Differences In Senescence Research Articles

Minimal assay detects population-level senescence in the aquatic plant <i>Lemna minor</i>

At the population level, senescence occurs when older individuals have increased risk of death and reduced reproduction compared to younger individuals. We investigated senescence in the aquatic plant <i>Lemna minor</i> (common duckweed), an important species for plant senescence research. Our objectives were to (1) confirm or refute the presence of population-level senescence in this model species; (2) develop a minimal assay of senescence requiring only once-weekly data collection; and (3) test whether there were appreciable differences in senescence in plants grown in glass compared to polystyrene petri dishes, with an aim to reducing single-use plastic waste and long-term research materials costs. We found that weekly survival arced downward with age when viewed on a semi-log plot, and weekly production of descendants decreased with age, with both findings indicating population-level senescence that matched previous work using more frequent data-collection (per Objectives 1 and 2). Additionally, we found no noteworthy differences in senescence between plants grown in glass versus polystyrene petri dishes (per Objective 3). The use of weekly data collection could liberate personnel resources for other research-group functions, and could make the <i>Lemna</i> system suitable for senescence- or demography-education exercises. The use of glass dishes could reduce lab waste and expense.

Exploration of the tumorigenic, metabolic, and cognitive consequences of tau protein removal

AbstractBackgroundTau accumulation causes tauopathies and drives cellular senescence, which can lead to inflammation, neurodegeneration, and cognitive impairment. The association between intracellular tau deposition and pathogenesis has prompted therapeutic strategies that reduce tau expression. However, tau is also critical in microtubule stabilization, synaptic plasticity, and maintaining DNA integrity. We investigated the impact of tau removal on brain cell senescence and associated neurocognitive behaviors in aged tau knockout (Mapt0/0) and wild type control (Mapt+/+) mice. We also assessed physical, metabolic, histological, and biochemical outcomes in Mapt0/0 and Mapt+/+ mice and in response to high fat diet (HFD), a stressor that drives DNA damage.Method20‐month‐old female Mapt0/0 and Mapt+/+ mice were subjected to the Elevated Plus Maze to assess anxiety‐like behavior. Mice were then fed control (CTL) or HFD (60% kcal fat) for 9 weeks. Behavioral and physical measures were then assessed, and brain tissue was further analyzed via gene expression, biochemistry, and histological assays.ResultTau knockout and HFD, separately and additively, caused weight gain and insulin resistance. Removing tau primed cells to proliferate, as Mapt0/0 mice had increased body size, organ size, and tumor burden compared to Mapt+/+. We observed no difference in senescence between genotypes on CTL diet. The HFD increased senescence only in Mapt+/+ mice, whereas Mapt0/0 mice displayed increased tumor burden. Mapt0/0 mice displayed anxiety‐ and depressive‐like behaviors on both diets. Transcriptomic and protein expression data revealed that several molecules responded similarly to tau removal and HFD exposure, but Mapt+/+ and Mapt0/0 mice responded differently to HFD. Genotype differences in DNA damage and cell cycle dysregulation were also observed.ConclusionMapt0/0 mice did not accumulate senescent cells but demonstrated anxiety‐like behaviors in the presence of elevated DNA damage; thus tau knockout may drive neuropsychiatric phenotypes which can be dissociated from obesity and senescence. Mapt0/0 mice also developed tumors, suggesting that tau plays a critical role in cell fate decisions, including senescence versus cancer. Overall, we found that tau removal prevents senescent cell accumulation with the tradeoff of tumorigenic, metabolic, and cognitive consequences. We caution against removing tau until a better understanding of its physiological roles are defined.

Sex difference and immunosenescence affect transplantation outcomes.

Kidney transplantation is a well-established alternative to renal replacement therapy. Although the number of patients with end-stage renal disease (ESRD) is increasing, the availability of kidney for transplantation is still insufficient to meet the needs. As age increases, the prevalence of ESRD increases; thus, the population of aged donors and recipients occupies large proportion. Accumulated senescent cells secrete pro-inflammatory factors and induce senescence. Additionally, it is gradually becoming clear that biological sex differences can influence aging and cause differences in senescence. Here, we review whether age-related sex differences affect organ transplant outcomes and what should be done in the future.

Raising offspring increases ageing: Differences in senescence among three populations of a long-lived seabird, the Atlantic puffin.

Actuarial senescence, the decline of survival with age, is well documented in the wild. Rates of senescence vary widely between taxa, to some extent also between sexes, with the fastest life histories showing the highest rates of senescence. Few studies have investigated differences in senescence among populations of the same species, although such variation is expected from population-level differences in environmental conditions, leading to differences in vital rates and thus life histories. We predict that, within species, populations differing in productivity (suggesting different paces of life) should experience different rates of senescence, but with little or no sexual difference in senescence within populations of monogamous, monomorphic species where the sexes share breeding duties. We compared rates of actuarial senescence among three contrasting populations of the Atlantic puffin Fratercula arctica. The dataset comprised 31 years (1990-2020) of parallel capture-mark-recapture data from three breeding colonies, Isle of May (North Sea), Røst (Norwegian Sea) and Hornøya (Barents Sea), showing contrasting productivities (i.e. annual breeding success) and population trends. We used time elapsed since first capture as a proxy for bird age, and productivity and the winter North Atlantic Oscillation Index (wNAO) as proxies for the environmental conditions experienced by the populations within and outside the breeding season, respectively. In accordance with our predictions, we found that senescence rates differed among the study populations, with no evidence for sexual differences. There was no evidence for an effect of wNAO, but the population with the lowest productivity, Røst, showed the lowest rate of senescence. As a consequence, the negative effect of senescence on the population growth rate (λ) was up to 3-5 times smaller on Røst (Δλ=-0.009) than on the two other colonies. Our findings suggest that environmentally induced differences in senescence rates among populations of a species should be accounted for when predicting effects of climate variation and change on species persistence. There is thus a need for more detailed information on how both actuarial and reproductive senescence influence vital rates of populations of the same species, calling for large-scale comparative studies.

TERT promoter mutations and methylation for telomerase activation in urothelial carcinomas: New mechanistic insights and clinical significance.

Telomerase, an RNA-dependent DNA polymerase synthesizing telomeric TTAGGG sequences, is primarily silent in normal human urothelial cells (NHUCs), but widely activated in urothelial cell-derived carcinomas or urothelial carcinomas (UCs) including UC of the bladder (UCB) and upper track UC (UTUC). Telomerase activation for telomere maintenance is required for the UC development and progression, and the key underlying mechanism is the transcriptional de-repression of the telomerase reverse transcriptase (TERT), a gene encoding the rate-limiting, telomerase catalytic component. Recent mechanistic explorations have revealed important roles for TERT promoter mutations and aberrant methylation in activation of TERT transcription and telomerase in UCs. Moreover, these TERT-featured genomic and epigenetic alterations have been evaluated for their usefulness in non-invasive UC diagnostics, recurrence monitoring, outcome prediction and response to treatments such as immunotherapy. Importantly, the detection of the mutated TERT promoter and TERT mRNA as urinary biomarkers holds great promise for urine-based UC liquid biopsy. In the present article, we review recent mechanistic insights into altered TERT promoter-mediated telomerase activation in UCs and discuss potential clinical implications. Specifically, we compare differences in senescence and transformation between NHUCs and other types of epithelial cells, address the interaction between TERT promoter mutations and other factors to affect UC progression and outcomes, evaluate the impact of TERT promoter mutations and TERT-mediated activation of human endogenous retrovirus genes on UC immunotherapy including Bacillus Calmette-Guérin therapy and immune checkpoint inhibitors. Finally, we suggest the standardization of a TERT assay and evaluation system for UC clinical practice.

Chronic hyperinsulinemia promotes human hepatocyte senescence

ObjectiveCellular senescence, an irreversible proliferative cell arrest, is caused by excessive intracellular or extracellular stress/damage. Increased senescent cells have been identified in multiple tissues in different metabolic and other aging-related diseases. Recently, several human and mouse studies emphasized the involvement of senescence in development and progression of NAFLD. Hyperinsulinemia, seen in obesity, metabolic syndrome, and other conditions of insulin resistance, has been linked to senescence in adipocytes and neurons. Here, we investigate the possible direct role of chronic hyperinsulinemia in the development of senescence in human hepatocytes. MethodsUsing fluorescence microscopy, immunoblotting, and gene expression, we tested senescence markers in human hepatocytes subjected to chronic hyperinsulinemia in vitro and validated the data in vivo by using liver-specific insulin receptor knockout (LIRKO) mice. The consequences of hyperinsulinemia were also studied in senescent hepatocytes following doxorubicin as a model of stress-induced senescence. Furthermore, the effects of senolytic agents in insulin- and doxorubicin-treated cells were analyzed. ResultsResults showed that exposing the hepatocytes to prolonged hyperinsulinemia promotes the onset of senescence by increasing the expression of p53 and p21. It also further enhanced the senescent phenotype in already senescent hepatocytes. Addition of insulin signaling pathway inhibitors prevented the increase in cell senescence, supporting the direct contribution of insulin. Furthermore, LIRKO mice, in which insulin signaling in the liver is abolished due to deletion of the insulin receptor gene, showed no differences in senescence compared to their wild-type counterparts despite having marked hyperinsulinemia indicating these are receptor-mediated effects. In contrast, the persistent hyperinsulinemia in LIRKO mice enhanced senescence in white adipose tissue. In vitro, senolytic agents dasatinib and quercetin reduced the prosenescent effects of hyperinsulinemia in hepatocytes. ConclusionOur findings demonstrate a direct link between chronic hyperinsulinemia and hepatocyte senescence. This effect can be blocked by reducing the levels of insulin receptors or administration of senolytic drugs, such as dasatinib and quercetin.

Sex-specific aging in bite force in a wild vertebrate.

The manifold differences between the sexes provide wide scope for sex differences in senescence. However, detecting physiological decline in old age and evaluating any sex difference in aging in a wild population can be challenging. This applies especially to long-lived species that require marking around birth in order to recognize elderly individuals, perhaps decades later. Here, we used bite force of known-age, long-lived Nazca boobies (Sula granti, a seabird) as a functional measure of muscle strength; surprisingly, only a single study has evaluated the possibility of senescent decline in muscle strength in a wild vertebrate. The male-biased adult sex ratio of this population constrains breeding opportunities across the lifespan for males, so we predicted that slower accumulation of reproductive costs would delay senescent decline in bite force in males compared to females, matching observed patterns in some non-muscle traits in this species. Data were collected from 349 adults using a force transducer at the start of the breeding season in November 2017 on Isla Española, Galápagos. Both sexes achieved less bite force in late life. The decline began at a later age in males, providing evidence of sex-specific schedules of decline in muscle function in a wild vertebrate.

Differences in senescence of late Endothelial Progenitor Cells in non-smokers and smokers.

INTRODUCTIONEndothelial Progenitor Cells (EPCs) are part of hematopoietic stem cells that differentiate into endothelial cells during their blood vessels’ maturation process. The role of EPCs is widely known to contribute to repair of the vascular wall when endothelial dysfunction occurs. However, various risk factors for cardiovascular disease (CVD) influence EPC performance, leading to endothelial dysfunction. One EPC dysfunction is decreased amount of EPC mobilization to the injured tissue. EPC dysfunction reduces the angiogenetic function of EPCs. The vital maturation process that the EPCs must pass is the late phase. The dysfunction of late EPCs is known as senescence. This study aimed to identify and compare senescence of late EPCs, through CD62E and CD41 markers, in non-smokers and smokers as a risk factor for CVD.METHODSEPC collection was from peripheral mononuclear cells (PBMCs) in non-smokers (n=30) and smokers (n=31). The EPCs were then marked by CD62E/CD41 and senescence β-galactosidase assay using FACS. Identification of senescence cells was based on fluorescence with DAPI.RESULTSPositive percentage of late EPCs in non-smokers was not significantly different from that in smokers (p=0.014). The number of senescent late EPCs in smokers was higher than in non-smokers (p<0.0001).CONCLUSIONSEndothelial progenitor cells that experienced senescence in the smokers showed EPC dysfunction, which resulted in decreased cell angiogenic function. Further research is needed to explain the mechanism of re-endothelialization failure in EPC dysfunction due to smoking.

Chronic senescent human mesenchymal stem cells as possible contributor to the wound healing disorder after exposure to the alkylating agent sulfur mustard

Wound healing is a complex process, and disturbance of even a single mechanism can result in chronic ulcers developing after exposure to the alkylating agent sulfur mustard (SM). A possible contributor may be SM-induced chronic senescent mesenchymal stem cells (MSCs), unable to fulfil their regenerative role, by persisting over long time periods and creating a proinflammatory microenvironment. Here we show that senescence induction in human bone marrow derived MSCs was time- and concentration-dependent, and chronic senescence could be verified 3 weeks after exposure to between 10 and 40 µM SM. Morphological changes, reduced clonogenic and migration potential, longer scratch closure times, differences in senescence, motility and DNA damage response associated genes as well as increased levels of proinflammatory cytokines were revealed. Selective removal of these cells by senolytic drugs, in which ABT-263 showed initial potential in vitro, opens the possibility for an innovative treatment strategy for chronic wounds, but also tumors and age-related diseases.

Does facial hair greying in chimpanzees provide a salient progressive cue of aging?

The greying of human head hair is arguably the most salient marker of human aging. In wild mammal populations, greying can change with life history or environmental factors (e.g., sexual maturity in silverback gorillas). Yet, whether humans are unique in our pattern of age-related hair depigmentation is unclear. We examined the relationship between pigmentation loss in facial hair (greying) to age, population, and sex in wild and captive chimpanzees (Pan troglodytes). Digital facial photographs representing three chimpanzee populations (N = 145; ages 1–60 years) were scored for hair greying on a scale of one [~100% pigmented] to six [~0% pigmented]. Our data suggest that chimpanzee head and facial hair generally greys with age prior to mid-life (~30 years old), but afterwards, greying ceases to increase incrementally. Our results highlight that chimpanzee pigmentation likely exhibits substantial variation between populations, and that both 'grey' and pigmented phenotypes exist across various age classes. Thus, chimpanzee facial hair greying is unlikely a progressive indicator of age beyond mid-life, and thus facial greying in chimpanzees seems different from the pattern observed in humans. Whether this reflects neutral differences in senescence, or potential differences in selection pressures (e.g. related to conspecific communication), is unclear and worthy of more detailed examination across populations and taxa.

Link between increased cellular senescence and extracellular matrix changes in COPD.

Chronic obstructive pulmonary disease (COPD) is associated with features of accelerated aging, including cellular senescence, DNA damage, oxidative stress, and extracellular matrix (ECM) changes. We propose that these features are particularly apparent in patients with severe, early-onset (SEO)-COPD. Whether fibroblasts from COPD patients display features of accelerated aging and whether this is also present in relatively young SEO-COPD patients is unknown. Therefore, we aimed to determine markers of aging in (SEO)-COPD-derived lung fibroblasts and investigate the impact on ECM. Aging hallmarks and ECM markers were analyzed in lung fibroblasts from SEO-COPD and older COPD patients and compared with fibroblasts from matched non-COPD groups (n = 9-11 per group), both at normal culture conditions and upon Paraquat-induced senescence. COPD-related differences in senescence and ECM expression were validated in lung tissue. Higher levels of cellular senescence, including senescence-associated β-galactosidase (SA-β-gal)-positive cells (19% for COPD vs. 13% for control) and p16 expression, DNA damage (γ-H2A.X-positive nuclei), and oxidative stress (MGST1) were detected in COPD compared with control-derived fibroblasts. Most effects were also different in SEO-COPD, with SA-β-gal-positive cells only being significant in SEO-COPD vs. matched controls. Lower decorin expression in COPD-derived fibroblasts correlated with higher p16 expression, and this association was confirmed in lung tissue. Paraquat treatment induced cellular senescence along with clear changes in ECM expression, including decorin. Fibroblasts from COPD patients, including SEO-COPD, display higher levels of cellular senescence, DNA damage, and oxidative stress. The association between cellular senescence and ECM expression changes may suggest a link between accelerated aging and ECM dysregulation in COPD.

Abscisic acid responses match the different patterns of autumn senescence in roots and leaves of Iris versicolor and Sparganium emersum

In seasonal climates with cold winters, leaves of deciduous trees and herbs senesce in the fall remobilizing nutrients in a tightly-regulated process with hormonal signaling. In contrast to leaves, not much data exist about root senescence. There is some indication that also in roots similar processes exist, but the available data is scarce and contradictory. Here we investigate senescence in the different plant organs by comparing temporal patterns of phytohormone levels during autumn senescence in two herbaceous perennial species both with senescing leaves, but with roots differing in their overwintering strategy. Roots of Sparganium emersum senesce in autumn, while roots of Iris versicolor overwinter without senescing. Levels of phytohormones, antioxidants and lipid peroxidation were monitored from late August until almost complete above-ground senescence at the end of October. Leaves of S. emersum senesced 4–6 weeks before those of I. versicolor, with peaks in ABA levels during the early weeks of senescence in both species. S. emersum roots showed a peak in ABA levels 4 weeks after that in leaves, possibly indicating a delayed senescence of roots. Roots of I. versicolor did not senesce and had low levels of ABA throughout. None of the other hormones showed patterns matching the interspecific differences in senescence. For example, jasmonate levels declined both in senescing and non-senescing roots. In leaves, lipid peroxidation pattern matched the patterns of senescence, whereas roots showed low levels of lipid peroxidation. Before total above-ground senescence, some gibberellins and cytokinins increased in leaves of both species, probably in association with formation of small overwintering leaves with arrested growth, embedded in the senescing shoot. In conclusion, the temporal pattern of ABA in roots of S. emersum indicates the presence of coordinated end-of-the-season processes in roots, similar to leaves, while the non-senescing roots of I. versicolor do not show such a pattern.

Modeling canopy senescence to calculate soybean maturity date using NDVI

AbstractSoybeans [Glycine max (L.) Merr.] are the second largest crop in the United States, and cultivar development is important to improve productivity on existing farms. High‐throughput phenotyping can assist breeders in characterizing new lines particularly for phenotypic traits of interest such as crop canopy color, leaf distribution, and seed yield. However, current methods for characterizing the maturity date of soybeans needs to be improved to further leverage high‐throughput phenotyping platforms. The objective of this study was to examine if relative differences in leaf senescence patterns of soybean cultivars could be used to accurately calculate the observed maturity date. A field study was conducted in 2016–2017 at two locations in Ohio. Leaf canopy senescence was measured using the normalized difference vegetation index (NDVI), and observed maturity was measured for each cultivar. Senescence was modeled for each cultivar, and relative differences in senescence calculated from NDVI reductions were compared with the relative differences in observed maturity for each cultivar. The relative differences between cultivars in the date when NDVI was reduced by 85% during senescence (compared with NDVI at the R5 growth stage) were accurate to calculate maturity differences to within 1.5 d of the observed values for 21 of the 24 cultivar × site‐year combinations. This practice has potential to contribute additional data to enhance the high‐throughput phenotyping process using existing equipment (or data being collected) in many programs.

Senescence in the city: exploring ageing patterns of a long‐lived raptor across an urban gradient

In many vertebrates, productivity and survival usually increase with age and then start to decline above a certain age; processes known as reproductive and actuarial senescence. Senescence is widely believed to be driven by the accumulation of somatic damage or mutations. Thus, levels of such cellular damage, and therefore senescence could, in theory, differ between different habitats if they experience different stressors. Urban environments expose animals to a wide range of stressors that pose a challenge to physiological systems and might accelerate the ageing process. We studied productivity and survival of black sparrowhawks across an urban gradient in Cape Town, South Africa. We hypothesise that productivity and survival will first increase with age, but that productivity and survival will then decline above a certain age, due to senescence. Furthermore, we hypothesise that rates of senescence will be accelerated in more urban areas. We used 17 years of data from colour‐ringed individuals. We found no indication of any improvement in productivity with age in early‐life, but we did detect reproductive senescence, with productivity declining above six years of age. However, contrary to our predictions, there were no differences in reproductive senescence along the urban gradient. Similarly, we found that survival rates of adults did not show any strong improvement with age in early life, but decreased with age amongst older birds, providing support for actuarial senescence. However, once again no differences in this pattern were apparent along the urban gradient. This study represents one of the first to examine differences in senescence rates in different habitats. Our results suggest that for this urban adapted species, senescence patterns do not vary according to levels of urbanisation. Whether this pattern holds for species more sensitive to urbanisation remains worthy of exploration.

Senescence in nature: New insights from a long-term seabird study.

In Focus: Tompkins, E. M., & Anderson, D. J. (2019). Sex-specific patterns of senescencein Nazca boobies linked to mating system. Journal of Animal Ecology, 88, 986-1000. https://doi.org/10.1111/1365-2656.12944. Sex-specific differences in senescence and environmental impacts on senescence in both sexes remain poorly understood. Tompkins and Anderson (2019) studied senescence in survival (hereafter called actuarial senescence) and in reproduction (hereafter called reproductive senescence) in Nazca boobies using 33years of individual-based capture-recapture data. Senescence patterns (life-history traits, ages at onset, senescence rates) differed between sexes and were affected by environmental conditions (food availability) faced by individuals during their younger ages. Patterns of sex differences in senescence may result from the mating dynamics due to the population's male-biased sex ratio.

Tooth wear as a practical indicator of sexual differences in senescence and mastication investment in ecology studies

Abstract Teeth of many mammalian species do not grow further after they have emerged, nor are they replaced or repaired if they break or wear. These dental properties have been used to test evolutionary hypotheses on life expectancy relative to actual age (senescence, aging), as the animal is expected to die when all its dental crown tissue has been depleted due to the wearing effect of mastication. Females of polygynous mammals with small litter size are expected to live longer than males of the same species, as female reproductive fitness is maximised by having a long reproductive life. In contrast, maleś reproductive success is limited to the short period when they are in prime condition, as it is in this period that they are most successful in intra-sexual competition for mating opportunities. Consequently, it has been predicted that femaleś teeth should be more durable and so wear more slowly than maleś teeth. However, these predictions are affected by potential sex differences in the hardness of dental tissues, which have not been assessed in depth in the literature. I tested sexual differences in the hardness of enamel and dentine on a balanced, by sex and age, sample of 156 lower first molars of Scottish red deer of known age using Vickers micro-hardness indentation measures as a proxy of the resilience of the tooth to wear. My results clearly indicate that there are no sexual differences in enamel and dentine hardness, and that tooth hardness has a negligible effect on predicting tooth wear, which supports the use of tooth wear relative to body size as a convenient proxy for assessing sexual differences in senescence in polygynous ungulates. I warn on making conclusions from comparisons between populations or species in tooth wear when tooth hardness was controlled for.

Sex-specific patterns of senescence in Nazca boobies linked to mating system.

Under life-history theories of ageing, increased senescence should follow relatively high reproductive effort. This expectation has rarely been tested against senescence varying between and within the two sexes, although such an approach may clarify the origins of sex-specific ageing in the context of a given mating system. Nazca boobies (Sula granti; a seabird) practise serial monogamy and biparental care. A male-biased population sex ratio results in earlier and more frequent breeding by females. Based on sex-specific reproductive schedules, females were expected to show faster age-related decline for survival and reproduction. Within each sex, high reproductive effort in early life was expected to reduce late-life performance and accelerate senescence. Longitudinal data were used to (a) evaluate the sex specificity of reproductive and actuarial senescence and then (b) test for early-/late-life fitness trade-offs within each sex. Within-sex analyses inform an interpretation of sex differences in senescence based on costs of reproduction. Analyses incorporated individual heterogeneity in breeding performance and cohort-level differences in early-adult environments. Females showed marginally more intense actuarial senescence and stronger age-related declines for fledging success. The opposite pattern (earlier and faster male senescence) was found for breeding probability. Individual reproductive effort in early life positively predicted late-life reproductive performance in both sexes and thus did not support a causal link between early-reproduction/late-life fitness trade-offs and sex differences in ageing. A high-quality diet in early adulthood reduced late-life survival (females) and accelerated senescence for fledging success (males). This study documents clear variation in ageing patterns-by sex, early-adult environment and early-adult reproductive effort-with implications for the role mating systems and early-life environments play in determining ageing patterns. Absent evidence for a disposable soma mechanism, patterns of sex differences in senescence may result from age- and condition-dependent mate choice interacting with this population's male-biased sex ratio and mate rotation.

Nitrogen Supply Drives Senescence-Related Seed Storage Protein Expression in Rapeseed Leaves.

In general, yield and fruit quality strongly rely on efficient nutrient remobilization during plant development and senescence. Transcriptome changes associated with senescence in spring oilseed rape grown under optimal nitrogen supply or mild nitrogen deficiency revealed differences in senescence and nutrient mobilization in old lower canopy leaves and younger higher canopy leaves. Having a closer look at this transcriptome analyses, we identified the major classes of seed storage proteins (SSP) to be expressed in vegetative tissue, namely leaf and stem tissue. Expression of SSPs was not only dependent on the nitrogen supply but transcripts appeared to correlate with intracellular H2O2 contents, which functions as well-known signaling molecule in developmental senescence. The abundance of SSPs in leaf material transiently progressed from the oldest leaves to the youngest. Moreover, stems also exhibited short-term production of SSPs, which hints at an interim storage function. In order to decipher whether hydrogen peroxide also functions as a signaling molecule in nitrogen deficiency-induced senescence, we analyzed hydrogen peroxide contents after complete nitrogen depletion in oilseed rape and Arabidopsis plants. In both cases, hydrogen peroxide contents were lower in nitrogen deficient plants, indicating that at least parts of the developmental senescence program appear to be suppressed under nitrogen deficiency.

Developmental stress and telomere dynamics in a genetically polymorphic species.

A central objective of evolutionary biology is understanding variation in life-history trajectories and the rate of aging, or senescence. Senescence can be affected by trade-offs and behavioural strategies in adults but may also be affected by developmental stress. Developmental stress can accelerate telomere degradation, with long-term longevity and fitness consequences. Little is known regarding whether variation in developmental stress and telomere dynamics contributes to patterns of senescence during adulthood. We investigated this question in the dimorphic white-throated sparrow (Zonotrichia albicollis), a species in which adults of the two morphs exhibit established differences in behavioural strategy and patterns of senescence, and also evaluated the relationship between oxidative stress and telomere length. Tan morph females, which exhibit high levels of unassisted parental care, display faster reproductive senescence than white females, and faster actuarial senescence than all of the other morph-sex classes. We hypothesized that high oxidative stress and telomere attrition in tan female nestlings could contribute to this pattern, since tan females are small and potentially at a competitive disadvantage even as nestlings. Nestlings that were smaller than nest mates had higher oxidative stress, and nestlings with high oxidative stress and fast growth rates displayed shorter telomeres. However, we found no consistent morph-sex differences in oxidative stress or telomere length. Results suggest that oxidative stress and fast growth contribute to developmental telomere attrition, with potential ramifications for adults, but that developmental oxidative stress and telomere dynamics do not account for morph-sex differences in senescence during adulthood.

Divergent N Deficiency-Dependent Senescence and Transcriptome Response in Developmentally Old and Young Brassica napus Leaves.

In the spring oilseed rape (OSR) cultivar ‘Mozart’ grown under optimal N supply (NO) or mild N deficiency (NL) the transcriptome changes associated with progressing age until early senescence in developmentally old lower canopy leaves (leaf #4) and younger higher canopy leaves (leaf #8) were investigated. Twelve weeks old NO and NL plants appeared phenotypically and transcriptomically identical, but thereafter distinct nutrition-dependent differences in gene expression patterns in lower and upper canopy leaves emerged. In NO leaves #4 of 14-week-old compared to 13-week-old plants, ∼600 genes were up- or downregulated, whereas in NL leaves #4 ∼3000 genes were up- or downregulated. In contrast, in 15-week-old compared to 13-week-old upper canopy leaves #8 more genes were up- or downregulated in optimally N-supplied plants (∼2000 genes) than in N-depleted plants (∼750 genes). This opposing effect of N depletion on gene regulation was even more prominent among photosynthesis-related genes (PSGs). Between week 13 and 14 in leaves #4, 99 of 110 PSGs were downregulated in NL plants, but none in NO plants. In contrast, from weeks 13 to 16 in leaves #8 of NL plants only 11 PSGs were downregulated in comparison to 66 PSGs in NO plants. Different effects of N depletion in lower versus upper canopy leaves were also apparent in upregulation of autophagy genes and NAC transcription factors. More than half of the regulated NAC and WRKY transcription factor, autophagy and protease genes were specifically regulated in NL leaves #4 or NO leaves #8 and thus may contribute to differences in senescence and nutrient mobilization in these leaves. We suggest that in N-deficient plants the upper leaves retain their N resources longer than in amply fertilized plants and remobilize them only after shedding of the lower leaves.