SsMet1 is a Critical Gene in Methionine Biosynthesis in Sclerotinia sclerotiorum
In this study, we characterized SsMet1 in S. sclerotiorum by creating SsMet1-deletion mutants, Met1-2 and Met1-4, using a split marker technique. The SsMet1-deletion mutants were unable to grow on minimal medium and did not produce sclerotia. Supplementation with methionine and homocysteine rescued the defects in mycelial growth, but not sclerotia development of the SsMet1-deletion mutants. These results indicate that SsMet1-deletion mutants are auxotrophic for methionine.
In addition, the SsMet1-deletion mutants exhibited increased sensitivity to osmotic and oxidative stresses, cell walldamaging agents, and thermal stress. The mutants were avirulent on detached bean leaves, but virulence was also restored with methionine supplementation in minimal media. All the defects were restored by genetic complementation of the mutant with wildtype SsMet1 allele. The results of this study indicate that SsMet1 plays a critical role in the regulation of various cellular processes in S. sclerotiorum.
homocysteine, cysteine, SAMe (S-adenosylmethionine), methyl donor, sulfur amino acids, transsulfuration pathway, folate cycle, vitamin B12, liver detoxification, antioxidant defense, glutathione synthesis, methionine restriction, amino acid metabolism, DNA methylation, one-carbon metabolism, metabolic health, taurine biosynthesis, nutritional biochemistry, methionine adenosyltransferase
#Methionine, #AminoAcids, #ProteinSynthesis, #Methylation, #SAMe, #Homocysteine, #Cysteine, #FolateCycle, #VitaminB12, #LiverHealth, #Antioxidants, #Glutathione, #Transsulfuration, #DNAHealth, #Epigenetics, #OneCarbonMetabolism, #MetabolicPathways, #NutritionalBiochemistry, #Taurine, #HealthResearch
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