Topic: Single-cell analysis

Yun Xia presents macrophage–kidney assembloids that address missing immune and vascular components in stem-cell organoids. Directed differentiation, self-organization, genetic perturbation, xenotransplantation and single-cell analysis reveal immune–epithelial interactions. Macrophages from the same parental cells acquire resident phenotypes; diabetic and polycystic kidney models show context-dependent effects on inflammation, epithelial injury and disease progression. Minoru Takasato addresses kidney organoids’ missing urinary outflow by generating bladder tissue from human pluripotent cells.

Tim Ebbels presents interpretable machine-learning models for metabolomics and multi-omics using pathway and chemical-class scores. Sparse coverage of the metabolome and uncertain annotations make conventional results difficult to interpret; pathway-based features aim to connect model output directly to biological function. The webinar examines applications from multi-assay mass spectrometry and multi-omics integration to single-cell and mass-spectrometry imaging, discusses methodological challenges and attempts to resolve them, and demonstrates how these approaches can clarify complex biologi

Matthew J. Girgenti discusses how research on individual brain cells and the three-dimensional organization of DNA is changing the biological understanding of post-traumatic stress disorder. The seminar examines how these approaches reveal trauma-associated brain changes and identify possible targets for more effective, personalized treatments. Girgenti is a neuroscientist in Yale School of Medicine’s Department of Psychiatry. Jeffrey Borenstein moderates this Meet the Scientist session. Online via the BBRF Zoom webinar. Tuesday 13 October 2026, 14:00 EDT (America/New_York; UTC−4). Follow Reg

The advent of next generation sequencing ushered in a ten-year period of exuberant technology development, enabling the quantification of gene expression and epigenetic features within individual cells, and within intact tissue sections. In this seminar, I will outline our technological contributions, beginning with the development of Drop-seq, a method for high-throughput single cell analysis, followed by the development of Slide-seq, a technique for measuring genome-wide expression at 10 micron spatial resolution. Using a combination of these techniques, we recently constructed a compreh

Three intimately related dimensions of the mammalian genome—linear DNA sequence, gene transcription, and 3D genome architecture—are crucial for the development of nervous systems. Changes in the linear genome (e.g., de novo mutations), transcriptome, and 3D genome structure lead to debilitating neurodevelopmental disorders, such as autism and schizophrenia. However, current technologies and data are severely limited: (1) 3D genome structures of single brain cells have not been solved; (2) little is known about the dynamics of single-cell transcriptome and 3D genome after birth; (3) true de nov

One of the major roadblocks to medical progress in the field of neurodegeneration is the absence of animal models that fully recapitulate features of the human diseases. Unprecedented opportunities to tackle this challenge are emerging e.g. from genome engineering and stem cell technologies, and there are intense efforts to develop models with a high translational value. Simultaneously, single-cell, multi-omics and optogenetics technologies now allow longitudinal, molecular and functional analysis of human disease processes in these models at high resolution. During this workshop, 12 experts w

The thalamic reticular nucleus (TRN), the major source of thalamic inhibition, is known to regulate thalamocortical interactions critical for sensory processing, attention and cognition. TRN dysfunction has been linked to sensory abnormality, attention deficit and sleep disturbance across multiple neurodevelopmental disorders. Currently, little is known about the organizational principles underlying its divergent functions. In this talk, I will start with an example of how dysfunction of TRN contributes to attention deficit and sleep disruption using a mouse model of Ptchd1 mutation, which in