Book Description

The maize kernel is at the heart of research efforts geared to elucidate the molecular mechanisms governing its development and the accumulation of oil and starch in its two major compartments, embryo and endosperm. Here, we present the molecular and phenotypic characterisation of two maize kernel mutants, the embryo-specific PPR8522 and the miniature PPR2263 mutant. Despite dissimilar phenotypes both mutations concerned genes coding for pentatricopeptide repeat (PPR) proteins predicted to act in organellar RNA processing. The gene responsible for the embryo-lethal phenotype of PPR8522 was identified by transposon tagging and confirmed by fine mapping. PPR8522 contains 10 PPR motifs, is targeted to plastids and required for the transcription of nearly all plastid-encoded genes. Mutant embryos deviate as early as the 3-cell stage from normal development but can be rescued in vitro in certain genetic backgrounds. Rescued mutant plantlets have an albino lethal phenotype due to a substantial cellular desorganisation of their plastids including a total lack of thylakoid stacks. The mutation responsible for the miniature kernel phenotype of PPR2263 was identified by a novel cDNA transposon display technique. The cloning was confirmed by transgenic complementation via Agrobacterium-mediated maize transformation. PPR2263 contains 10 PPR motifs, a mitochondrial-targeting sequence and a DYW domain, suggesting a role in organellar RNA editing. Mutant plants hardly ever reach sexual maturity and are characterised by slow growth.