Abstract
Plastid gene expression (PGE) is essential for chloroplast biogenesis and function and, hence, for plant development. However, many aspects of PGE remain obscure due to the complexity of the process. A hallmark of nuclear-organellar coordination of gene expression is the emergence of nucleus-encoded protein families, including nucleic-acid binding proteins, during the evolution of the green plant lineage. One of these is the mitochondrial transcription termination factor (mTERF) family, the members of which regulate various steps in gene expression in chloroplasts and/or mitochondria. Here, we describe the molecular function of the chloroplast-localized mTERF2 in Arabidopsis thaliana. The complete loss of mTERF2 function results in embryo lethality, whereas directed, microRNA (amiR)-mediated knockdown of MTERF2 is associated with perturbed plant development and reduced chlorophyll content. Moreover, photosynthesis is impaired in amiR-mterf2 plants, as indicated by reduced levels of photosystem subunits, although the levels of the corresponding messenger RNAs are not affected. RNA immunoprecipitation followed by RNA sequencing (RIP-Seq) experiments, combined with whole-genome RNA-Seq, RNA gel-blot, and quantitative RT-PCR analyses, revealed that mTERF2 is required for the splicing of the group IIB introns of ycf3 (intron 1) and rps12.
Highlights
Plastids of the group Plantae arose more than one-billion years ago from a single endosymbiosis event, in which a heterotrophic protist was engulfed and retained a cyanobacterium in its cytoplasm [1]
In order to experimentally define and investigate the intracellular localization of mTERF2 in more depth, chloroplasts from three-week-old Col-0 plants overexpressing mTERF2-c-myc were prepared and membrane- and stroma-enriched fractions were first isolated essentially according to the protocol that was used by Kauss et al [37]
23S ribosomal RNAs (rRNAs) in amiR1–mterf2 plants can, at least in part, account for the general reduction in chloroplast translation capacity and the delay in chloroplast development. These findings suggest that the reduced accumulation of photosynthesis proteins in plants lacking mTERF2 is not caused by differential accumulation of transcripts, but implies the presence of a disturbance in another step in plastid gene expression (PGE)
Summary
Plastids of the group Plantae arose more than one-billion years ago from a single endosymbiosis event, in which a heterotrophic protist was engulfed and retained a cyanobacterium in its cytoplasm [1]. Plastids lost most of their genes to the nucleus [2] and they have only retained a reduced genome of approximately 120 loci. Both nucleus- and plastid-encoded components are required for processes that take place in chloroplasts, including the formation of the photosystems, the Rubisco complex, and plastid ribosomes. The lack of nucleus-encoded proteins necessary for plastid gene expression (PGE) often results in pale green plants and even seedling- or embryo-lethality [3], which underlines the importance of PGE for plant development and photosynthesis. With one exception (the plastid-encoded maturase MatK), all of the proteins that are needed for organellar
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