The transmembrane autophagy protein ATG9 is essential for autophagosome formation. Peng et al. show that scramblase-attenuatedC. elegans ATG-9 mutants rescue the autophagy defect and lysosome damage caused by nondegradative autolysosomes. This uncovers the role of ATG-9 in regulating lysosome function and integrity.

The study reveals that individual mitotic cyclins’ roles are more flexible than previously thought. Deficiency of B-type cyclins inhibits mitotic entry, leading to pre-NEBD mitotic slippage. Remarkably, elevating cyclin A levels can restore mitosis independently of B-type cyclins. These findings challenge traditional views on cyclin functions.

TDP-43 exhibits rhythmic expression, and its rhythmicity persists despite BMAL1 depletion in vivo, may modulate phospho-AMPKα(Thr172)/PFKP to alter glucose uptake/ATP production, and regulate USP13 mRNA splicing to affect BMAL1 ubiquitination. Its dysfunction disrupts murine circadian rhythms and cognition, linking TDP-43 to circadian-metabolic coupling in neurodegeneration.

Men and Hirayama et al. show that misfolded protein aggregates are degraded through microautophagy, a process mediated by the UBAP1-containing ESCRT-I complex and PTPN23. Their findings provide new insights into the mechanisms of misfolded protein aggregate clearance in cells.

This study uncovers Rab GTPases as evolutionarily conserved signals mediating selective autophagy, targeting damaged mitochondria, lipid droplets, and pathogens for degradation. The research reveals a conserved mechanism across species, demonstrating how Rab GTPases regulate mitophagy, lipophagy, and xenophagy, with implications for maintaining cellular homeostasis.

Miranda-Alban et al. uncover a synergistic interaction between the cytoplasmic tyrosine kinase Abelson and the Nedd4 family ubiquitin ligases that regulates the transit of the Notch receptor through late endosomal vesicles, thereby modulating activation of the signaling pathway in both ligand-exposed and -unexposed cells.

Deraniyagala et al. explore the poorly understood mechanism of “intracellular counting” using the developing oral apparatus of the ciliateTetrahymena as a model. An ortholog of importin-9 and a TPR protein MpH were found to increase and decrease the number of forming oral ciliary rows, respectively.