The Arabidopsis organelle-localized glycyl-tRNA synthetase encoded by EMBRYO DEFECTIVE DEVELOPMENT1 is required for organ patterning

Abstract

Leaves develop as planar organs, with a morphology that is specialized for photosynthesis. Development of a planar leaf requires genetic networks that set up opposing adaxial and abaxial sides of the leaf, which leads to establishment of dorsoventral polarity. While many genes have been identified that regulate adaxial and abaxial fate there is little information on how this is integrated with cellular function. EMBRYO DEFECTIVE DEVELOPMENT1 (EDD1) is a nuclear gene that encodes a plastid and mitochondrial localized glycyl-tRNA synthetase. Plants with partial loss of EDD1 function have changes in patterning of margin and distal regions of the leaf. In combination with mutations in the MYB domain transcription factor gene ASYMMETRIC LEAVES1 (AS1), partial loss of EDD1 function results in leaves with reduced adaxial fate. EDD1 may influence leaf dorsoventral polarity through regulating the abaxial fate genes KANADI1 (KAN1) and ETTIN (ETT)/AUXIN RESPONSE FACTOR3 (ARF3) since these genes are upregulated in the edd1 as1 double mutant. SCABRA3 (SCA3), a nuclear gene that encodes the plastid RNA polymerase is also required for leaf adaxial fate in the absence of AS1. These results add a novel component to networks of genetic regulation of leaf development and suggest that organelles, particularly plastids, are required in leaf patterning. Potentially, signalling from organelles is essential for coordination of different cell fates within the developing leaf.

The Pentatricopeptide Repeat Protein EMB2654 Is Essential for Trans-Splicing of a Chloroplast Small Ribosomal Subunit Transcript

“…Cotyledons and leaves of the rescued emb2394 line were greenish-yellow, and the leaves serrated (Fig. 1, C and E), a pattern already observed for chloroplast translation mutants (Pinon et al, 2008;Moschopoulos et al, 2012). The rescued emb2654 seedlings had pale green cotyledons and albino leaves (Fig.…”

Pattern Dynamics in Adaxial-Abaxial Specific Gene Expression Are Modulated by a Plastid Retrograde Signal during Arabidopsis thaliana Leaf Development

“…One possible scenario is that ABI4 and GLK1 also affect the expression levels of FIL , miR165/166 and other adaxial- and abaxial-specific genes through the transcriptional regulation. Among the adaxial- and abaxial-specific genes, KAN1 and ETTIN / ARF3 are known to be up-regulated in response to the impaired plastid gene expression though the involvement of GUN1 in the up-regulation is unclear [62]. On the other hand, it is also possible that the slow FMB shifting is a more indirect effect than such direct transcriptional regulations.…”

“…On the other hand, it is also possible that the slow FMB shifting is a more indirect effect than such direct transcriptional regulations. For example, there are some reports pointing out that lincomycin-treated plant differently express the genes encoding cytosolic ribosomal proteins [85] and that some mutants of the genes for cytosolic ribosomal proteins form the partially abaxialized leaves as plastid-defective mutants do [62], [86]–[89]. Another study shows the importance of abscisic acid metabolism for the leaf morphological phenotype of a plastid-defective mutant [63].…”

ASYMMETRIC LEAVES2 and FASCIATA2 cooperatively regulate the formation of leaf adaxial-abaxial polarity in Arabidopsis thaliana

“…Interestingly, most of the single modifier mutants show the common phenotype, formation of slightly narrow leaves with pointed tip (pointed leaves). (Horiguchi et al 2011;Ishibashi et al 2012;Moschopoulos et al 2012;Pinon et al 2008). Mutations in the FASCIATA2 (FAS2) gene, which encodes a component of Chromatin Assembly Factor-1 (CAF-1) complex, a histone chaperone, also generate such a leaf phenotype (Kaya et al 2001).…”