Upon stress, JNK stimulates microtubule dynamics in human epithelial cell lines. Henrie et al. show that JNK phosphorylates the rescue factor CLIP-170, increasing its retention frequency on the lattice behind comets, at locations that correspond to potential future rescue sites.

Autophagosomes engulf a variety of targets, from a portion of cytosol to large organelles, by regulating the size of the autophagosomal membrane. Yamamoto et al. identify ERdj8, a novel ER membrane protein that affects the size of autophagosomes.

Trafficking of matrix metalloproteinases (MMPs) through the Golgi remains enigmatic in the field. Pacheco-Fernandez et al. find that nucleobindin-1 (NUCB1), a cis-Golgi localized Ca2+-binding protein, plays a major role in this process by binding to MMPs, regulating their intra-Golgi trafficking, and thereby modulating cell invasion and matrix degradation.

Cancer cell dissemination is facilitated by small actin-rich plasma membrane protrusions called invadopodia. Pedersen et al. now show that invadopodia maturation and function depend on contact site formation between the endoplasmic reticulum and late endosomes, which promotes translocation of the latter to growing invadopodia.

Paul et al. use cryo-ET to show that microtubules can contain actin filaments in their lumen. Two types of F-actin structure are distinguished, Class I and Class II, with slightly different helical symmetries and outer microtubule diameters. They call these filaments microtubule lumenal actin (ML-actin).

Autophagy selectively degrades a wide range of cellular components to regulate cellular functions or maintain cellular homeostasis. Tomioka et al. reveal that the nuclear pore complex and nucleoporins are degraded by selective autophagy upon inactivation of Tor kinase complex 1 in Saccharomyces cerevisiae.

Autophagy requires the synthesis of PI(3)P and the conjugation of LC3 to the phagophore membrane. We reconstituted these two reactions and their coupling by WIPI2 and showed that positive feedback between PI3KC3-C1 and WIPI2 leads to rapid LC3 lipidation by the ATG16L1 complex.