Effects of Exogenous Application of GA4+7 and NAA on Sugar Accumulation and Related Gene Expression in Peach Fruits During Developing and Ripening Stages

Sweetness is one of the key factors determining peach fruit quality. To better understand the molecular basis of gibberellic acid (GA) and 1-naphthaleneacetic acid (NAA) interference with sugar biosynthesis, a middle-late maturing commercial cultivar, ‘Jinxiu’ yellow peach fruit, was treated with three different concentrations of GA₄₊₇ and four of NAA. Fruit weight, firmness, total soluble solids, different sugar contents and the expression level of sugar-related genes were evaluated. The results showed that maximum increase in cv. ‘Jinxiu’ peach fruit size and sucrose content was with 1.25 mM GA₄₊₇, compared to control fruits and the other treatments during the ripening stages. The sucrose-phosphate synthase gene (PpSPS₂) which had a high level of expression and positive correlation with sucrose content was significantly regulated by 1.25 mM GA₄₊₇ in the final ripening stages. 0.5 mM NAA treatments significantly reduced the sucrose content and fruit size. Ninety percent of the fruits were deformed or dropped from the trees with treatments of 1 mM NAA and 2 mM NAA in the early development period. The crosstalk of different phytohormones and the related genes will be further investigated to get an insight into the inherent association between hormone control and sugar accumulation.

     

Ascorbate distribution during hibernation is independent of ascorbate redox state

Distribution of ascorbate into tissues is an essential process in ascorbate antioxidant defense. Hibernating animals are studied as a model of tolerance to ischemia-reperfusion because of their tolerance to fluctuations in blood flow associated with prolonged torpor and periodic arousal episodes. Throughout hibernation, plasma ascorbate concentration ([Asc](p)) repetitively increases during torpor, then falls during periodic arousal bouts. We previously proposed that high [Asc](p) provides a ready source of antioxidant protection for distribution to the central nervous system and peripheral tissues during arousal. Here we tested whether deliberate oxidation of plasma ascorbate by intravenous administration of ascorbate oxidase (AO), prior to arousal, compromised tissue levels of ascorbate or the other water-soluble antioxidants, glutathione (GSH) and urate. Although AO decreased [Asc](p) to below the level of detection during torpor and after arousal, ascorbate oxidation did not decrease post-arousal tissue levels of reduced ascorbate, glutathione, or urate in any tissue examined, except liver. The data imply that ascorbate is taken up equally well into brain and other tissues as either ascorbate or its oxidized product dehydroascorbate, with subsequent intracellular reduction of dehydroascorbate. Lack of effect of ascorbate oxidation on tissue levels of GSH or urate indicates that dehydroascorbate uptake and reduction do not compromise tissue concentrations of these other water-soluble antioxidants. Thus, we show equal availability of reduced and oxidized plasma ascorbate during metabolically demanding thermogenesis and reperfusion associated with arousal from hibernation.     

Distribution,levels, and activation of MEK1 in Alzheimer's disease

Extracellular-signal-regulated kinase (ERK) has been implicated in the pathogenesis of Alzheimer's disease (AD), but the upstream cascade leading to ERK activation has not been elucidated. In this study, we focused on one of the physiological activators of ERK, mitogen-activated protein kinase (MAPK)/ERK kinase 1 (MEK1). Although there was no significant difference in the level and distribution of total MEK1 between AD and age-matched control cases, increased levels of activated phospho-MEK1 were specifically localized to neuronal intracytoplasmic granular structures in severe AD (Braak stage V-VI). The considerable overlap between MEK1 and its downstream effector, phospho-ERK, suggests both a functional and mechanistic link. Nuclear localization of phospho-MEK1 was a prominent feature in both mild AD cases (Braak stage III-IV) and control cases with limited pathology (Braak stage I-II). Since MEK1 is normally cytoplasmic due to the active export from nucleus because of the presence of nuclear export signal in its amino-terminus, we suspect that the apparent nuclear accumulation of phospho-MEK1 in AD patients at early stages suggests that abnormal nuclear trafficking may contribute to the pathogenesis of AD. By immunoblot analyses, phospho-MEK1 was significantly increased in AD over control cases. Together, these findings lend further credence to the notion that the ERK pathway is dysregulated in AD and also indicate an active role for this pathway in disease pathogenesis.     

Comparative biology and pathology of oxidative stress in Alzheimer and other neurodegenerative diseases: beyond damage and response

In this review, we consider comparative aspects of the biology and pathology of oxygen radicals in neurodegenerative disease and how these findings have influenced our concept of oxidative stress. The common definition of oxidative stress is a breach of antioxidant defenses by oxygen radicals leading to damage to critical molecules and disrupted physiology. Inherent in this definition is that oxidative stress is an unstable situation, for if there is net damage, viability of the system decreases with time, leading to disequilibria and death. While this circumstance defines acute conditions, such as stroke and head trauma which result in dysfunction and death, it does not fit physiological situations or chronic diseases closely aligned to normal physiology. Therefore, we propose that oxidative modifications in Alzheimer disease may actually serve as a homeostatic response to stress resulting in a shift of neuronal priority from normal function to basic survival. This phenomenon is comparable to normal physiological conditions of metabolic decrease, such as those seen in hibernation and estivation. Thus, Alzheimer disease could be seen as part of normal aging that includes additional pathology due to inadequate homeostatic response.     

玉米重金属铅含量的配合力分析与育种对策

选择有代表性的12个玉米自交系,按Griffing4模式组配获得66个组合(F1),用温室盆栽,在3个Pb2+污染水平下对叶片和子粒Pb2+含量配合力和遗传参数进行分析。结果表明:玉米叶片和子粒的Pb2+含量一般配合力与特殊配合力差异均达到显著水平,非加性方差大于加性方差,遗传方差大于环境方差,广义遗传率大于狭义遗传率,该性状的变异主要来自遗传因素,遗传力较强。玉米种质筛选过程中,土壤Pb2+浓度在333.32 mg/kg以下,用亲本郑58组配的组合在筛选时不仅注重子粒Pb2+含量未超标而且要注重叶片Pb2+高富集,其主要是兼顾饲料和粮食安全的同时进行土壤Pb2+污染的生物修复;土壤Pb2+浓度高于715.46 mg/kg时,用亲本178组配的组合筛选应注意叶片和子粒低Pb2+积累的种质选育,对今后在不同Pb2+污染土壤中开展玉米品种筛选和规避污染育种策略的选择具有一定的指导意义。     

Compensatory responses induced by oxidative stress in Alzheimer disease

Oxidative stress occurs early in the progression of Alzheimer disease, significantly before the development of the pathologic hallmarks, neurofibrillary tangles and senile plaques. In the first stage of development of the disease, amyloid-beta deposition and hyperphosphorylated tau function as compensatory responses and downstream adaptations to ensure that neuronal cells do not succumb to oxidative damage. These findings suggest that Alzheimer disease is associated with a novel balance in oxidant homeostasis.