In higher plants, many mitochondrial genes contain group II-type introns that are removed from RNAs by splicing to produce mature transcripts that are then translated into functional proteins. However, the factors involved in the splicing of mitochondrial introns and their biological functions are not well understood in maize. Here, we isolated an empty pericarp 10 (emp10) mutant and identified the underlying gene by map-based cloning. Emp10 encodes a P-type mitochondria-targeted pentatricopeptide repeat (PPR) protein with 10 PPR motifs. Loss of Emp10 function results in splicing defect of the first intron of nad2, a gene encoding subunit 2 of NADH dehydrogenase (also called complex I). The emp10 mutant has undetectable activity of complex I and has arrested development of embryo and endosperm, and thus defective seeds with empty pericarp. Additionally, the basal endosperm transfer layer cells were severely affected, indicating the deficiency of cell wall ingrowths in the emp10 kernels. Moreover, the alternative respiratory pathway involving alternative oxidase was significantly induced in the emp10 mutant. These results suggest that EMP10 is specifically required for the cis-splicing of mitochondrial nad2 intron 1, embryogenesis and endosperm development in maize.

A new pentatricopeptide repeat (PPR) gene in maize differs from previously reported genes, as it is required for splicing of all four introns of nad1.

SummaryGroup VII ethylene response factors (ERFVIIs) play important roles in ethylene signalling and plant responses to flooding. However, natural ERFVII variations in maize (ZmERFVIIs) that are directly associated with waterlogging tolerance have not been reported. Here, a candidate gene association analysis of the ZmERFVII gene family showed that a waterlogging‐responsive gene, ZmEREB180, was tightly associated with waterlogging tolerance. ZmEREB180 expression specifically responded to waterlogging and was up‐regulated by ethylene; in addition, its gene product localized to the nucleus. Variations in the 5ʹ‐untranslated region (5ʹ‐UTR) and mRNA abundance of this gene under waterlogging conditions were significantly associated with survival rate (SR). Ectopic expression of ZmEREB180 in Arabidopsis increased the SR after submergence stress, and overexpression of ZmEREB180 in maize also enhanced the SR after long‐term waterlogging stress, apparently through enhanced formation of adventitious roots (ARs) and regulation of antioxidant levels. Transcriptomic assays of the transgenic maize line under normal and waterlogged conditions further provided evidence that ZmEREB180 regulated AR development and reactive oxygen species homeostasis. Our study provides direct evidence that a ZmERFVII gene is involved in waterlogging tolerance. These findings could be applied directly to breed waterlogging‐tolerant maize cultivars and improve our understanding of waterlogging stress.

Plant mitochondrial transcription termination factor (mTERF) genes comprise a large family with important roles in regulating organelle gene expression. In this study, a comprehensive database search yielded 31 potential mTERF genes in maize (Zea mays L.) and most of them were targeted to mitochondria or chloroplasts. Maize mTERF were divided into nine main groups based on phylogenetic analysis, and group IX represented the mitochondria and species-specific clade that diverged from other groups. Tandem and segmental duplication both contributed to the expansion of the mTERF gene family in the maize genome. Comprehensive expression analysis of these genes, using microarray data and RNA-seq data, revealed that these genes exhibit a variety of expression patterns. Environmental stimulus experiments revealed differential up or down-regulation expression of maize mTERF genes in seedlings exposed to light/dark, salts and plant hormones, respectively, suggesting various important roles of maize mTERF genes in light acclimation and stress-related responses. These results will be useful for elucidating the roles of mTERF genes in the growth, development and stress response of maize.

The expression systems of the mitochondrial genes are derived from their bacterial ancestors, but have evolved many new features in their eukaryotic hosts. Mitochondrial RNA splicing is a complex process regulated by families of nucleus-encoded RNA-binding proteins, few of which have been characterized in maize ( Zea mays L.). Here, we identified the Zea mays small kernel 3 ( Zmsmk3 ) candidate gene, which encodes a mitochondrial transcription termination factor (mTERF) containing two mTERF motifs, which is conserved in monocotyledon; and the target introns were also quite conserved during evolution between monocotyledons and dicotyledons. The mutations of Zmsmk3 led to arrested embryo and endosperm development, resulting in small kernels. A transcriptome of 12 days after pollination endosperm analysis revealed that the starch biosynthetic pathway and the zein gene family were down-regulated in the Zmsmk3 mutant kernels. ZmSMK3 is localized in mitochondria. The reduced expression of ZmSmk3 in the mutant resulted in the splicing deficiency of mitochondrial nad4 intron1 and nad1 intron4, causing a reduction in complex I assembly and activity, impairing mitochondria structure and activating the alternative respiratory pathway. So, the results suggest that ZmSMK3 is required for the splicing of nad4 intron 1 and nad1 intron 4, complex I assembly and kernel development in maize.

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Activation of PAR2 inhibits the expression of IL-10 in B cells, which can be reversed by treating B cells with Bcl2L12 shRNA-carrying liposomes. The data suggest that regulation of Bcl2L12 may be a novel approach in the treatment for AR.

Aberrant PDGF-PDGFR signaling and its effects on downstream effectors have been implicated in glioma development. A crucial AKT regulator, ACK1 (TNK2) has been shown to be a downstream mediator of PDGF signaling; however, the exact underlying mechanisms in gliomas remain elusive. Here, we report that in glioma cells, PDGFR-b activation enhanced the interaction between ACK1 and AKT, resulting in AKT activation. PDGF treatment consistently promoted the formation of complexes containing PDGFR-b and ACK1. Mutational analysis suggested that Y635 of ACK1 is a PDGFR-b phosphorylation site and that the ACK1 Y635F mutant abrogated the sequential activation of AKT. Moreover, PDK1 interacted with ACK1 during PDGF stimulation, which is required for the binding of ACK1 to PDGFR-b. Further mutational analysis showed that T325 of ACK1 was crucial for the ACK1 and PDK1 interaction. ACK1 Y635F or T325A mutants abolished PDGFR-b-induced AKT activation, the subsequent nuclear translocation of bcatenin and the expression of cyclin D1. Glioma cell cycle progression, proliferation and tumorigenesis were accordingly blocked by ACK1 Y635F or T325A. In glioblastoma multiforme samples from 51 patients, increased ACK1 tyrosine phosphorylation correlated with upregulated PDGFR-b activity and AKT activation. Taken together, our data demonstrate that ACK1 plays a pivotal role in PDGF-PDGFR-induced AKT signaling in glioma tumorigenesis. This knowledge contributes to our understanding of glioma progression and may facilitate the identification of novel therapeutic targets for future glioma treatment.