Notch1 has an indispensable role in initiating the T lineage program from progenitors in the thymus. This study defines stage-specific regulation of Notch target genes and shows that Notch2 also amplifies inductive and lineage-restrictive Notch signals in early T cell development.

Super-resolution imaging shows that G1/S transcription factors in budding yeast are spatially organized in small clusters that increase in number, not molecular content, as the transcription factor copy number increases with cell growth in G1. This spatial and temporal organization of the G1/S regulon might help coordinate the Start transition.

Cytoplasmic cilia, which are found in human and Drosophila sperm, are unique in that the axoneme is exposed to the cytoplasm. Fingerhut and Yamashita show that localization of a novel RNP granule containing axonemal dynein mRNAs facilitates incorporation of these axonemal proteins, promoting cytoplasmic cilia formation.

Synaptic properties are controlled by trans-synaptic adhesion complexes. Neurexins are central components of these complexes, but how neurexins are regulated remains largely unknown. Khalaj et al. identify FAM19A1-A4 as neuronal activity–regulated proteins that form covalent complexes with neurexins and regulate their post-translational modifications, thus shaping neurexin–ligand interactions and synapse properties.

Combining in vivo lineage tracing and single-cell RNA- and ATAC-seq, Wang et al. identified a repertoire of stereotyped neurogenic lineages in the developing zebrafish retina, revealing the lineage logic of neuron type/subtype specification and respecification in a vertebrate CNS structure.

In this article, Osseni et al. show that by controlling acetylation of microtubules at neuromuscular junctions, HDAC6 regulates the insertion and removal of acetylcholine receptors. Accordingly, these findings provide key novel insights into the mechanisms involved in the stability and structure of neuromuscular junctions.

Chiusa et al. show that the RNA-DNA binding protein FUS plays a profibrotic role by binding to the collagen IV gene promoter and commencing its transcription. Reducing nuclear FUS inhibits collagen IV transcription, suggesting that targeting FUS offers a new antifibrotic therapy.