Volume 22 Issue 9, September 2020

Ferroptosis is an iron-dependent mode of cell death driven by lipid peroxidation, capable of explosively propagating through a field of cells. Two studies now explore the mechanisms underlying ferroptotic cell death and its spread, as well as its possible in vivo significance, shedding light on some of the burning questions surrounding ferroptosis.

While the formation and concentration of urine are better understood, how kidney epithelial cells generate the energy to drive these functions has remained unclear. A study now reveals that shear stress originating from urinary flow is sensed by the primary cilia of cortical epithelial cells and stimulates lipolysis and oxidative metabolism.

PD-L1 has been extensively described as the membrane-bound ligand of PD-1. A recent study discovered a previously unknown role for PD-L1, which is able to bind DNA and thus govern different pathways linked to either evasion of immune surveillance or tumour microenvironment inflammation.

The intestinal stem cell niche McCarthy, Kraiczy and Shivdasani review the cellular and molecular organisation of the mammalian intestinal stem cell niche and its functions.

Two complementary studies from the laboratories of Riegman et al. and Katikaneni et al., respectively, identify a key role for controlled wave-like propagation of lipid peroxide signalling during wound detection in vivo and in ferroptotic cell death.

Two complementary studies from the laboratories of Riegman et al. and Katikaneni et al., respectively, identify a key role for controlled wave-like propagation of lipid peroxide signalling during wound detection in vivo, and in ferroptotic cell death.

Liu et al. characterize a mechanism of UFL1-mediated UFMylation of p53 at multiple lysine residues and show how this dampens MDM2-induced ubiquitination of p53 to enhance its stability and tumour-suppressive function.

Gao et al. uncover p300-induced acetylation and HDAC2-mediated deacetylation of PD-L1, which modulate its nuclear translocation to affect the expression of immune genes and the efficacy of anti-PD-1 therapy.

Nowosad et al. show that during amino acid starvation, the cell-cycle inhibitor p27 binds LAMTOR1 on lysosomes to inhibit mTOR and promote autophagy, linking cell division and cell growth machineries.

Here Miceli et al. show that shear stress on primary cilia induces mitochondrial biogenesis and metabolic reprogramming in kidney epithelial cells through lipophagy stimulation.

Ilina et al. investigate the balance between cell adhesion and matrix density on patterns of collective breast cancer cell invasion using three-dimensional models of the extracellular matrix, in vivo imaging and in silico modelling

Aeby et al. report that DCP1A negatively regulates Tsix RNA abundance by suppressing its transcriptional elongation and RNA stability, thus contributing to X-chromosome inactivation.

Moro et al. show that hypermethylation-induced silencing of the ubiquitin ligase FBXL7 rescues c-SRC from ubiquitin-mediated degradation and enhances epithelial-to-mesenchymal transition and metastasis.

Moghadam et al. developed a CRISPR transcriptional repressor to silence MyD88 expression in vivo to modulate immune response against AAV gene therapy and septicaemia.