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...

The endogenous circadian clock regulates many physiological processes related to plant survival and adaptability. GIGANTEA (GI), a clock-associated protein, contributes to the maintenance of circadian period length and amplitude, and also regulates flowering time and hypocotyl growth in response to day length. Similarly, EARLY FLOWERING 4 (ELF4), another clock regulator, also contributes to these processes. However, little is known about either the genetic or molecular interactions between GI and ELF4 in Arabidopsis. In this study, we investigated the genetic interactions between GI and ELF4 in the regulation of circadian clock-controlled outputs. Our mutant analysis shows that GI is epistatic to ELF4 in flowering time determination, while ELF4 is epistatic to GI in hypocotyl growth regulation. Moreover, GI and ELF4 have a synergistic or additive effect on endogenous clock regulation. Gene expression profiling of gi, elf4, and gi elf4 mutants further established that GI and ELF4 have differentially dominant influences on circadian physiological outputs at dusk and dawn, respectively. This phasing of GI and ELF4 influences provides a potential means to achieve diversity in the regulation of circadian physiological outputs, including flowering time and hypocotyl growth.

PurposeThe purpose of this paper is to explore the notion of “Third Place” in an arts context by exploring the consumption of two arts venues, Tate Modern and the Southbank Centre (SBC) on the regenerated South Bank in London, UK.Design/methodology/approachAn interpretative phenomenological approach was taken drawing on 45 qualitative interviews that were conducted in and around Tate Modern and the SBC during Autumn 2009.FindingsFour audience groups were identified segmented by their motivations, experiences and feelings about the two buildings. The first group “Place to see” visit Tate Modern and the SBC to attend exhibitions and performances. The second meet friends and spend time in the cafes and bars using them as a “Place to hang‐out and meet”. The third group use the buildings as a “Place to drop‐in” on their way to somewhere else. The fourth group use the SBC as a “Third Place”, to study, for meetings, to read, escape and rejuvenate.Research limitations/implicationsThis was an exploratory paper. Further research is required to test the findings in other art museums, arts venues, libraries, parks and other public and private spaces within communities.Originality/valueThe paper fills a gap by drawing on the “Third Place” literature to explore the consumption of art museums and venues. It provides us with a better understanding of the meanings these public buildings have to individuals, the way they are used by the public and how arts managers might attract new audiences from their communities. It also provides insights for planners and town centre managers as to the types of places individuals are seeking during their daily lives.

The homeostatic maintenance of the genomic DNA is crucial for regulating aging processes. However, the role of RNA homeostasis in aging processes remains unknown. RNA helicases are a large family of enzymes that regulate the biogenesis and homeostasis of RNA. However, the functional significance of RNA helicases in aging has not been explored. Here, we report that a large fraction of RNA helicases regulate the lifespan of Caenorhabditis elegans. In particular, we show that a DEAD-box RNA helicase, helicase 1 (HEL-1), promotes longevity by specifically activating the DAF-16/forkhead box O (FOXO) transcription factor signaling pathway. We find that HEL-1 is required for the longevity conferred by reduced insulin/insulin-like growth factor 1 (IGF-1) signaling (IIS) and is sufficient for extending lifespan. We further show that the expression of HEL-1 in the intestine and neurons contributes to longevity. HEL-1 enhances the induction of a large fraction of DAF-16 target genes. Thus, the RNA helicase HEL-1 appears to promote longevity in response to decreased IIS as a transcription coregulator of DAF-16. Because HEL-1 and IIS are evolutionarily well conserved, a similar mechanism for longevity regulation via an RNA helicase-dependent regulation of FOXO signaling may operate in mammals, including humans.arious genetic and environmental factors, including insulin/ insulin-like growth factor 1 (IGF-1) signaling (IIS), target of rapamycin signaling, dietary restriction, mitochondrial respiration, and reproductive systems, influence aging across phyla (reviewed in refs. 1-3). IIS is one of the most evolutionarily conserved pathways involved in the regulation of aging. Mutations in Caenorhabditis elegans daf-2, which encodes an insulin/IGF-1 receptor homolog, double the lifespan of C. elegans (4). Inhibition of DAF-2 reduces phosphatidylinositide 3 (PI3)-kinase signaling, which upregulates several transcription factors, including DAF-16/forkhead box O (FOXO), heat shock factor-1 (HSF-1), and SKN-1/NRF2 (reviewed in refs. 1, 3, and 5). DAF-16 is one of the best characterized of these longevity factors; reduced PI3-kinase signaling leads to the dephosphorylation and nuclear translocation of DAF-16, which up-regulates the expression of various target genes. DAF-16 target genes contribute to longevity by promoting stress resistance, reproductive span, innate immunity, and protein homeostasis.RNA helicases are essential for biogenesis, maturation, processing, and homeostasis of various types of RNAs (reviewed in ref. 6). In addition, RNA helicases work with factors, such as a CREBbinding protein, RNA polymerases I and II, and histone deacetylases, to regulate transcriptional activity (7,8). For example, DDX5 (p68), a DEAD-box RNA helicase, interacts with Smad3, a transcriptional activator and intracellular effector of TGF-β (9), and with RNA polymerase II to modulate transcriptional activity (10). Because RNA helicases comprise a large family of housekeeping proteins essential for RNA biogenesis and homeostasis, their importanc...

Small RNAs that originate from transfer RNA (tRNA) species, tRNA-derived fragments (tRFs), play diverse biological functions but little is known for their association with aging. Moreover, biochemical aspects of tRNAs limit discovery of functional tRFs by high throughput sequencing. In particular, genes encoding tRNAs exist as multiple copies throughout genome, and mature tRNAs have various modified bases, contributing to ambiguities for RNA sequencing-based analysis of tRFs. Here, we report age-dependent changes of tRFs in Caenorhabditis elegans. We first analyzed published RNA sequencing data by using a new strategy for tRNA-associated sequencing reads. Our current method used unique mature tRNAs as a reference for the sequence alignment, and properly filtered out false positive enrichment for tRFs. Our analysis successfully distinguished de novo mutation sites from differences among homologous copies, and identified potential RNA modification sites. Overall, the majority of tRFs were upregulated during aging and originated from 5′-ends, which we validated by using Northern blot analysis. Importantly, we revealed that the major source of tRFs upregulated during aging was the tRNAs with abundant gene copy numbers. Our analysis suggests that tRFs are useful biomarkers of aging particularly when they originate from abundant homologous gene copies.