A single alteration 20 nt 5' to an editing target inhibits chloroplast RNA editing in vivo

ABSTRACT RNA editing in higher-plant chloroplasts involves C-to-U conversions at specific sites. Although in vivo analyses have been performed, little is known about the biochemical aspects of chloroplast editing reactions. Here we improved our original in vitro system and devised a procedure for preparing active chloroplast extracts not only from tobacco plants but also from pea plants. Using our tobacco in vitro system, cis-acting elements were defined for psbE and petB mRNAs. Distinct proteins were found to bind specifically to each cis-element, a 56-kDa protein to the psbE site and a 70-kDa species to the petB site. Pea chloroplasts lack the corresponding editing site in psbE since T is already present in the DNA. Parallel in vitro analyses with tobacco and pea extracts revealed that the pea plant has no editing activity for psbE mRNAs and lacks the 56-kDa protein, whereas petB mRNAs are edited and the 70-kDa protein is also present. Therefore, coevolution of an editing site and its cognate trans-factor was demonstrated biochemically in psbE mRNA editing between tobacco and pea plants.

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MORF2 tightly associates with MORF9 to regulate chloroplast RNA editing in Arabidopsis

Plant Science ◽

10.1016/j.plantsci.2018.10.020 ◽

2019 ◽

Vol 278 ◽

pp. 64-69 ◽

Cited By ~ 5

Author(s):

Chao Huang ◽

Zi-Ran Li ◽

Qing-Bo Yu ◽

Lin-Shan Ye ◽

Yong-Lan Cui ◽

...

Keyword(s):

Rna Editing ◽

Chloroplast Rna

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Genome-Wide Analysis of Multiple Organellar RNA Editing Factor (MORF) Family in Kiwifruit (Actinidia chinensis) Reveals Its Roles in Chloroplast RNA Editing and Pathogens Stress

Plants ◽

10.3390/plants11020146 ◽

2022 ◽

Vol 11 (2) ◽

pp. 146

Author(s):

Yuhong Xiong ◽

Jing Fang ◽

Xiaohan Jiang ◽

Tengfei Wang ◽

Kangchen Liu ◽

...

Keyword(s):

Rna Editing ◽

Chloroplast Development ◽

Structural Features ◽

Resistance Mechanisms ◽

Actinidia Chinensis ◽

Rna Seq ◽

Good Taste ◽

Genome Wide ◽

Solid Foundation ◽

Chloroplast Rna

Kiwifruit (Actinidia chinensis) is well known for its high vitamin C content and good taste. Various diseases, especially bacterial canker, are a serious threat to the yield of kiwifruit. Multiple organellar RNA editing factor (MORF) genes are pivotal factors in the RNA editosome that mediates Cytosine-to-Uracil RNA editing, and they are also indispensable for the regulation of chloroplast development, plant growth, and response to stresses. Although the kiwifruit genome has been released, little is known about MORF genes in kiwifruit at the genome-wide level, especially those involved in the response to pathogens stress. In this study, we identified ten MORF genes in the kiwifruit genome. The genomic structures and chromosomal locations analysis indicated that all the MORF genes consisted of three conserved motifs, and they were distributed widely across the seven linkage groups and one contig of the kiwifruit genome. Based on the structural features of MORF proteins and the topology of the phylogenetic tree, the kiwifruit MORF gene family members were classified into six groups (Groups A–F). A synteny analysis indicated that two pairs of MORF genes were tandemly duplicated and five pairs of MORF genes were segmentally duplicated. Moreover, based on analysis of RNA-seq data from five tissues of kiwifruit, we found that both expressions of MORF genes and chloroplast RNA editing exhibited tissue-specific patterns. MORF2 and MORF9 were highly expressed in leaf and shoot, and may be responsible for chloroplast RNA editing, especially the ndhB genes. We also observed different MORF expression and chloroplast RNA editing profiles between resistant and susceptible kiwifruits after pathogen infection, indicating the roles of MORF genes in stress response by modulating the editing extend of mRNA. These results provide a solid foundation for further analyses of the functions and molecular evolution of MORF genes, in particular, for clarifying the resistance mechanisms in kiwifruits and breeding new cultivars with high resistance.

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Wilms' Tumor Suppressor GeneWT1

Journal of the American Society of Nephrology ◽

10.1681/asn.v11suppl_2s106 ◽

2000 ◽

Vol 11 (suppl 2) ◽

pp. S106-S115 ◽

Cited By ~ 3

Author(s):

CHRISTIAN MROWKA ◽

ANDREAS SCHEDL

Keyword(s):

Tumor Suppressor ◽

Rna Editing ◽

Kidney Development ◽

Wilms Tumor ◽

Suppressor Gene ◽

Structural Features ◽

Genomic Locus ◽

Developmental Abnormalities ◽

Complex Process

Abstract.Normal development of the kidney is a highly complex process that requires precise orchestration of proliferation, differentiation, and apoptosis. In the past few years, a number of genes that regulate these processes, and hence play pivotal roles in kidney development, have been identified. The Wilms' tumor suppressor geneWT1has been shown to be one of these essential regulators of kidney development, and mutations in this gene result in the formation of tumors and developmental abnormalities such as the Denys-Drash and Frasier syndromes. A fascinating aspect of theWT1gene is the multitude of isoforms produced from its genomic locus. In this review, our current understanding of the structural features ofWT1, how they modulate the transcriptional and post-transcriptional activities of the protein, and how mutations affecting individual isoforms can lead to diseased kidneys is summarized. In addition, results from transgenic experiments, which have yielded important findings regarding the function of WT1in vivo, are discussed. Finally, data on the unusual feature of RNA editing ofWT1transcripts are presented, and the relevance of RNA editing for the normal functioning of the WT1 protein in the kidney is discussed.

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