Regulated cell shape change requires the induction of cortical cytoskeletal domains. Often, local changes to plasma membrane (PM) topography are involved. Centrosomes organize cortical domains and can affect PM topography by locally pulling the PM inward. Are these centrosome effects coupled? At the syncytial Drosophila embryo cortex, centrosome-induced actin caps grow into dome-like compartments for mitoses. We found the nascent cap to be a collection of PM folds and tubules formed over the astral centrosomal MT array. The localized infoldings require centrosome and dynein activities, and myosin-based surface tension prevents them elsewhere. Centrosome-engaged PM infoldings become specifically enriched with an Arp2/3 induction pathway. Arp2/3 actin network growth between the infoldings counterbalances centrosomal pulling forces and disperses the folds for actin cap expansion. Abnormal domain topography with either centrosome or Arp2/3 disruption correlates with decreased exocytic vesicle association. Together, our data implicate centrosome-organized PM infoldings in coordinating Arp2/3 network growth and exocytosis for cortical domain assembly.

Recent technological advances have transformed our understanding of the human thymus. Innovations such as high-resolution imaging, single-cell omics, and organoid cultures, including thymic epithelial cell (TEC) differentiation and culture, and improvements in biomaterials, have further elucidated the thymus architecture, cellular dynamics, and molecular mechanisms underlying T cell development, and have unraveled previously unrecognized levels of stromal cell heterogeneity. These advancements offer unprecedented insights into thymic biology and hold promise for the development of novel therapeutic strategies for immune-related disorders.

How are Rab GTPases regulated during lysosome-related organelle (LRO) biogenesis? Li et al. (https://doi.org/10.1083/jcb.202402016) identify LYSMD proteins as crucial activators of Rab32-family GTPases in LRO development, shedding light on the previously ambiguous mechanisms governing Rab functionality in this process.

Learning through cooperation with conspecifics-'cooperative learning'-is critical to cultural evolution and survival. Recent progress has established that interbrain synchronization (IBS) between individuals predicts success in cooperative learning. However, the likely sources of IBS during learning interactions remain poorly understood. To address this dearth of knowledge, we tested whether movement synchrony serves as an exogenous factor that drives IBS, taking an embodiment perspective. We formed dyads of individuals with varying levels of prior knowledge (high-high (HH), high-low (HL), low-low (LL) dyads) and instructed them to collaboratively analyse an ancient Chinese poem. During the task, we simultaneously recorded their brain activity using functional near-infrared spectroscopy and filmed the entire experiment to parse interpersonal movement synchrony using the computer-vision motion energy analysis. Interestingly, the homogeneous groups (HH and/or LL) exhibited stronger movement synchrony and IBS compared with the heterogeneous group. Importantly, mediation analysis revealed that spontaneous and synchronized body movements between individuals contribute to IBS, hence facilitating learning. This study therefore fills a critical gap in our understanding of how interpersonal transmission of information between individual brains, associated with behavioural entrainment, shapes social learning. This article is part of the theme issue 'Minds in movement: embodied cognition in the age of artificial intelligence'.

αβ T cells are critical components of the adaptive immune system; they maintain tissue and immune homeostasis during health, provide sterilizing immunity after pathogen infection, and are capable of eliminating transformed tumor cells. Fundamental to these distinct functions is the ligand specificity of the unique antigen receptor expressed on each mature T cell (TCR), which endows lymphocytes with the ability to behave in a cell-autonomous, disease context-specific manner. Clone-specific behavioral properties are initially established during T cell development when thymocytes use TCR recognition of major histocompatibility complex (MHC) and MHC-like ligands to instruct survival versus death and to differentiate into a plethora of inflammatory and regulatory T cell lineages. Here, we review the ligand specificity of the preselection thymocyte repertoire and argue that developmental stage-specific alterations in TCR signaling control cross-reactivity and foreign versus self-specificity of T cell sublineages.