MORF9-dependent specific plastid RNA editing inhibits root growth under sugar starvation in Arabidopsis.

Multiple organellar RNA editing factor (MORF) complex was shown to be highly associated with C-to-U RNA editing of vascular plant editosome. However, mechanisms by which MORF9-dependent plastid RNA editing controls plant development and responses to environmental alteration remain obscure. In this study, we found that loss of MORF9 function impaired PSII efficiency, NDH activity, and carbohydrate production, rapidly promoted nuclear gene expression including sucrose transporter and sugar/energy responsive genes, and attenuated root growth under sugar starvation conditions. Sugar repletion increased MORF9 and MORF2 expression in wild-type seedlings and reduced RNA editing of matK-706, accD-794, ndhD-383 and ndhF-290 in the morf9 mutant. RNA editing efficiency of ndhD-383 and ndhF-290 sites was diminished in the gin2/morf9 double mutants, and that of matK-706, accD-794, ndhD-383 and ndhF-290 sites were significantly diminished in the snrk1/morf9 double mutants. In contrast, overexpressing HXK1 or SnRK1 promoted RNA editing rate of matK-706, accD-794, ndhD-383 and ndhF-290 in leaves of morf9 mutants, suggesting that HXK1 partially impacts MORF9 mediated ndhD-383 and ndhF-290 editing, while SnRK1 may only affect MORF9-mediated ndhF-290 site editing. Collectively, these findings suggest that sugar and/or its intermediary metabolites impair MORF9-dependent plastid RNA editing resulting in derangements of plant root development.

Modulating carbon dioxide activation on carbon nanotube immobilized salophen complexes by varying metal centers for efficient electrocatalytic reduction.

Electrocatalytic CO2 reduction (ECR) into valuable chemicals, especially driven by renewable energy, presents a promising pattern to realize carbon neutrality. Site-isolated metal complexes flourish in the area of ECR as single-atom-like catalysts because of their competent and tailorable activity. In this study, salophen-based metal (Fe, Co, Ni and Cu) complexes were anchored onto carbon nanotubes (CNTs) to construct efficient catalysts for electrochemically converting CO2 to CO. Both experimental and theoretical results verified that CO2 activation was the rate-determining step for the catalytic performance of these hybrid molecular catalysts. The coordinate activation ability can be manipulated by varying the metal centers. The as-synthesized Fe-salophen hybrid CNT (Fe-salophen/CNT) shows the best activity and selectivity of -13.24 mA·cm-2 current density with 86.8% Faradaic efficiency for generating CO (FECO) at -0.76 V vs. RHE in aqueous solution, whereas Cu-salophen/CNT only achieved a -2.22 mA·cm-2 current density and 57.9% FECO under the same reaction conditions. These distinct catalytic performances resulted from the different coordination activation abilities of CO2 on various metal centers.

Triple-localized WHIRLY2 Influences Leaf Senescence and Silique Development via Carbon Allocation.

Coordination of gene expression in mitochondria, plastids, and nucleus is critical for plant development and survival. Although WHIRLY2 (WHY2) is involved in mitochondrial genome repair and affects the DNA copy number of the mitochondrial genome, the detailed mechanism of action of the WHY2 protein is still elusive. In this study, we found that WHY2 was triple-localized among the mitochondria, plastids, and the nucleus during Arabidopsis (Arabidopsis thaliana) aging. Overexpressing WHY2 increased starch granule numbers in chloroplasts of pericarp cells, showing a partially dry, yellowing silique and early senescence leaves. Accordingly, WHY2 protein could directly activate the expression of jasmonic acid carboxyl methyltransferase and senescence associated gene 29 (SWEET15) gene expression and repress SWEET11 gene expression in the nucleus, leading to alteration of starch accumulation and transport in pericarp cells. In contrast, loss of WHY2 decreased starch and sugar content in pericarp cells but promoted starch accumulation in leaves and seeds. These phenotypes of WHY2-overexpressing plants were enhanced in response to methyl jasmonate. Our results suggest that WHY2 in plastids, mitochondria, and the nucleus plays a vital role in alteration of carbon reallocation from maternal tissue to filial tissue.

MORF9 Functions in Plastid RNA Editing with Tissue Specificity.

RNA editing in plant mitochondria and plastids converts specific nucleotides from cytidine (C) to uridine (U). These editing events differ among plant species and are relevant to developmental stages or are impacted by environmental conditions. Proteins of the MORF family are essential components of plant editosomes. One of the members, MORF9, is considered the core protein of the editing complex and is involved in the editing of most sites in chloroplasts. In this study, the phenotypes of a T-DNA insertion line with loss of MORF9 and of the genetic complementation line of Arabidopsis were analyzed, and the editing efficiencies of plastid RNAs in roots, rosette leaves, and flowers from the morf9 mutant and the wild-type (WT) control were compared by bulk-cDNA sequencing. The results showed that most of the known MORF9-associated plastid RNA editing events in rosette leaves and flowers were similarly reduced by morf9 mutation, with the exception that the editing rate of the sites ndhB-872 and psbF-65 declined in the leaves and that of ndhB-586 decreased only in the flowers. In the roots, however, the loss of MORF9 had a much lower effect on overall plastid RNA editing, with nine sites showing no significant editing efficiency change, including accD-794, ndhD-383, psbZ-50, ndhF-290, ndhD-878, matK-706, clpP1-559, rpoA-200, and ndhD-674, which were reduced in the other tissues. Furthermore, we found that during plant aging, MORF9 mRNA level, but not the protein level, was downregulated in senescent leaves. On the basis of these observations, we suggest that MORF9-mediated RNA editing is tissue-dependent and the resultant organelle proteomes are pertinent to the specific tissue functions.