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Association of ability to rank sweet and fat taste intensities with sweet and fat food propensity ratios of children, adolescents and adults: the I.Family study
Get PDFHow to improve sustainability of nutrient dense diets for children and adolescents: an exemplary assessment in Germany
Get PDFSmoking trends in Poland (2012–2021)—insights from the comprehensive cardiovascular risk prevention program
Get PDFThe transsulfuration pathway suppresses the embryonic lethal phenotype of glutathione reductase mutants in Caenorhabditis elegans
Get PDFThe gsr-1 gene encodes the only glutathione reductase in Caenorhabditis elegans and gsr-1 loss-of-function alleles have a fully penetrant embryonic lethal phenotype. Therefore, maintenance of glutathione redox homeostasis is essential for nematode survival. We report here that impairment of the nonsense-mediated mRNA decay (NMD) pathway suppresses the embryonic lethality of gsr-1 mutants, allowing their normal development and growth. This NMD pathway dependent suppression requires cth-1 and cth-2 that encode 2 isoforms of cystathionine-γ-lyase that catalyze the conversion of cystathionine to cysteine through the transsulfuration pathway. In contrast, the thioredoxin system that can also provide cysteine through the cystine reduction pathway appears to be dispensable for the suppression of the lethal phenotype of gsr-1 embryos when the NMD pathway is inactivated. Together, our data indicate that increasing the activity of the reverse transsulfuration pathway can compensate the detrimental effect of the gsr-1 mutation, raising the interesting question of why C. elegans has not preserved such compensatory mechanism to avoid the embryonic lethality of these mutants
Becoming a Family and Community Nurse: Navigating Role Identity in a Fragmented System. A Phenomenological Study
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