Aging induces gradual yet massive cell death in higher organisms, including annual plants. Even so, the underlying regulatory mechanisms are barely known, despite the long-standing interest in this topic. Here, we demonstrate that ORE1, which is a NAC (NAM, ATAF, and CUC) transcription factor, positively regulates aging-induced cell death in Arabidopsis leaves. ORE1 expression is up-regulated concurrently with leaf aging by EIN2 but is negatively regulated by miR164. miR164 expression gradually decreases with aging through negative regulation by EIN2, which leads to the elaborate up-regulation of ORE1 expression. However, EIN2 still contributes to aging-induced cell death in the absence of ORE1. The trifurcate feed-forward pathway involving ORE1, miR164, and EIN2 provides a highly robust regulation to ensure that aging induces cell death in Arabidopsis leaves.

Plant leaves, harvesting light energy and fixing CO 2 , are a major source of foods on the earth. Leaves undergo developmental and physiological shifts during their lifespan, ending with senescence and death. We characterized the key regulatory features of the leaf transcriptome during aging by analyzing total-and small-RNA transcriptomes throughout the lifespan of Arabidopsis (Arabidopsis thaliana) leaves at multidimensions, including age, RNA-type, and organelle. Intriguingly, senescing leaves showed more coordinated temporal changes in transcriptomes than growing leaves, with sophisticated regulatory networks comprising transcription factors and diverse small regulatory RNAs. The chloroplast transcriptome, but not the mitochondrial transcriptome, showed major changes during leaf aging, with a strongly shared expression pattern of nuclear transcripts encoding chloroplast-targeted proteins. Thus, unlike animal aging, leaf senescence proceeds with tight temporal and distinct interorganellar coordination of various transcriptomes that would be critical for the highly regulated degeneration and nutrient recycling contributing to plant fitness and productivity.Most organisms undergo age-dependent developmental changes during their lifespans. The timely decision of developmental changes during the lifespan is a critical evolutionary characteristic that maximizes fitness in a given ecological setting (Leopold, 1961;Fenner, 1998;Samach and Coupland, 2000). Plants use unique developmental strategies throughout their lifespans as opposed to animals. In plants, most organs are formed postnatally from sets of stem cells in the seed. In addition, plants are sessile and cope with encountering environments physiologically, rather than behaviorally. Thus, they have developed highly plastic and interactive developmental programs to incorporate environmental changes into their developmental decisions (Pigliucci, 1998;Sultan, 2000).The leaf is an organ that characterizes the fundamental aspects of plants. Leaves harvest light energy, fix CO 2 to produce carbohydrates, and, as primary producers in our ecosystem, serve as a major food source on the earth. Leaves undergo a series of developmental and physiological shifts during their lifespans. A leaf is initially formed as a leaf primordium derived from the stem cells at the shoot apical meristem and develops into a photosynthetic organ through biogenesis processes involving cell division, differentiation, and expansion (Tsukaya, 2013). In the later stages of their lifespans, leaves undergo organ-level senescence and eventually death. Organlevel senescence in plants involves postmitotic senescence and is a term used similarly as "aging" in animals. During the senescence stage, leaf cells undergo dramatic shifts in physiology from biogenesis to the sequential 1 This research was supported by the Institute for Basic Science (IBS-R013-D1 and IBS-R013-G1), the DGIST R&D Program (2014010043, 2015010004, 2015010011, 20150100012, and 15-01-HRLA-01), Basic Science Research Program (2010-0...

Sensory adaptation is an essential part of biological neural systems for sustaining human life. Using the light-induced halide phase segregation of CsPb­(Br1–x I x )3 perovskite, we introduce neuromorphic phototransistors that emulate human sensory adaptation. The phototransistor based on a hybrid structure of perovskite and transition-metal dichalcogenide (TMD) emulates the sensory adaptation in response to a continuous light stimulus, similar to the neural system. The underlying mechanism for the sensory adaptation is the halide segregation of the mixed halide perovskites. The phase separation under visible-light illumination leads to the segregation of I and Br into separate iodide- and bromide-rich domains, significantly changing the photocurrent in the phototransistors. The devices are reversible upon the removal of the light stimulation, resulting in near-complete recovery of the photosensitivity before the phase segregation (sensitivity recovery of 96.65% for 5 min rest time). The proposed phototransistor based on the perovskite–TMD hybrid structure can be applied to other neuromorphic devices such as neuromorphic photonic devices, intelligent sensors, and selective light-detecting image sensors.

We report highly efficient ethyl cellulose with CsPbBr perovskite QD films for white light generation in LED application. Ethyl cellulose with CsPbBr quantum dots is applied with SrSiN : Eu red phosphor on an InGaN blue chip, achieving a highly efficient luminous efficacy of 67.93 lm W under 20 mA current.

Background and PurposeSeveral imaging-based indices were constructed quantitatively using the emphysema index (EI) and fibrosis score (FS) on high-resolution computed tomography (HRCT). We evaluated the ability of these indices to predict mortality compared to physiologic results. Additionally, prognostic predictive factors were compared among subgroups with biopsy-proven fibrotic idiopathic interstitial pneumonia (IIP) (biopsy-proven CPFE) and in a separate cohort with subclinical CPFE.Materials and MethodsThree chest radiologists independently determined FS. EI was automatically quantified. PFTs, smoking history, and composite physiologic index (CPI) were reviewed. Predictors of time to death were determined based on clinico-physiologic factors and CT-based CPFE indices.ResultsThe prevalence of biopsy-proven CPFE was 26% (66/254), with an EI of 9.1±7.1 and a FS of 19.3±14.2. In patients with CPFE, median survival and 5-year survival rates were 6.0 years and 34.8%, respectively, whereas those in fibrotic IIP without emphysema were 10.0 years and 60.9% (p = 0.013). However, the extent of fibrosis did not differ significantly between the two cohorts. In subclinical CPFE, prevalence was 0.04% (93/20,372), EI was 11.3±10.4, and FS was 9.1±7.1. FVC and a fibrosis-weighted CT index were independent predictors of survival in the biopsy-proven CPFE cohort, whereas only the fibrosis-weighted CT index was a significant prognostic factor in the subclinical CPFE cohort.ConclusionsRecognition and stratification using CT quantification can be utilized as a prognostic predictor. Prognostic factors vary according to fibrosis severity and among cohorts of patients with biopsy-proven and subclinical CPFE.

Biocontrol offers a promising alternative to synthetic fungicides for the control of a variety of pre- and post-harvest diseases of crops. Black rot, which is caused by the pathogenic fungus Ceratocytis fimbriata, is the most destructive post-harvest disease of sweet potato, but little is currently known about potential biocontrol agents for this fungus. Here, we isolated several microorganisms from the tuberous roots and shoots of field-grown sweet potato plants, and analyzed their ribosomal RNA gene sequences. The microorganisms belonging to the genus Pantoea made up a major portion of the microbes residing within the sweet potato plants, and fluorescence microscopy showed these microbes colonized the intercellular spaces of the vascular tissue in the sweet potato stems. Four P. dispersa strains strongly inhibited C. fimbriata mycelium growth and spore germination, and altered the morphology of the fungal hyphae. The detection of dead C. fimbriata cells using Evans blue staining suggested that these P. dispersa strains have fungicidal rather than fungistatic activity. Furthermore, P. dispersa strains significantly inhibited C. fimbriata growth on the leaves and tuberous roots of a susceptible sweet potato cultivar (“Yulmi”). These findings suggest that P. dispersa strains could inhibit black rot in sweet potato plants, highlighting their potential as biocontrol agents.

Reactive oxygen species (ROS) are inevitable by-products of aerobic metabolic processes, causing non-specific oxidative damage and also acting as second messengers. Superoxide is a short-lived ROS that functions in various cellular responses, including aging and cell death. However, it is unclear as to how superoxide brings about age-dependent cell death and senescence. Here, we show that the accumulation and signaling of superoxide are mediated by three Arabidopsis proteins-RPK1, CaM4, and RbohF-which trigger subsequent cellular events leading to age-dependent cell death. We demonstrate that the NADPH oxidase RbohF is responsible for RPK1-mediated transient accumulation of superoxide, SIRK kinase induction, and cell death, all of which are positively regulated by CaM4. RPK1 physically interacts with and phosphorylates CaM4, which, in turn, interacts with RbohF. Overall, we demonstrate how the protein trio governs the superoxide accumulation and signaling at the cell surface to control senescence and cell death.

These authors contributed equally to this work. SUMMARYThe plant-specific transcription factor (TF) NAC103 was previously reported to modulate the unfolded protein response in Arabidopsis under endoplasmic reticulum (ER) stress. Alternatively, we report here that NAC103 is involved in downstream signaling of SOG1, a master regulator for expression of DNA damage response (DDR) genes induced by genotoxic stress. Arabidopsis NAC103 expression was strongly induced by genotoxic stress and nac103 mutants displayed substantial inhibition of DDR gene expression after gamma radiation or radiomimetic zeocin treatment. DDR phenotypes, such as true leaf inhibition, root cell death and root growth inhibition, were also suppressed significantly in the nac103 mutants, but to a lesser extent than in the sog1-1 mutant. By contrast, overexpression of NAC103 increased DDR gene expression without genotoxic stress and substantially rescued the phenotypic changes in the sog1-1 mutant after zeocin treatment. The putative promoters of some representative DDR genes, RAD51, PARP1, RPA1E, BRCA1 and At4g22960, were found to partly interact with NAC103. Together with the expected interaction of SOG1 with the promoter of NAC103, our study suggests that NAC103 is a putative SOG1-dependent transcriptional regulator of plant DDR genes, which are responsible for DDR phenotypes under genotoxic stress.