Interplay between vitamin E and phosphorus availability in the control of longevity in Arabidopsis thaliana

Background and Aims Vitamin E helps to control the cellular redox state by reacting with singlet oxygen and preventing the propagation of lipid peroxidation in thylakoid membranes. Both plant ageing and phosphorus deficiency can trigger accumulation of reactive oxygen species, leading to damage to the photosynthetic apparatus. This study investigates how phosphorus availability and vitamin E interact in the control of plant longevity in the short-lived annual Arabidopsis thaliana.Methods The responses of tocopherol cyclase (VTE1)- and γ-tocopherol methyltransferase (VTE4)-null mutants to various levels of phosphorus availability was compared with that of wild-type plants. Longevity (time from germination to rosette death) and the time taken to pass through different developmental stages were determined, and measurements were taken of photosynthetic efficiency, pigment concentration, lipid peroxidation, vitamin E content and jasmonate content.Key Results The vte1 mutant showed accelerated senescence under control conditions, excess phosphorus and mild phosphorus deficiency, suggesting a delaying, protective effect of α-tocopherol during plant senescence. However, under severe phosphorus deficiency the lack of α-tocopherol paradoxically increased longevity in the vte1 mutant, while senescence was accelerated in wild-type plants. Reduced photoprotection in vitamin E-deficient mutants led to increased levels of defence chemicals (as indicated by jasmonate levels) under severe phosphorus starvation in the vte4 mutant and under excess phosphorus and mild phosphorus starvation in the vte1 mutant, indicating a trade-off between the capacity for photoprotection and the activation of chemical defences (jasmonate accumulation).Conclusions Vitamin E increases plant longevity under control conditions and mild phosphorus starvation, but accelerates senescence under severe phosphorus limitation. Complex interactions are revealed between phosphorus availability, vitamin E and the potential to synthesize jasmonates, suggesting a trade-off between photoprotection and the activation of chemical defences in the plants.     

Early‐onset aging and mitochondrial defects associated with loss of histone acetyltransferase 1 (Hat1)

Histone acetyltransferase 1 (Hat1) is responsible for the acetylation of newly synthesized histone H4 on lysines 5 and 12 during the process of chromatin assembly. To understand the broader biological role of Hat1, we have generated a conditional mouse knockout model of this enzyme. We previously reported that Hat1 is required for viability and important for mammalian development and genome stability. In this study, we show that haploinsufficiency of Hat1 results in a significant decrease in lifespan. Defects observed in Hat1^+/? mice are consistent with an early‐onset aging phenotype. These include lordokyphosis (hunchback), muscle atrophy, minor growth retardation, reduced subcutaneous fat, cancer, and paralysis. In addition, the expression of Hat1 is linked to the normal aging process as Hat1 mRNA and protein becomes undetectable in many tissues in old mice. At the cellular level, fibroblasts from Hat1 haploinsufficient embryos undergo early senescence and accumulate high levels of p21. Hat1^+/? mouse embryonic fibroblasts (MEFs) display modest increases in endogenous DNA damage but have significantly higher levels of reactive oxygen species (ROS). Consistently, further studies show that Hat1^?/? MEFs exhibit mitochondrial defects suggesting a critical role for Hat1 in mitochondrial function. Taken together, these data show that loss of Hat1 induces multiple hallmarks of early‐onset aging.     

cDNA cloning and differential gene expression of three catalases in pumpkin

Three cDNA clones (cat1, cat2, cat3) for catalase (EC 1.11.1.6) were isolated from a cDNA library of pumpkin (Cucurbita sp.) cotyledons. In northern blotting using the cDNA-specific probe, the cat1 mRNA levels were high in seeds and early seedlings of pumpkin. The expression pattern of cat1 was similar to that of malate synthase, a characteristic enzyme of glyoxysomes. These data suggest that cat1 might encode a catalase associated with glyoxysomal functions. Furthermore, immunocytochemical analysis using cat1-specific anti-peptide antibody directly showed that cat1 encoding catalase is located in glyoxysomes. The cat2 mRNA was present at high levels in green cotyledons, mature leaf, stem and green hypocotyl of light-grown pumpkin plant, and correlated with chlorophyll content in the tissues. The tissue-specific expression of cat2 had a strong resemblance to that of glycolate oxidase, a characteristic enzyme of leaf peroxisomes. During germination of pumpkin seeds, cat2 mRNA levels increased in response to light, although the increase in cat2 mRNA by light was less than that of glycolate oxidase. cat3 mRNA was abundant in green cotyledons, etiolated cotyledons, green hypocotyl and root, but not in young leaf. cat3 mRNA expression was not dependent on light, but was constitutive in mature tissues. Interestingly, cat1 mRNA levels increased during senescence of pumpkin cotyledons, whereas cat2 and cat3 mRNAs disappeared during senescence, suggesting that cat1 encoding catalase may be involved in the senescence process. Thus, in pumpkin, three catalase genes are differentially regulated and may exhibit different functions.     

草酸氧化酶在水稻胚芽鞘衰老中的作用

草酸氧化酶（OxO）催化草酸氧化产生CO2和H2O2,其在植物发育及防御过程中可能具有重要作用。本文以水稻品种‘湘糯1号’（‘Xiangnuo 1’）为材料,对胚芽鞘中的OxO及其生理功能进行了研究。结果表明,胚芽鞘中的H2O2含量在其衰老时增加;OxO活性在浸种后96h时较低,之后也迅速增加,在240h达到最高;而可溶性蛋白、O2-·和草酸含量以及过氧化氢酶（CAT）活性则随着胚芽鞘的衰老迅速降低。由于H2O2能够诱导细胞死亡,推测OxO可能通过降解草酸产生H2O2参与胚芽鞘的衰老。     

Delayed kinetics of DNA double-strand break processing in normal and pathological aging

Accumulation of DNA damage may play an essential role in both cellular senescence and organismal aging. The ability of cells to sense and repair DNA damage declines with age. However, the underlying molecular mechanism for this age-dependent decline is still elusive. To understand quantitative and qualitative changes in the DNA damage response during human aging, DNA damage-induced foci of phosphorylated histone H2AX (γ-H2AX), which occurs specifically at sites of DNA double-strand breaks (DSBs) and eroded telomeres, were examined in human young and senescing fibroblasts, and in lymphocytes of peripheral blood. Here, we show that the incidence of endogenous γ-H2AX foci increases with age. Fibroblasts taken from patients with Werner syndrome, a disorder associated with premature aging, genomic instability and increased incidence of cancer, exhibited considerably higher incidence of γ-H2AX foci than those taken from normal donors of comparable age. Further increases in γ-H2AX focal incidence occurred in culture as both normal and Werner syndrome fibroblasts progressed toward senescence. The rates of recruitment of DSB repair proteins to γ-H2AX foci correlated inversely with age for both normal and Werner syndrome donors, perhaps due in part to the slower growth of γ-H2AX foci in older donors. Because genomic stability may depend on the efficient processing of DSBs, and hence the rapid formation of γ-H2AX foci and the rapid accumulation of DSB repair proteins on these foci at sites of nascent DSBs, our findings suggest that decreasing efficiency in these processes may contribute to genome instability associated with normal and pathological aging.     

Progressive loss of SIRT1 with cell cycle withdrawal

Sir2 is an NAD+-dependent deacetylase that regulates lifespan in yeast, worms and flies. The mammalian orthologs of Sir2 include SIRT1 in humans and mice. In this study, we analyzed the level of SIRT1 in human lung fibroblasts (IMR90) and mouse embryonic fibroblasts (MEFs) from mice with normal, accelerated, and delayed aging. SIRT1 protein, but not mRNA, decreased significantly with serial cell passage in both human and murine cells. Mouse SIRT1 decreased rapidly in prematurely senescent (p44 Tg) MEFs, remained high in MEFs with delayed senescence (Igf-1r-/-), and was inversely correlated with senescence-activated beta-galactosidase (SA-betaGal) activity. Reacquisition of mitotic capability following spontaneous immortalization of serially passaged wild-type MEFs restored the level of SIRT1 to that of early passage, highly proliferative MEFs. In mouse and human fibroblasts, we found a significant positive correlation between the levels of SIRT1 and proliferating cell nuclear antigen (PCNA), a DNA processing factor expressed during S-phase. In the animal, we found that SIRT1 decreased with age in tissues in which mitotic activity also declines, such as the thymus and testis, but not in tissues such as the brain in which there is little change in mitotic activity throughout life. Again, the decreases in SIRT1 were highly correlated with decreases in PCNA. Finally, loss of SIRT1 with age was accelerated in mice with accelerated aging but was not observed in long-lived growth hormone-receptor knockout mice. Thus, as mitotic activity ceases in mouse and human cells in the normal environment of the animal or in the culture dish, there is a concomitant decline in the level of SIRT1.     

冷型小麦旗叶衰老和活性氧代谢特性研究

以典型的冷型小麦和暖型小麦为试验材料,研究了同一环境背景下不同温度型小麦开花后的旗叶衰老和活性氧代谢特性。结果表明,与暖型小麦相比,冷型小麦籽料灌浆期旗叶叶绿素和可溶性蛋白质含量下降缓慢、含量高,整个业粒形成和灌浆期ＭＤＡ积累速度慢、含量低,籽粒灌浆期防御活性氧伤害的关键性保护酶（ＳＯＤ、ＣＡＴ和ＰＯＤ）活性下隆幅度小,灌浆中后期活性水平高。由此认为,小麦旗叶衰老和活性氧代谢特性与其温度型的归属关     

Effect of vitamin C depletion on age-related hearing loss in SMP30/GNL knockout mice

Using senescence marker protein 30 (SMP30)/gluconolactonase (GNL) knockout (KO) mice, which cannot synthesize vitamin C (VC), we examined whether modulating VC level affects age-related hearing loss (AHL). KO and wild-type (WT) C57BL/6 mice were given water containing 1.5 g/L VC [VC(+)] or 37.5 mg/L VC [VC(−)]. At 10 months of age, KO VC(−) mice showed significant reduction in VC level in the inner ear, plasma, and liver, increase in auditory brainstem response (ABR) thresholds, and decrease in the number of spiral ganglion cells compared to WT VC(−), WT VC(+), and KO VC(+) mice. There were no differences in VC level in the inner ear, ABR thresholds, or the number of spiral ganglion cells among WT VC(−), WT VC(+), and KO VC(+) mice. These findings suggest that VC depletion can accelerate AHL but that supplementing VC may not increase VC level in the inner ear or slow AHL in mice.