Ken Kamiya

morphoDE asks a deliberately simple question: where two cell types meet, the boundary bulges outward in some places and caves inward in others—do the cells on a bulge express different genes than the cells in a dent? We tested it across 11 published 3D spatial-transcriptomics datasets and 126 interface–strata, from a human lymph-node tumor to an Arabidopsis leaf. The correspondence holds almost everywhere: 125 of 126 interface–strata carry signal that survives a geometry-breaking null (which shuffles the shape while keeping the biology fixed), signal appears in all 11 datasets, and 16 reach a perfect 12/12 in species sharing no common ancestry. On the human tumor the difference is 93% within a single cell type—convex bulges carry immune and cholesterol programs, concave dents carry hypoxia and invasion (PTHLH, KRT17). Why it matters: interface shape and cell state are linked as a general property of tissue architecture, not a tumor quirk—giving a geometry-readable spatial map of cell state, from cancer to plants.