Metabolic reprogramming and mitochondrial dysfunction underlie β gonia arrest and niche cell dysfunction in sterile triploid oysters.

Complementary to the classical view that triploid sterility results from meiotic failure, female triploid pacific oysters exhibit partial sterility also characterized by the impairment of the differentiation of germ cells, forming β gonia. However, the molecular basis underlying this sterility remains unclear, partly due to the diffuse nature of oyster gonads, which lack distinct structural boundaries, making cell-type identification challenging. Here, we integrate high-resolution spatial transcriptomics (Stereo-seq) and single-nucleus RNA sequencing (snRNA-seq) to construct a spatially resolved molecular atlas of sterile triploid oyster gonads, enabling precise characterization of β gonia transcriptional dysregulation and their disrupted interactions with niche cells. We find that β gonia exhibit germplasm mRNA downregulation, impaired ATP synthesis, and excessive mitochondrial autophagy, likely driven by the silencing of SOHLH2, a key regulator of oocyte differentiation. Additionally, triploid niche cells undergo G