A mutation in the nuclear-encoded plastid ribosomal protein S9 leads to early embryo lethality in maize.

Seeds of the lethal embryo 1 (lem1) mutant in maize (Zea mays) display a non-concordant lethal phenotype: whereas the embryo aborts very early, before the transition stage, the endosperm develops almost normally. The mutant was identified in a collection of maize lines that carried the transposon Activation (Ac) at different locations in the genome. Co-segregation and reversion analysis showed that lem1 was tagged by Ac. The lem1 gene encodes a protein that is highly similar to the rice plastid 30S ribosomal protein S9 (PRPS9). lem1 maps to chromosome 1L and appears to be the only copy of prps9 in the maize genome. Green fluorescent protein (GFP) fusion constructs containing only the putative transit peptide (TP) of LEM1 localize exclusively to the plastids, confirming that the LEM1 protein is a PRP. In contrast, GFP fusion constructs containing the entire LEM1 protein co-localize to the plastids and to the nucleus, suggesting a possible dual function for this protein. Two alternative, although not mutually exclusive, explanations are considered for the lem phenotype of the lem1 mutant: (i) functional plastids are required for normal embryo development; and (ii) the PRPS9 has an extra-ribosomal function required for embryogenesis.