Linear ubiquitination at damaged lysosomes induces local NFKB activation and controls cell survival.

Lysosomes are the major cellular organelles responsible for nutrient recycling and degradation of cellular material. Maintenance of lysosomal integrity is essential for cellular homeostasis and lysosomal membrane permeabilization (LMP) sensitizes toward cell death. Damaged lysosomes are repaired or degraded via lysophagy, during which glycans, exposed on ruptured lysosomal membranes, are recognized by galectins leading to K48- and K63-linked poly-ubiquitination (poly-Ub) of lysosomal proteins followed by recruitment of the macroautophagic/autophagic machinery and degradation.

Mapping autophagosome contents identifies interleukin-7 receptor-α as a key cargo modulating CD4+ T cell proliferation.

CD4+ T cells are pivotal cells playing roles in the orchestration of humoral and cytotoxic immune responses. It is known that CD4+ T cell proliferation relies on autophagy, but identification of the autophagosomal cargo involved is missing. Here we create a transgenic mouse model, to enable direct mapping of the proteinaceous content of autophagosomes in primary cells by LC3 proximity labelling.

Correction: A computational reproducibility study of PLOS ONE articles featuring longitudinal data analyses.

[This corrects the article DOI: 10.1371/journal.pone.

Standardized Headache Therapy in the Pediatric Emergency Department Using Improvement Methodology.

Introduction: Primary headache is a common cause of pediatric emergency department (PED) visits. Without published guidelines to direct treatment options, various strategies lacking evidence are often employed. This study aims to standardize primary headache treatment in the PED by promoting evidence-based therapies, reducing nonstandard abortive therapies, and introducing dihydroergotamine (DHE) into practice.