Cell growth articles from across Nature Portfolio

Additional roles of metabolic enzymes in cancer remain to be explored. Here, the authors show nuclear localized PYCR1 undergoes IGF1R-mediated phosphorylation under hypoxia, binds with ELK4 and recruits SIRT7 to modulate transcription of target genes to promote colorectal cancer progression.

Shapiro, Chang, et al. identify a conserved role for the iron-binding histone demethylase KDM3B in sensing iron levels and regulating mTORC1 through transcriptional repression of key mTORC1 pathway components.

Neutrophils provide a critical early defense as part of our innate immune system. Here, authors performed a genome-wide assessment of the molecular factors critical to proliferation, differentiation, and cell migration in a neutrophil-like cell.

Mitochondrial DNA is critical for cell function, but how growing cells maintain stable concentrations is unclear. Seel et al. find that cells couple mitochondrial DNA copy number directly to cell volume through nuclear-encoded limiting factors, whose amount increases with cell volume.

Okreglak et al. explore the molecular mechanisms that link organellar pH dynamics with the cell cycle, and find that vacuolar pH oscillates during cell cycle phases to ensure an adequate supply of amino acids during cell division. This study offers metabolic insight into the fundamental mechanisms that couple amino acid availability to the cell cycle through pH fluctuations.

Cells use various metabolic pathways to synthesize the building blocks for growth and proliferation. To ensure balanced growth, these biosynthetic processes must be tightly coordinated. We describe a molecular machinery that senses the cellular capacity to make lipids to regulate other biosynthetic processes — such as protein synthesis — accordingly.

A new study shows that the enzymes involved in de novo pyrimidine synthesis and ferroptosis form a complex called the pyrimidinosome, which is controlled by AMPK. Cancer cells low in AMPK expression rely on the pyrimidinosome, suggesting that co-inhibition of AMPK and the pyrimidinosome represents a potential cancer treatment strategy.

In this Tools of the Trade article, Benjamin Jackson (at the Finley lab) describes the use of genetic co-essentiality analysis to interrogate the assembly of metabolic networks, fuelling discovery of new aspects of metabolism.

Dai and colleagues show that activation of AMPK by glucose starvation leads to phosphorylation of GATOR2 and affects nutrient-dependent activation of mTORC1.