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Tran, T. T. T.

Publications and source records attributed to Tran, T. T. T..

3 recordsLinked to original sources

A novel GLYCEROPHOSPHODIESTER PHOSPHODIESTERASE 13 is involved in the Phosphate starvation-induced lipid remodeling in rice

Phosphorus (P) is one of the most vital macronutrient determinants in plant development and productivity. However, the bioavailability of inorganic phosphate (Pi), the only form that plants can assimilate, is limited in the soil, thus significantly affecting plant development. Plants have adopted various specialized strategies to modify their morphological, physiological, and biochemical properties for better adaptation to Pi deficiency conditions. GLYCEROPHOSPHODIESTER PHOSPHODIESTERASES (GDPDs), generally known as phospholipid remodeling proteins, have been suggested to play essential roles in maintaining phosphate homeostasis. The previous genome-wide association studies (GWAS) in a Vietnamese rice collection led to the discovery of a robust QTL named qRST9.14 associating with the phosphate adaption in rice, in which OsGDPD13 is located within this locus. Interestingly, we discovered an absence of OsGDPD13 from the Indica reference genome. A subcellular localization study showed that the GDPD13 protein localizes to the plasma membrane, cytoplasmic speckles, and plasmodesmata. The osgdpd13 knockout mutant was generated in the Japonica cv Kitaake background to characterize its function. Phenotypic analysis indicated that mutation of OsGDPD13 significantly lowered crown root number and reduced the plant height under Pi deficient condition. Moreover, osgdpd13 lines reduce the capability to degrade total phospholipids compared to the wild type under Pi starvation conditions. This finding suggests the involvement of the OsGDPD13 gene in rice growth and the Phosphate starvation-induced lipid remodeling under P deficiency. This work will provide valuable information for developing crop plants with higher Phosphate use efficiency.

plant biology↗

Fiber-associated Lachnospiraceae reduce colon tumorigenesis by modulation of the tumor-immune microenvironment

Patients with colorectal cancer (CRC) harbor gut microbiomes that differ in structure and function from those of healthy individuals, suggesting this altered microbiome could contribute to tumorigenesis. Despite increasing evidence implicating the gut microbiome in CRC, the collective role of different microbial consortia in CRC carcinogenesis is unclear. We have previously described these consortia as co-abundance groups that co-exist at different abundance levels in the same patient. Here, we report that tumor biopsy tissue from patients with a "high-risk" Pathogen-type microbiome had a different immune transcriptome and immune cell infiltrate from those with a "low-risk" Lachnospiraceae-type microbiome. Transplantation from patients of the two fecal microbiome types into mice with an orthotopic tumor differentially affected tumor growth and the systemic anti-tumor immune response. The differences in tumor volume and immunophenotype between mice receiving the high-risk and the low-risk microbiome correlated with differences in the engrafted human microbial species and predicted microbiome-encoded metabolites in the two groups. Of twelve taxa whose abundance in recipient mice led to increased tumor onset, seven corresponded with differentially abundant taxa in a global dataset of 325 CRC patients versus 310 healthy controls. These data suggest that the enrichment for a Lachnospiraceae-type configuration of the gut microbiome may influence colon cancer progression and disease outcome by modulating the local and systemic anti-tumor immune response. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=159 SRC="FIGDIR/small/432654v2_ufig1.gif" ALT="Figure 1"> View larger version (45K): org.highwire.dtl.DTLVardef@1de9ff5org.highwire.dtl.DTLVardef@d790d5org.highwire.dtl.DTLVardef@65be8aorg.highwire.dtl.DTLVardef@1c096da_HPS_FORMAT_FIGEXP M_FIG C_FIG Proposed model of how the high-risk Pathogen and low-risk Lachnospiraceae CAGs differentially modulate the tumor immune response.

microbiology↗

Association between Apolipoprotein E genotype and the gut microbiome composition in humans and mice

Apolipoprotein E (APOE) genotype is the strongest prevalent genetic risk factor for Alzheimers disease. Numerous studies have provided insights into the pathological mechanisms. However, a comprehensive understanding of the impact of APOE genotype on microflora speciation and metabolism is completely lacking. The aim of this study was to investigate the association between APOE genotype and the gut microbiome composition in human and APOE-targeted replacement (TR, APOE3 and APOE4) transgenic mice. Faecal microbiota amplicon sequencing from matched individuals with different APOE genotypes revealed no significant differences in overall microbiota diversity (alpha or beta diversity) in group-aggregated human APOE genotypes. However, several bacterial taxa showed significantly different relative abundance between APOE genotypes. Notably, we detected an association of Prevotellaceae and Ruminococcaceae and several butyrate-producing genera abundances with APOE genotypes. These findings were confirmed by comparing the gut microbiota of APOE-TR mice. Furthermore, metabolomic analysis of faecal water from murine samples detected significant differences in microbe-associated amino acids and short-chain fatty acids between APOE genotypes. Together, the findings indicate that APOE genotype associated with specific gut microbiome profiles in both humans and in APOE-TR mice. This suggests that the gut microbiome is worth further investigation as a potential therapeutic target to mitigate the deleterious impact of the APOE4 allele on cognitive decline and the prevention and treatment of AD.

genomics↗