A novel metabolic network analysis method enables large-scale computational predictions of biosynthetic capabilities across the human oral microbiome, revealing a unique cluster of fastidious microorganisms and potential metabolic interdependencies.
The endoplasmic reticulum E3 ubiquitin ligase Doa10 and the mitochondrial AAA-ATPase Msp1 govern targeting fidelity of outer mitochondrial tail-anchored proteins by controlling cytoplasmic concentration and extracting mistargeted and orphan species.
Antigen receptor control of methionine transport is critical to co-ordinate protein synthesis and the production of methyl donors for nucleotide and protein methylations which are required for T cell differentiation.
A near-complete flux balance analysis model of a minimal cell demonstrates the high essentiality of its metabolic genes, agrees well with experimental essentiality data and suggests some further gene removals.
UBIAD1 mediates a unique geranylgeranyl pyrophosphate-sensing mechanism that when disrupted, inhibits degradation of HMG CoA reductase and triggers overproduction of corneal cholesterol that characterizes the eye disease Schnyder Corneal Dystrophy.