Cells constantly change their molecular state in response to internal and external cues1. Mapping cellular activity in tissues with spatiotemporal precision is essential for understanding organ physiology, pathology and regenerative processes. Current cell-sensing modalities primarily rely on either end point analysis that takes static snapshots2 or real-time sensing that monitors a small subset of cells3,4. Here we introduce granularly expanding memory for intracellular narrative integration (GEMINI), an in cellulo recording platform that leverages a computationally designed protein assembly as an intracellular memory device to record the history of individual cells. GEMINI grows predictably within live cells, capturing cellular events as tree-ring-like fluorescent patterns for imaging-based retrospective readout. Absolute chronological information of activity histories is attainable with hour-level accuracy. GEMINI effectively maps differential NF-κB-mediated transcriptional changes, resolving fast dynamics of 15 min and providing quantifiable signal amplitudes. In a xenograft model, GEMINI records inflammation-induced signalling dynamics across tissue, revealing spatial heterogeneity linked to vascular density. When expressed in the mouse brain, GEMINI minimally impacts neuronal functions and can resolve both transcriptional changes and activity patterns of neurons. Together, GEMINI provides a robust and generalizable means for spatiotemporal mapping of cell dynamics underlying physiological and pathological processes in both culture and intact tissues.

Socioeconomic status (SES) significantly influences mental health outcomes and treatment access, yet its reporting in psychedelic-assisted therapy trials remains underexplored. Here we systematically reviewed 98 articles (49 primary trials and 49 secondary analyses) published between 2006 and 2024 examining classic psychedelics and MDMA for mental health conditions. Only 12% of primary trials reported participant income data, and 31% reported educational attainment. In USA-based trials, participants showed markedly higher SES than the general population: 93% had some college education (versus 62% nationally), and median incomes in major trials substantially exceeded the national median for all workers. Non-US trials showed variable patterns. This widespread underreporting of SES data and evidence of socioeconomic disparities, particularly in US trials, highlights an urgent need for standardized SES reporting and targeted strategies to improve socioeconomic diversity in psychedelic-assisted therapy research, ensuring broader generalizability and access to these emerging treatments.

The repair of DNA double-strand breaks by homologous recombination is essential for genomic integrity, and its dysregulation is a hallmark of cancer1. Central to homologous recombination is the RAD51 recombinase, whose assembly into a nucleoprotein filament is governed by five RAD51 paralogues (RAD51B, RAD51C, RAD51D, XRCC2 and XRCC3)2. Mutations in any of these proteins predispose individuals to multiple cancers or genetic disorders3-6. These paralogues are thought to form two functionally separate complexes RAD51B-RAD51C-RAD51D-XRCC2 (BCDX2) and RAD51C-XRCC3 (CX3), that act independently at different stages of homologous recombination7-11. Here we demonstrate that all five paralogues can assemble into a single, ATP-dependent BCDX2-CX3-RAD51 supercomplex. The architecture of this assembly bound to single-stranded DNA reveals a contiguous filament where the CX3 module stacks atop BCDX2, creating a protofilament template for RAD51 filament formation. We further identify a novel, RAD51B-independent DX2-CX3 complex (RAD51D-XRCC2-RAD51C-XRCC3) functioning as a stable RAD51 anchor on single-stranded DNA, and we capture it in multiple states, including capping RAD51 filament segment. These distinct assemblies are differentially regulated by ATPase activity, defining a dynamic BCDX2-CX3 'loader' and a stable DX2-CX3 'anchor' that provide functional modularity to the homologous recombination machinery. This work provides a unifying mechanism for human RAD51 paralogue function and delivers an atomic blueprint for interpreting disease-causing mutations.