Seeds provide plant embryos with the remarkable ability to endure extended periods of times and extreme environmental conditions. Orthodox – or desiccation-tolerant – seeds, in particular, feature a number of adaptations to optimise resistance against extreme environments. Those traits must be established during seed maturation, since metabolism is reduced to a minimum during the desiccated phase and cannot support active defence. A characteristic of the maturation of most orthodox seeds is de-greening of the embryo, i.e. the regulated disassembly of the chloroplast thylakoid systems and chlorophyll degradation. While de-greening was shown to be under hormonal control, the physiological significance of thylakoid disassembly and reassembly remains unclear. Here we isolated an Arabidopsis lea48 lea42 line, as a model for depleted LEA function specifically in mitochondria and plastids of seeds. lea48 lea42 features a stay-green phenotype due to incomplete thylakoid degradation of the chloroplast, as evidenced by proteomic, transcriptomic and transmission electron microscopy analyses, yet without apparent signs of disrupted ABA homeostasis. While fresh lea48 lea42 seeds were unaffected in their germination properties, mutants were compromised in longevity at high-temperature/ high-humidity aging. Organelle-specific genetic complementation revealed that reduced longevity is linked to LEA ablation in the plastid, rather than the mitochondria. Strikingly, ‘light-ageing’, i.e. illumination of mature dry seeds, also reduced longevity delayed germination, which was associated with an accumulation of oxidised lipids. Our study pinpoints a novel role for LEA proteins in the regulated remodelling of seed mitochondria and plastids before desiccation. We identify embryo de-greening under the partial control of LEA as a key contributor to seed longevity, with direct evolutionary and ecological implications, as well as for strategies in plant breeding and agriculture.