Xin Jin

The paper introduces distributed AI agents to analyze large-scale biological datasets, demonstrating their ability to rapidly extract insights and predict outcomes across a Perturb-seq atlas.

The paper develops Perturb-CLEAR to study dendritic morphogenesis in the developing mouse cortex, revealing gene-specific multimodal phenotypes linked to NDD risk genes.

The paper maps gene expression responses to loss of 1,947 disease-associated genes across the mouse brain using Perturb-seq, revealing cell-type-specific essentiality and transcriptional programs.

This paper develops an in vivo multiomic Perturb-seq platform to improve gRNA recovery and applies it to study neurodevelopmental disorder risk genes in the cortex.

Deleting Piezo1 and Piezo2 together in mice weakens uterine contractions and prolongs labor; uterine and sensory-neuron deletions act additively, and knockout uteri show reduced Gja1 (connexin43).

This study develops a high-throughput in vivo Perturb-seq platform to analyze gene function across diverse cell types in the brain and peripheral nervous system, identifying cell type-specific transcriptional networks.

The paper identifies neuron-class specific signals that drive differential myelination across cortical layers using single-cell data from mouse neocortex.

The paper investigates how PTEN heterozygous mutations affect different cell types in human cortical organoids and shows that these effects lead to abnormal circuit activity regardless of genetic background.

The paper presents a single-cell multiomics atlas of human cortical organoid development, revealing molecular programs of cellular diversification and identifying human-specific gene roles in lineage establishment.

This study uses in vivo Perturb-Seq to analyze the effects of 35 autism risk genes on neuronal and glial cells in the developing brain.

This study shows C. elegans can discriminate colors using a system unrelated to opsins, guiding foraging behavior based on light absorption by toxins.

This study identifies a GPCR, str-217, in C. elegans that mediates DEET resistance by altering chemotaxis behavior through increased pause length.