Plastids affect embryo patterning

Abstract

Plastids are essential for plant cells and serve as biochemical hubs during embryogenesis. Therefore, many knockout mutants of genes encoding plastid-targeted proteins are embryonic lethal in Arabidopsis. However, until now, the reason for such embryonic lethal phenotypes was thought to be related to a general lack of essential plastid-generated metabolites, such as lipids or amino acids. Much less was known about a potential specific role of plastids during embryogenesis. GENOMES UNCOUPLED 1 (GUN1) and DELAYED GREENING 1 (DG1) are plastid-localized proteins that are involved in RNA editing when bound to MULTIPLE ORGANELLAR RNA-EDITING FACTOR 2 (MORF2). However, at least for GUN1, an enigmatic role in retrograde signalling is known to affect nuclear gene expression in response to plastid signals.

The researchers identify a recessive dg1 mutant that leads to embryo arrest at the globular stage in a quarter of the progeny from heterozygous plants — presumably the homozygous embryos. Expression of WUS and STM, which is normally confined to the inter-cotyledonary zone, is expanded in these mutants, and vascular identity does not reach the cotyledon primordia. In wild-type embryos, DG1 is expressed broadly except in the incipient shoot apical meristem, in line with the idea that DG1 represses WUS and STM. This role of DG1 is independent of its interaction with MORF2 and consequently of plastid RNA editing, which depends on the MORF2 interaction. Instead, the defect in dg1 embryos is partially suppressed by the gun1 mutant, with double mutants progressing to the torpedo stage and showing normal expression of WUS and STM. These results suggest that expression of WUS and STM is influenced by a plastid retrograde signal, which contributes to embryo patterning.