qGW11a/OsCAT8,encoding an amino acid permease,negatively regulates grain size and weight in rice

Grain size is a key factor influencing grain weight in rice.In this study,a chromosome segment substitution line(CSSL9-17)was identified,that exhibits a significant reduction in both grain size and weight compared to its donor parent 93-11.Further investigation identified two quantitative trait loci(QTL)on chromosome 11,designated qGW11a and qGW11b,which contribute to 1000-grain weight with an additive effect.LOC_Os11g05690,encoding the amino acid permease OsCAT8,is the target gene of qGW11a.Overexpression of OsCAT8 resulted in decreased grain weight,while OsCAT8 knockout mutants exhibited increased grain weight.The 287-bp located within the OsCAT8 promoter region of 93-11 negatively regulates its activity,which is subsequently correlated with an increase in grain size and weight.These results suggest that OsCAT8 functions as a negative regulator of grain size and grain weight in rice.

A single nucleotide substitution at 5'-UTR of GSN1 represses its translation and leads to an increase of grain length in rice

Rice grain size is an important trait that affects rice yield and quality, and thus the identification of genes related to grain size is of great significance for improving rice yield and quality. Many genes related to grain size, such as DEP1(Huang et al., 2009),GW5(Liu et al., 2017).

Glutamine mitigates murine burn sepsis by supporting macrophage M2 polarization through repressing the SIRT5-mediated desuccinylation of pyruvate dehydrogenase

Background:Alternative(M2)-activated macrophages drive the anti-inflammatory response against sepsis,a leading cause of death in patients suffering from burn injury.Macrophage M2 polarization is intrinsically linked with dominant oxidative phosphorylation(OXPHOS).Glutamine serves as a major anaplerotic source to fuel OXPHOS,but it remains unknown whether glutamine can modulate metabolic checkpoints in OXPHOS that favour M2 polarization.The study aims to explore whether glutamine essentially supports M2 polarization in IL-4-stimulated murine macrophages by sustaining the activity of PDH and whether glutamine augments macrophage M2 polarization and thus alleviates inflammation and organ injury in a murine burn sepsis model.Methods:To understand how glutamine promotes M2 activation in interleukin(IL-4)-treated murine macrophages,we detected glutamine-dependent M2 polarization and its relationship with the pyruvate dehydrogenase(PDH)complex by RT-PCR,flow cytometry and western blot.To explore how glutamine modulates PDH activity and thus supports M2 polarization,we compared the expression,phosphorylation and succinylation status of PDHA1 and then examined sirtuin SIRT5-dependent desuccinylation of PDHA1 and the effects of SIRT5 overexpression on M2 polarization by RT-PCR,flow cytometry and western blot.To determine whether glutamine or its metabolites affect M2 polarization,macrophages were cocultured with metabolic inhibitors,and then SIRT5 expression and M2 phenotype markers were examined by RT-PCR,flow cytometry and western blot.Finally,to confirm the in vivo effect of glutamine,we established a burn sepsis model by injecting Pseudomonas aeruginosa into burn wounds and observing whether glutamine alleviated proinflammatory injuries by RT-PCR,flow cytometry,western blot,immunofluorescent staining,hematoxylin-eosin staining and enzyme-linked immuno sorbent assay.Results:We showed that consumption of glutamine supported M2 activation in IL-4-treated murine macrophages by upregulating the activity of PDH.Mechanistically,glutamine did not affect the expression or alter the phosphorylation status of PDHA1 but instead downregulated the expression of SIRT5 and repressed SIRT5-dependent desuccinylation on PDHA1,which in turn recovered PDH activity and supported M2 polarization.This effect was implemented by its secondary metaboliteα-ketoglutarate(αKG)rather than glutamine itself.Finally,we demonstrated that glutamine pro-moted macrophage M2 polarization in a murine burn sepsis model,thereby repressing excessive inflammation and alleviating organ injury in model mice.Conclusions:Glutamine mitigates murine burn sepsis by essentially supporting macrophage M2 polarization,with a mechanism involving the repression of the SIRT5-mediated desuccinylation of pyruvate dehydrogenase that replenishes OXPHOS and sustains M2 macrophages.

The impact of gut microbiota changes on the intestinal mucus barrier in burned mice:a study using 16S rRNA and metagenomic sequencing

Background:The gut microbiota is a complex ecosystem that plays a critical role in human health and disease.However,the relationship between gut microbiota and intestinal damage caused by burns is not well understood.The intestinal mucus layer is crucial for maintaining intestinal homeostasis and providing a physiological barrier against bacterial invasion.This study aims to investigate the impact of gut microbiota on the synthesis and degradation of intestinal mucus after burns and explore potential therapeutic targets for burn injury.Methods:A modified histopathological grading system was employed to investigate the effects of burn injury on colon tissue and the intestinal mucus barrier in mice.Subsequently,16S ribosomal RNA sequencing was used to analyze alterations in the gut microbiota at days 1-10 post-burn.Based on this,metagenomic sequencing was conducted on samples collected at days 1,5 and 10 to investigate changes in mucus-related microbiota and explore potential underlying mechanisms.Results:Our findings showed that the mucus barrier was disrupted and that bacterial translocation occurred on day 3 following burn injury in mice.Moreover,the gut microbiota in mice was significantly disrupted from days 1 to 3 following burn injury,but gradually recovered to normal as the disease progressed.Specifically,there was a marked increase in the abundance of symbiotic and pathogenic bacteria associated with mucin degradation on day 1 after burns,but the abundance returned to normal on day 5.Conversely,the abundance of probiotic bacteria associated with mucin synthesis changed in the opposite direction.Further analysis revealed that after a burn injury,bacteria capable of degrading mucus may utilize glycoside hydrolases,flagella and internalins to break down the mucus layer,while bacteria that synthesize mucus may help restore the mucus layer by promoting the production of short-chain fatty acids.Conclusions:Burn injury leads to disruption of colonic mucus barrier and dysbiosis of gut microbiota.Some commensal and pathogenic bacteria may participate in mucin degradation via glycoside hydrolases,flagella,internalins,etc.Probiotics may provide short-chain fatty acids(particularly butyrate)as an energy source for stressed intestinal epithelial cells,promote mucin synthesis and accelerate repair of mucus layer.