A seedling-lethal mutation affects chloroplast biogenesis and photosynthetic gene expression in kiwifruit

We identified a developmental disorder in a segregating population of yellow kiwifruit ( Actinidia chinensis ), characterized by interveinal chlorosis in upper leaves, culminating in growth arrest and seedling death after developing 9–10 leaves. This study aimed to elucidate the physiological and molecular basis of this phenotype through integrated phenotypic, transcriptomic, and genomic analyses. Through phenotypic characterization, we identified key alterations in chloroplast size, lower net CO 2 assimilation rate, a decrease in the maximum quantum yield of PSII photochemistry Fv/Fm, and an altered accumulation of the nutrients phosphorus, potassium, sulfur, boron, and extractable iron in chlorotic leaves. At the transcriptional level, leaves of chlorotic plantlets overexpressed genes involved in chlorophyll metabolism, the photosynthetic apparatus and protein translation machinery, resembling a compensatory mechanism to up-regulate chloroplast and protein translation processes, which was also found in photosynthesis deficient mutants from other species. Our results pointed to a putative monogenic recessive mutation, designated chlorotic terminal ( cht ), which localized in a wide region of chromosome 18 by Bulked Segregant Analysis (BSA) and gene mapping, and affected chloroplast biogenesis, photosynthetic activity, and iron-related metabolic processes. These findings provided insight into the molecular mechanisms underlying leaf chlorosis in kiwifruit and highlighted candidate genes for further functional characterization.