cells, connective tissue progenitors, and vascular smooth muscle cells. By integrating scRNA-seq, scATAC-seq, and functional validation, we identified key enhancer-driven gene regulatory networks (eGRNs) governing adipogenesis, with DBI emerging as a critical regulator through its interaction with PPARG. Additionally, we delineated developmental trajectories and unique eGRNs underlying angiogenesis, osteogenesis, chondrogenesis, and myogenesis associated with fat formation. Our findings provide novel insights into embryonic adipogenesis in mammals and reveal critical regulons governing lineage specialization.

Includes long-term monitoring of water quantity data, total nitrogen, nitrate-nitrogen data and isotope data

Avian Pathogenic Escherichia coli (APEC) is a strain of extraintestinal pathogenic E. coli that is the primary cause of economic loss, has acquired antibiotic resistance, and poses a significant challenge to medical microbiologists in impoverished countries. In APEC, cysN is essential for cysteine synthesis, which is required for protein synthesis, along with the creation of numerous sulfur-containing compounds for bacterial growth and metabolism. However, the involvement of cysN in APEC pathogenicity has not been investigated. To investigate the function of cysN in APEC, cysN gene mutant and complemented strains were constructed and biologically characterized. The results determined that Quorum Sensor regulator LsrR directly binds to the cysN promoter to a region between -289 to -319 of the cysN promoter and inactivation of the cysN gene decreased biofilm formation (P < 0.01), serum resistance (P < 0.05), adhesion (P < 0.01), invasion capacity (P < 0.05) of APEC94 towards host cells, reduced transcription levels of fimbrial, flagellar, and virulence genes (P < 0.05), altered antibiotic resistance characteristic, and reducing APEC94 colonization in blood, lungs, liver, spleen, and intestine (P < 0.05) in mice, and the mortality rate of mutant APEC94∆cysN and APEC94 was 12.5% and 87.5% in a mice infection model respectively. In addition, the results revealed that cysN positively affects the expression of flagellar, type 1 fimbria, and virulence genes in APEC. However, the expression levels of virulence genes such as csgF, fyuA, yjaA, chuA, ompA, and iss were not influenced compared to the wild-type strain. Similarly, the transcription level of the inflammatory cytokines IL-2, IL-4, IL-6, IL-10, TNF-α, and INF-ƴ was significantly decreased in mutant APEC94ΔcysN strain infected tissues compared with the wild-type strain (P < 0.05). These results indicate that regulator cysN contributes to the virulence and pathogenicity of APEC.

Avian Pathogenic Escherichia coli (APEC) is a strain of extraintestinal pathogenic E. coli that is the primary cause of economic loss, has acquired antibiotic resistance, and poses a significant challenge to medical microbiologists in impoverished countries. In APEC, cysN is essential for cysteine synthesis, which is required for protein synthesis, along with the creation of numerous sulfur-containing compounds for bacterial growth and metabolism. However, the involvement of cysN in APEC pathogenicity has not been investigated. To investigate the function of cysN in APEC, cysN gene mutant and complemented strains were constructed and biologically characterized. The results determined that Quorum Sensor regulator LsrR directly binds to the cysN promoter to a region between -289 to -319 of the cysN promoter and inactivation of the cysN gene decreased biofilm formation (P < 0.01), serum resistance (P < 0.05), adhesion (P < 0.01), invasion capacity (P < 0.05) of APEC94 towards host cells, reduced transcription levels of fimbrial, flagellar, and virulence genes (P < 0.05), altered antibiotic resistance characteristic, and reducing APEC94 colonization in blood, lungs, liver, spleen, and intestine (P < 0.05) in mice, and the mortality rate of mutant APEC94∆cysN and APEC94 was 12.5% and 87.5% in a mice infection model respectively. In addition, the results revealed that cysN positively affects the expression of flagellar, type 1 fimbria, and virulence genes in APEC. However, the expression levels of virulence genes such as csgF, fyuA, yjaA, chuA, ompA, and iss were not influenced compared to the wild-type strain. Similarly, the transcription level of the inflammatory cytokines IL-2, IL-4, IL-6, IL-10, TNF-α, and INF-ƴ was significantly decreased in mutant APEC94ΔcysN strain infected tissues compared with the wild-type strain (P < 0.05). These results indicate that regulator cysN contributes to the virulence and pathogenicity of APEC.

Supplemental figures and tables for the Article "Unraveling the Molecular Mechanisms of Physiological Fruit Abscission via Comparative Transcriptomics in Actinidia arguta"

The accuracy of the transcriptome was validated through qPCR, demonstrating gene expression differences at various stages within the abscission zone of Actinidia arguta fruits with distinct abscission characteristics. It also confirmed the interactions between different plant hormones caused by overexpressed genes and revealed changes in the expression levels of related genes within the abscission zone of Actinidia arguta fruits in response to the application of various growth regulators.

These data are supporting materials for the article "Trichinella spiralis Excretory Secretory Antigens Ameliorate Porcine Epidemic Diarrhea Virus-Induced Mucosal Damage in Porcine Intestinal Oganoids by Alleviating Inflammation and Promoting Tight Junction". The data encompasses the raw information regarding the proteomic results of porcine intestinal organoids that are either uninfected, infected with PEDV, or infected with PEDV and then treated with TsEs.

original data related to: Non-canonical OsATG8 and OsATG1 regulate nutrient stress–induced immunity via ROP GTPase signaling

African swine fever (ASF), one of the most harmful diseases prevalent in pig farms nowadays, caused by the African swine fever virus (ASFV) that cause enormous economic losses. Viremia usually develops within a few days after ASFV infection. However, the metabolic changes in pig serum after ASFV infection remain unclear. In this study, serum samples collected from ASFV-infected pig at different times were analyzed using pseudotargeted metabolomics method. Metabolomic analysis revealed 225 metabolites decreased and 65 metabolites increased in serum collected in ASFV infected 5 days post-infection (dpi), 254 metabolites decreased and 58 metabolites increased in serum collected ASFV infected 10 dpi. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of the significant changed metabolites indicated that dopaminergic synapse has the highest rich factor in both ASFV5 (ASFV infected 5 dpi) VS ASFV0 (ASFV infected 0 dpi) and ASFV10 (ASFV infected 10 dpi) VS ASFV0.