The activity, localization, and essentiality of TbFUT1, together with its ability to complement Leishmania parasites lacking the homologous gene, suggest the presence of an uncommon and conserved mitochondrial fucosylation pathway required for kinetoplastid parasites viability.

Globotriaosylcermide directly impacts neuronal integrity and ion channel function as potential mechanism underlying small fiber pathology in Fabry disease.

Yeast cells can tune the modality of a nutrient response on physiological and evolutionary timescales by adapting the expression and sequence of a sensor protein.

Regulation of Pax6 expression through the α-enhancer fine-tunes amacrine cell subtype number, and consequently, the visual output of the retina.

Ggta1 deletion in mice shapes and reduces the microbiota pathogenicity and probably contributed to the natural selection of GGTA1 loss-of-function mutations in the ancestral primates that gave rise to humans.

Post-phosphoryl modification of α-dystroglycan requires the glucuronyltransferase B4GAT1; this enzyme synthesizes the acceptor glycan that serves as a primer for the glycosyltransferase LARGE to synthesize the laminin-binding glycan.

Pain behaviors in a Fabry mouse model are associated with the accumulation of a fat molecule that disrupts sodium ion channels in small fiber neurons.

Disruption of the LG domain-binding phospho-ribitol-containing O-mannose structures on α-dystroglycan results in congenital muscular dystrophy.

Dorsal paired medial neurons, which are required for memory consolidation, promote sleep by inhibiting the excitation of mushroom body neurons.

Activated Drosophila macrophages undergo transient metabolic remodeling towards Hypoxia inducible factor 1 α-driven aerobic glycolysis, a program that induces systemic metabolic changes and is crucial for resistance to infection.