Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Tumours reprogram their metabolism to maximize macromolecule biosynthesis for growth. However, which of the common tumour-associated metabolic activities are critical for proliferation remains unclear. Glutamate-derived glutamine is now shown to satisfy the glutamine needs of glioblastoma, indicating that glutamine anaplerosis is dispensable for growth.
The ciliary transition zone (TZ) at the base of cilia is thought to gate entry of proteins into the cilium. The authors characterize a role for TMEM107, a protein mutated in the ciliopathy Joubert syndrome, in organizing a submodule of the TZ.
The role of centrosome amplification in tumorigenesis has remained unclear. Using mice, Blanpain and colleagues find that overexpression of Plk4, which leads to centrosome amplification, can cause aneuploidy and tumour initiation in p53-deficient skin.
Gottlieb and colleagues demonstrate that glioblastoma cell proliferation under glutamine starvation conditions depends on the glutamine-synthetase-dependent conversion of glutamate to glutamine to fuel purine biosynthesis and cell growth.
Centriole duplication requires the loading of centriolar proteins to the daughter centriole during mitosis. Fu and colleagues analyse by 3D-structural illumination microscopy the sequential recruitment of centriolar proteins Cep135, Cep295 and Cep152.
Baskin et al. report that FAM126A, which is mutated in hypomyelination and congenital cataract, regulates PI4KIII, the kinase generating PtdIns(4)P. Loss of FAM126A in patients affects PI4KIIIα complex assembly and PtdIns(4)P synthesis at the plasma membrane.
By comparing the metabolomes, transcriptomes and epigenomes of human pluripotent stem cell lines, Sperber et al. show that interplay between the metabolome and histone modifications drives the metabolic switch from naive to primed pluripotency.
Samakovlis and colleagues perform a genome-wide, tissue-specific RNAi screen in the Drosophila larval and adult airway systems and find that an initial transient anisotropic distribution of aPKC drives fibre orientation during tube formation.
Through a proteomics approach, Qi and colleagues and Long and colleagues identify the sensor of the unfolded protein response IRE1α as an endogenous substrate of the E3 ubiquitin ligase involved in ER-associated degradation, Hrd1.
Using in vivo quantitative single-molecule fluorescence microscopy of kinesin II and OSM-3 motor dynamics in C. elegans cilia, Peterman and colleagues show that kinesin II loads cargo at the base, whereas OSM-3 transports the cargo to the tip.
Austen et al. generated talin biosensors to study integrin-based force transduction. They report that extracellular rigidity sensing requires talin’s mechanical engagement and find talin isoform-dependent effects in integrin-mediated mechanosensing.
The mechanisms underlying integrin-dependent signalling are a topic of continued study. Endocytosed integrins are now shown to drive assembly of signalling complexes on the cytoplasmic face of endocytic membranes to promote cancer cell survival and increase metastatic capacity following cell detachment.
Two studies show that the E3 ubiquitin ligase RNF138 is recruited to DNA double-strand break sites, where it ubiquitylates key repair factors to promote DNA-end resection and homologous recombination. These findings add insights into the multilayered regulatory mechanisms underlying DNA double-strand break repair pathway choice in mammalian cells.
Jackson and colleagues and Hendzel and colleagues reveal that the E3 ligase RNF138 functions in the repair of double-strand breaks by promoting CtIP accumulation and displacement of DNA-PK subunit Ku.
Ding and colleagues show that somatic cell reprogramming does not depend on Atg5-dependent canonical autophagy, but requires mitochondrial clearance in an Atg5-independent manner downstream of AMPK.
Jackson and colleagues and Hendzel and colleagues reveal that the E3 ligase RNF138 functions in the repair of double-strand breaks by promoting CtIP accumulation and displacement of DNA-PK subunit Ku.
Chiolo and colleagues find that, in a SUMOylation-dependent manner, heterochromatic double-strand breaks move to the nuclear periphery where Rad51 is recruited to continue repair.
Chen and colleagues report that the third enzyme in the oxidative pentose phosphate pathway (PPP), 6PGD, controls cancer cell proliferation by regulating LKB1–AMPK signalling. Inhibitors of 6PGD decrease tumorigenesis in mouse xenografts.
Humphries and colleagues analyse proteomic data of integrin adhesion complexes to derive a consensus integrin adhesome and characterize the temporal dynamics of adhesome component recruitment during adhesion complex assembly and disassembly.