The phosphate starvation response network in a commensal yeast evolved to expand its downstream targets via changes in the main transcription factor's dependence on its co-activator, potentially altering the physiological response.
Phosphate starvation in rice induces widespread, but transient, modulation of DNA methylation near stress responsive genes that is independent from the RNA-directed DNA methylation pathway.
Genetic and biochemical analysis of two enzymes reveals that inositol pyrophosphate signaling molecules allow plants to sense and regulate cellular phosphate levels, and to take up more phosphate when needed.
Proteasomes are protected from autophagic elimination upon carbon starvation by sequestration into cytoplasmic storage granules, which aid cell fitness by providing a cache of proteasomes that can be rapidly remobilized when carbon availability improves.
Steadily growing cells prepare for conditions that demand increased translation by producing excess ribosomes, at the expense of lower steady-state growth rate.
An image-based multiplex autophagosome RNAi screen targeting all Rab GTPases as well as their GAPs and GEFs identifies the Rab GEF SMCR8 as multifaceted autophagy modulator, which regulates kinase activity and gene expression of ULK1.
The stem cells of the postnatal muscle allow postnatal muscle growth and repair and withdraw from the cell cycle when the tyrosine phosphatase Ptpn11 (Shp2) is inhibited or mutated in mice.
Specific human mitofusin 2 mutations induce selective upper body obesity with suppressed leptin expression and severe adipose mitochondrial dysfunction.
