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Chronic kidney disease (CKD) is associated with accelerated atherosclerosis progression and high incidence of cardiovascular events, hinting that atherosclerotic plaques in CKD may be vulnerable. However, its cause and mechanism remain obscure. Here, it is shown that apolipoprotein E‐deficient (ApoE−/−) mouse with CKD (CKD/ApoE−/− mouse) is a useful model for investigating the pathogenesis of plaque vulnerability, and premature senescence and phenotypic switching of vascular smooth muscle cells (VSMCs) contributes to CKD‐associated plaque vulnerability. Subsequently, VSMC phenotypes in patients with CKD and CKD/ApoE−/− mice are comprehensively investigated. Using multi‐omics analysis and targeted and VSMC‐specific gene knockout mice, VSMCs are identified as both type‐I‐interferon (IFN‐I)‐responsive and IFN‐I‐productive cells. Mechanistically, mitochondrial damage resulting from CKD‐induced oxidative stress primes the cyclic GMP‐AMP synthase‐stimulator of interferon genes (cGAS‐STING) pathway to trigger IFN‐I response in VSMCs. Enhanced IFN‐I response then induces VSMC premature senescence and phenotypic switching in an autocrine/paracrine manner, resulting in the loss of fibrous cap VSMCs and fibrous cap thinning. Conversely, blocking IFN‐I response remarkably attenuates CKD‐associated plaque vulnerability. These findings reveal that IFN‐I response in VSMCs through immune sensing of mitochondrial damage is essential for the pathogenesis of CKD‐associated plaque vulnerability. Mitigating IFN‐I response may hold promise for the treatment of CKD‐associated cardiovascular diseases. [ABSTRACT FROM AUTHOR]

Summary: Marker‐based prediction holds great promise for improving current plant and animal breeding efficiencies. However, the predictabilities of complex traits are always severely affected by negative factors, including distant relatedness, environmental discrepancies, unknown population structures, and indeterminate numbers of predictive variables. In this study, we utilised two independent F1 hybrid populations in the years 2012 and 2015 to predict rice thousand grain weight (TGW) using parental untargeted metabolite profiles with a partial least squares regression method. A stable predictive model for TGW was built based on hybrids from the population in 2012 (r = 0.75) but failed to properly predict TGW for hybrids from the population in 2015 (r = 0.27). After integrating hybrids from both populations into the training set, the TGW of hybrids could be predicted but was largely dependent on population structures. Then, core hybrids from each population were determined by principal component analysis and the TGW of hybrids in both environments were successfully predicted (r > 0.60). Moreover, adjusting the population structures and numbers of predictive analytes increased TGW predictability for hybrids in 2015 (r = 0.72). Our study demonstrates that the TGW of F1 hybrids across environments can be accurately predicted based on parental untargeted metabolite profiles with a core hybridisation strategy in rice. Metabolic biomarkers identified from early developmental stage tissues, which are grown under experimental conditions, may represent a workable approach towards the robust prediction of major agronomic traits for climate‐adaptive varieties. [ABSTRACT FROM AUTHOR]

Summary: The pentatricopeptide repeat (PPR) protein family is a large family characterized by tandem arrays of a degenerate 35‐amino‐acid motif whose members function as important regulators of organelle gene expression at the post‐transcriptional level. Despite the roles of PPRs in RNA editing in organelles, their editing activities and the underlying mechanism remain obscure.Here, we show that a novel DYW motif‐containing PPR protein, PPS1, is associated with five conserved RNA‐editing sites of nad3 located in close proximity to each other in mitochondria, all of which involve conversion from proline to leucine in rice. Both pps1 RNAi and heterozygous plants are characterized by delayed development and partial pollen sterility at vegetative stages and reproductive stage.RNA electrophoresis mobility shift assays (REMSAs) and reciprocal competition assays using different versions of nad3 probes confirm that PPS1 can bind to cis‐elements near the five affected sites, which is distinct from the existing mode of PPR‐RNA binding because of the continuity of the editing sites. Loss of editing at nad3 in pps1 reduces the activity of several complexes in the mitochondrial electron transport chain and affects mitochondrial morphology.Taken together, our results indicate that PPS1 is required for specific editing sites in nad3 in rice. [ABSTRACT FROM AUTHOR]

The drought-induced 19 protein family consists of several atypical Cys2/His2-type zinc finger proteins in plants and plays an important role in abiotic stress. In this study, we found that overexpressing OsDi19-4 in rice altered the expression of a series of abscisic acid (ABA)-responsive genes, resulting in strong ABA-hypersensitive phenotypes including ABA-induced seed germination inhibition, early seedling growth inhibition and stomatal closure. On the contrary, OsDi19-4 knockdown lines were less sensitive to ABA. Additionally, OsCDPK14 was identified to interact with OsDi19-4 and be responsible for the phosphorylation of OsDi19-4, and the phosphorylation of OsDi19-4 was further enhanced after the treatment of ABA. Apart from these, OsDi19-4 was shown to directly bind to the promoters of OsASPG1 and OsNAC18 genes, two ABA-responsive genes, and regulate their expression. Transient expression assays confirmed the direct regulation role of OsDi19-4, and the regulation was further enhanced by the increased phosphorylation of OsDi19-4 after the treatment of ABA. Taken together, these data demonstrate that OsDi19-4 acts downstream of OsCDPK14 to positively regulate ABA response by modulating the expression of ABA-responsive genes in rice. [ABSTRACT FROM AUTHOR]

Cytoplasmic male sterility ( CMS) and restoration of fertility ( Rf) are widely distributed in plant species utilized by humans. RF5 and GRP162 are subunits of the restoration of fertility complex ( RFC) in Hong-Lian rice. Despite the fact that the RFC is 400-500 kDa in size, the other proteins or factors in the complex still remain unknown. Here, we identified RFC subunit 3, which encodes a DUF1620-containing and WD40-like repeat protein ( RFC3) that is present in all tissues but highly expressed in leaves., We established that RFC3 interacts with both RF5 and GRP162 in vitro and in vivo, and is transported into the mitochondria as a membrane protein. Furthermore, CMS RNA ( atp6-orfH79) and CMS cytotoxic protein ( ORFH79) accumulate when RFC3 is silenced in restorer lines., We presented the analysis with blue-native polyacrylamide gel electrophoresis, indicating that RFC is disrupted in the RNAi line. We concluded that RCF3 is indispensable as a scaffold protein for the assembly of the RFC complex., We unveil a new molecular player of the RFC in the Rf pathway in rice and propose the model of RFC based on these data. [ABSTRACT FROM AUTHOR]

Katanin, a microtubule-severing enzyme, consists of two subunits: the catalytic subunit P60, and the regulatory subunit P80. In several species, P80 functions in meiotic spindle organization, the flagella biogenesis, the neuronal development, and the male gamete production. However, the P80 function in higher plants remains elusive. In this study, we found that there are three katanin P80 orthologs ( OsKTN80a, OsKTN80b, and OsKTN80c) in Oryza sativa L. Overexpression of OsKTN80a caused the retarded root growth of rice seedlings. Further investigation indicates that the retained root growth was caused by the repressed cell elongation in the elongation zone and the stalled cytokinesis in the division zone in the root tip. The in vivo examination suggests that OsKTN80a acts as a microtubule stabilizer. We prove that OsKTN80a, possibly associated with OsKTN60, is involved in root growth via regulating the cell elongation and division. [ABSTRACT FROM AUTHOR]

The restoration fertility complex ( RFC) was previously identified in Honglian ( HL)-cytoplasmic male sterility ( CMS) rice ( Oryza sativa), and glycine-rich protein 162 ( GRP162) is responsible for binding to the CMS-associated transcript atp6-orfH79., Here, we engineered a recombinant GRP162 containing the mitochondrial transit peptide, termed Mt- GRP162, as an artificial restorer of fertility ( Rf) gene. Mt- GRP162 was confirmed to bind to CMS-associated RNA and to localize to the mitochondria. The transgenic plants showed restored fertility with partially functional pollen., We found that the expression of ORFH79 decreased in transgenic plants, while the expression of atp6-orfH79 was not changed. These findings indicate that Mt- GRP162 restores fertility by suppressing the expression of the cytotoxic protein ORFH79 at the post-transcriptional level rather than via the cleavage of atp6-orfH79 in the presence of RFC., These findings contribute to our understanding of the mechanisms of restoration through diverse pathways. [ABSTRACT FROM AUTHOR]

Cytoplasmic male sterility ( CMS) has attracted great interest because of its application in crop breeding. Despite increasing knowledge of CMS, not much is understood about its molecular mechanisms. Previously, orf H79 was cloned and identified as the CMS gene in Honglian rice, but how the ORFH79 protein causes pollen abortion is still unknown., Through bacterial two-hybrid library screening, P61, a subunit of the mitochondrial electron transport chain ( ETC) complex III, was selected as a candidate that interacts with ORFH79. Bimolecular fluorescence complementation ( Bi FC) and coimmunoprecipitation (co IP) assays verified their interaction inside mitochondria. Blue native polyacrylamide gel electrophoresis ( BN- PAGE) and western blotting showed ORF79 and P61 colocalized in mitochondrial ETC complex III of CMS lines., Compared with the maintainer line, Yuetai B ( YB), a significant decrease of enzyme activity was detected in mitochondrial complex III of the CMS line, Yuetai A ( YA), which resulted in decreased ATP concentrations and an increase in the reactive oxygen species ( ROS) content., We propose that the CMS protein, ORFH79, can bind to complex III and decrease its enzyme activity through interaction with P61. This defect results in energy production dysfunction and oxidative stress in mitochondria, which may work as retrograde signals that lead to abnormal pollen development. [ABSTRACT FROM AUTHOR]

Summary: • Post-pollination competition is reported here in cultivated rice (Oryza sativa ) and a perennial wild rice (O. rufipogon ) to investigate the occurrence of crop-to-wild gene flow. • Wild and cultivated rice (variety Minghui-63) were grown in a common garden in Hunan province, China, and crop-specific genetic markers were used to detect hybridization following hand-pollinations. Using 11 sequential pollination treatments, the effects of the relative timing of pollination on the success of foreign pollen was investigated. • Foreign pollen from the crop resulted in lower pollen germination, fewer pollen tubes per style, and a significant reduction of seed set, demonstrating a disadvantage of foreign pollen even in the absence of pollen competition. When 1: 1 pollen mixtures were applied, only 2% of the resulting seeds were hybrids, revealing a much stronger disadvantage of foreign pollen when competing with conspecific pollen. Testing the effects of the relative timing of pollination on the success of foreign pollen suggested that conspecific pollen is often more successful than foreign pollen. Nonetheless, hybridization is possible following the deposition of pollen mixtures, especially when foreign pollen arrives earlier than conspecific pollen. • Pollen competition between wild and cultivated rice could slow the rate of crop-to-wild gene flow, but even if pollen competition was ubiquitous it would not prevent gene flow from the crop. [ABSTRACT FROM AUTHOR]

Like the old Chinese saying that a solid dyke can collapse because of the presence of an ant hole, the "ants" uremic toxins make the "solid" fibrous cap of atherosclerotic plaques susceptible to collapse via innate immune activation in vascular smooth muscle cells, as described by Ke Yang, Jinghong Zhao, and co-workers in article number 2002738. Chronic Kidney Disease: Mitochondrial Damage-Induced Innate Immune Activation in Vascular Smooth Muscle Cells Promotes Chronic Kidney Disease-Associated Plaque Vulnerability (Adv. Sci. 5/2021). [Extracted from the article]