Lack of individual plastid ribosomal proteins (PRPs) can have diverse phenotypic effects in Arabidopsis thaliana, ranging from embryo lethality to compromised vitality, with the latter being associated with photosynthetic lesions and decreases in the expression of plastid proteins. In this study, reverse genetics was employed to study the function of eight PRPs, five of which (PRPS1, S20, L27, L28 and L35) have not been functionally characterised before. In the case of PRPS17, only leaky alleles or RNAi lines had been analysed previously. PRPL1 and PRPL4 have been described as essential for embryo development, but their mutant phenotypes are analysed in detail here. We found that PRPS20, L1, L4, L27 and L35 are required for basal ribosome activity, which becomes crucial at the globular stage and during the transition from the globular to the heart stage of embryogenesis. Thus, lack of any of these PRPs leads to alterations in cell division patterns, and embryo development ceases prior to the heart stage. PRPL28 is essential at the latest stages of embryo-seedling development, during the greening process. PRPS1, S17 and L24 appear not to be required for basal ribosome activity and the organism can complete the entire life cycle in their absence. Interestingly, despite the prokaryotic origin of plastids, the significance of individual plastid ribosomal proteins for plant development cannot be predicted from the relative phenotypic severity of the corresponding mutants in prokaryotic systems.