The kidney tissue of a single individual of the California minnow Gila bicolor (Girard) contained polyploid cells in about 1.7% frequency. Chromosome spreads of triploid, tetraploid, hexaploid, octaploid, and dodecaploid cells were observed and may have arisen through endoreduplication of ancestral diploid and triploid cells. The cytological mechanism producing the triploid cells is unknown. Diplochromosomes were not present. The distribution of ploidy in cells of this individual is not random. In particular, cells having undergone one round of chromosomal increase appear increasingly susceptible to additional rounds of chromosomal gain.

Human genome variation contributes to diversity in neurodevelopmental outcomes and vulnerabilities; recognizing the underlying molecular and cellular mechanisms will require scalable approaches. Here, we describe a cell village experimental platform we used to analyze genetic, molecular, and phenotypic heterogeneity across neural progenitor cells from 44 human donors cultured in a shared in vitro environment using algorithms (Dropulation and Census-seq) to assign cells and phenotypes to individual donors. Through rapid induction of human stem cell-derived neural progenitor cells, measurements of natural genetic variation, and CRISPR-Cas9 genetic perturbations, we identified a common variant that regulates antiviral IFITM3 expression and explains most inter-individual variation in susceptibility to the Zika virus. We also detected expression QTLs corresponding to GWAS loci for brain traits and discovered novel disease-relevant regulators of progenitor proliferation and differentiation such as CACHD1. This approach provides scalable ways to elucidate the effects of genes and genetic variation on cellular phenotypes.