PPR8522 encodes a chloroplast-targeted pentatricopeptide repeat protein necessary for maize embryogenesis and vegetative development

Abstract

The pentatricopeptide repeat (PPR) domain is an RNA binding domain allowing members of the PPR superfamily to participate in post-transcriptional processing of organellar RNA. Loss of PPR8522 from maize (Zea mays) confers an embryo-specific (emb) phenotype. The emb8522 mutation was isolated in an active Mutator (Mu) population and co-segregation analysis revealed that it was tightly linked to a MuDR insertion in the first exon of PPR8522. Independent evidence that disruption of PPR8522 caused the emb phenotype was provided by fine mapping to a region of 116kb containing no other gene than PPR8522 and complementation of the emb8522 mutant by a PPR8522 cDNA. The deduced PPR8522 amino acid sequence of 832 amino acids contains 10 PPR repeats and a chloroplast target peptide, the function of which was experimentally demonstrated by transient expression in Nicotiana benthamiana. Whereas mutant endosperm is apparently normal, mutant embryos deviate from normal development as early as 3 days after pollination, are reduced in size, exhibit more or less severe morphological aberrations depending on the genetic background, and generally do not germinate. The emb8522 mutation is the first to associate the loss of a PPR gene with an embryo-lethal phenotype in maize. Analyses of mutant plantlets generated by embryo-rescue experiments indicate that emb8522 also affects vegetative plant growth and chloroplast development. The loss of chloroplast transcription dependent on plastid-encoded RNA polymerase is the likely cause for the lack of an organized thylakoid network and an albino, seedling-lethal phenotype.

The Requirement of WHIRLY1 for Embryogenesis Is Dependent on Genetic Background in Maize

“…In K55 and Ky21 genetic backgrounds, ij conditions embryo lethality, but seedlings with stripe leaves in Mo17 and Oh51a backgrounds. Similar suppression was observed in emb8522 , which conditions embryo lethality in the original genetic background but in A188 and B73 backgrounds conditions albino seedlings [34]. Emb8522 encodes a plastid PPR protein with possible functions in plastid gene expression.…”

“…In maize, WHY1 is also essential for the biogenesis of plastid ribosome. The severe loss of function allele why1-1 in the standard genetic background and B73 conditions albino seedlings [33], [34].…”

Natural Variation in Sensitivity to a Loss of Chloroplast Translation in Arabidopsis

“…At first, it appeared that differences in fatty acid biosynthesis alone could explain the phenotypes observed. However, at least five mutants with severe defects in maize embryogenesis are disrupted in chloroplast translation: lem1 (Ma and Dooner, 2004), prpl35-1 (Magnard et al, 2004), ppr8522 (Sosso et al, 2012), emb16/why1 , and emb12 (Shen et al, 2013). Thus, a loss of chloroplast translation in maize is sometimes associated with embryo lethality.…”

Large-scale genetic analysis of chloroplast biogenesis in maize

“…140 Most mutants in the PML collection are seedling lethal, and die 141 at~three weeks post-germination when seed reserves are exhausted. 142 The mutations are recessive and are propagated by crossing heterozy- 143 gous plants. Genes that have been linked to phenotypes in the PML col- 144 lection thus far are represented by an average of~3.6 mutant alleles, 145 suggesting that the collection is nearing saturation for the chlorophyll- 146 deficiency screen that was used to assemble it.…”