Volume 2 Issue 12, December 2020

UCP2 is shown in yeast and mammalian cells to transport aspartate out of mitochondria, thus enabling KRAS-mutated pancreatic ductal adenocarcinoma cells to perform glutaminolysis to support cancer growth.

Osteoclasts are the body’s exclusive bone-resorbing cells; however, their differentiation trajectory remains unclear. Using single-cell RNA sequencing, Tsukasaki et al. provide a comprehensive road map of osteoclastogenesis, unveiling stepwise molecular events underlying osteoclast cell fate transitions.

Wei et al. identify the HDL receptor SR-B1 as a host factor that enhances infection of cultured cells with SARS-CoV-2 in the presence of ACE2, thus providing a possible molecular connection between lipoprotein metabolism and COVID-19.

A particularly aggressive subtype of lung cancer with mutations in KRAS and LKB1 is shown to depend on increased hexosamine biosynthesis mediated by the enzyme GFPT2.

Oncogenic transformation can render cancer cells dependent on aberrant expression of glycolytic enzyme isoforms. Lin et al. describe a novel enolase inhibitor, POMHEX, that can selectively kill ENO1-deleted glioblastomas.

The PI3K–PTEN signalling pathway is a central regulator of metabolic homeostasis. Brunner et al. find that cell-intrinsic PI3K signalling allows adipose tissue macrophages to buffer obesity-induced lipotoxicity by promoting lipid uptake and catabolism.

By using single-cell transcriptomics, Weng et al. reveal complex temporal gene control during pancreatic beta-cell differentiation from human embryonic stem cells, allowing for the construction of a unique lineage tree and optimization of differentiation protocols.

Hibernation is a state of extreme metabolic and physiological plasticity occurring in conjunction with physical inactivity and prolonged fasting. Using in vivo tracing, Rice et al. reveal that nitrogen recycling staves off ammonia toxicity during hibernation in ground squirrels.

Martin-Perez et al. show that the beneficial effects of rapamycin in a mouse model of Leigh syndrome are associated with downregulation of protein kinase C.

Telomere shortening in adipocyte progenitors, promoted by genetic Tert inactivation, is shown to compromise adipose tissue health and systemic metabolism, providing a possible mechanistic link between obesity, ageing and metabolic disease.