Blue light and UV radiation accelerate spring and autumn leaf phenology in temperate tree species

Non peer reviewe

Robustness of hierarchical spatial critical infrastructure networks

PhD ThesisThe economic state and wellbeing of a nation is dependent upon the critical infrastructure networks that deliver resources, goods and services. However, these are increasingly exposed to a number of hazards, both natural and man-made, which threaten to disrupt their ability to function. It is essential that in order to develop long-term strategic plans of infrastructure provision we are able to understand their current robustness to such hazards. The robustness of critical infrastructure networks has typically been investigated from a topological perspective as a means of simplifying the complexities associated with their analysis. Such work has led to many studies suggesting critical infrastructures exhibit a topological structure, from random to exponential degree distributions. However, often such analysis ignores the explicit spatial characteristics of the node and edge assets. Furthermore, the very nature of topological analysis means that flows/movements that take place over such networks cannot be considered. This work addresses these weaknesses by extending traditional topological analysis to consider emergent properties critical infrastructure networks exhibit when considering higher-order connectivity and flows. An analysis of a suite of synthetic networks with a spectrum of topologies alongside real infrastructure spatial networks, in terms of their basic topology and high-order connectivity, shows that a number of critical infrastructure networks seem to be better characterised as hierarchical networks. Subsequent failure modelling reveals that such hierarchical networks responded in a dramatically different manner to perturbations; complete failure occurring approximately 19 and 34 percent sooner for random and targeted failures compared to random networks. Such poor robustness is further exacerbated when flow simulation modelling over the resulting hierarchical networks is undertaken, revealing particular sensitivity to cascading failures from spatial hazards. In light of these results, it is suggested that it is essential to improve the robustness of critical infrastructure networks that exhibit a hierarchical spatial organisation.School of Civil Engineering and Geosciences, Newcastle University

Design of a low power 80386 based system

Call number: LD2668 .T4 EECE 1989 R63Master of ScienceElectrical and Computer Engineerin

Survival outcome and EMT suppression mediated by a lectin domain interaction of Endo180 and CD147

Epithelial cell-cell contacts maintain normal glandular tissue homeostasis, and their breakage can trigger epithelial-to-mesenchymal transition (EMT), a fundamental step in the development of metastatic cancer. Despite the ability of C-type lectin domains (CTLD) to modulate cell-cell adhesion, it is not known if they modulate epithelial adhesion in EMT and tumor progression. Here, the multi-CTLD mannose receptor, Endo180 (MRC2/uPARAP), was shown using the Kaplan-Meier analysis to be predictive of survival outcome in men with early prostate cancer. A proteomic screen of novel interaction partners with the fourth CTLD (CTLD4) in Endo180 revealed that its complex with CD147 is indispensable for the stability of three-dimensional acini formed by nontransformed prostate epithelial cells (PEC). Mechanistic study using knockdown of Endo180 or CD147, and treatment with an Endo180 mAb targeting CTLD4 (clone 39.10), or a dominant-negative GST-CTLD4 chimeric protein, induced scattering of PECs associated with internalization of Endo180 into endosomes, loss of E-cadherin (CDH1/ECAD), and unzipping of cell-cell junctions. These findings are the first to demonstrate that a CTLD acts as a suppressor and regulatory switch for EMT; thus, positing that stabilization of Endo180-CD147 complex is a viable therapeutic strategy to improve rates of prostate cancer survival

The influence of spectral composition on spring and autumn phenology in trees

Several recent reviews highlight the molecular mechanisms that underpin phenological responses to temperature and photoperiod; however, these have mostly overlooked the influence of solar radiation and its spectral composition on these processes. For instance, solar radiation in the blue and ultraviolet (UV) regions of the spectrum, as well as the red/far-red (R:FR) ratio, can influence spring and autumn phenology. Solar radiation reaching the Earth changes diurnally and seasonally; however, rising global temperatures, latitudinal range shifts and light pollution are likely to produce novel combinations of phenological cues for tree species. Here, we review the literature on phenological responses to spectral composition. Our objective was to explore the natural variation in spectral composition using radiative transfer models and to reveal any species-specific or ecotype-specific responses relating to latitudinal origin. These responses are likely to be most pronounced at high latitudes where spectral composition varies most throughout the year. For instance, trees from high latitudes tend to be more sensitive to changes in R:FR than those from low latitudes. The effects of blue light and UV radiation on phenology have not been studied as much as those of R:FR, but the limited results available suggest both could be candidate cues affecting autumn leaf colouration and senescence. Failure of more–southern species and ecotypes to adapt and use spectral cues during northwards range shifts could result in mistimed phenology, potentially resulting in frost damage, reduced fitness and limited range expansion. Future areas for research should look to establish how consistently different functional types of tree respond to spectral cues and identify photoreceptor-mediated mechanisms that allow plants to combine information from multiple light cues to coordinate the timing of phenological events. It should then be feasible to consider the synchronous or sequential action of light cues within a hierarchy of environmental factors regulating phenology.Peer reviewe

Understorey light quality affects leaf pigments and leaf phenology in different plant functional types

Forest understorey plants receive most sunlight in springtime before canopy closure, and in autumn following leaf-fall. We hypothesized that plant species must adjust their phenological and photoprotective strategies in response to large changes in the spectral composition of the sunlight they receive. Here, we identified how plant species growing in northern deciduous and evergreen forest understoreys differ in their response to blue light and ultraviolet (UV) radiation according to their functional strategy. We installed filters in a forest understorey in southern Finland, to create the following treatments attenuating: UV radiation < 350 nm, all UV radiation (< 400 nm), all blue light and UV radiation (< 500 nm), and a transparent control. In eight species, representing different functional strategies, we assessed leaf optical properties, phenology, and epidermal flavonoid contents over two years. Blue light accelerated leaf senescence in all species measured in the understorey, apart from Quercus robur seedlings, whereas UV radiation only accelerated leaf senescence in Acer platanoides seedlings. More light-demanding species accumulated flavonols in response to seasonal changes in light quality compared to shade-tolerant and wintergreen species and were particularly responsive to blue light. Reduction of blue and UV radiation under shade reveals an important role for microclimatic effects on autumn phenology and leaf photoprotection. An extension of canopy cover under climate change, and its associated suppression of understorey blue light and UV radiation, may delay leaf senescence for understorey species with an autumn niche.Peer reviewe

Deubiquitinating enzymes as oncotargets

Carcinogenesis is a complex process tightly regulated at multiple levels by post-translational modifications. Epigenetics plays a major role in cancer development, all stable changes to the gene expression process that are not a result of a direct change in the DNA code are described as epigenetics. Epigenetic processes are regulated by post-translational modifications including ubiquitination which can directly affect either histones or transcription factors or may target their co-factors and interacting partners exerting an indirect effect. Deubiquitination of these target proteins is equally important and alterations in this pathway can also lead to cancer development, progression and metastasis. Only the correct, unaltered balance between ubiquitination and deubiquitination ensures healthy cellular homeostasis. In this review we focus on the role of deubiquitinating (DUB) enzymes in various aspects of epigenetics including the regulation of transcription factors, histone modifications, DNA damage repair pathways and cell cycle regulation. We discuss the impact of those processes on tumourigenesis and potential therapeutic applications of DUBs for cancer treatment

Greater capacity to exploit warming temperatures in northern populations of European beech is partly driven by delayed leaf senescence

One of the most widespread consequences of climate change is the disruption of trees’ phenological cycles. The extent to which tree phenology varies with local climate is largely genetically determined, and while a combination of temperature and photoperiodic cues are typically found to trigger bud burst (BB) in spring, it has proven harder to identify the main cues driving leaf senescence (LS) in autumn. We used 905 individual field observations of BB and LS from six Fagus sylvatica populations, covering the range of environmental conditions found across the species distribution, to: (i) estimate the dates of BB and LS of these populations; (ii) assess the main drivers of LS; and (iii) predict the likely variation in growing season length (GSL; defined as the period from BB to LS timing) across populations under current and future climate scenarios. To this end, we first calibrated linear mixed-effects models for LS as a function of temperature, insolation and BB date. Secondly, we calculated GSL for each population as the number of days between BB and LS. We found that: i) there were larger differences among populations in the date of BB than in the date of LS; ii) the temperature through September, October and November was the main determinant of LS, although covariation of temperature with daily insolation and precipitation-related variables suggests that all three variables may affect LS timing; and iii) GSL was predicted to increase in northern populations and to shrink in central and southern populations under climate change. Consequently, the large present-day differences in GSL across the range of beech are likely to decrease under future climates where rising temperatures will alter the relationship between BB and LS. Northern populations are likely to increase their productivity as warmer conditions will enable them to extend their growing season.Peer reviewe

The histone demethylase enzyme KDM3A is a key estrogen receptor regulator in breast cancer

Endocrine therapy has successfully been used to treat estrogen receptor (ER)-positive breast cancer, but this invariably fails with cancers becoming refractory to treatment. Emerging evidence has suggested that fluctuations in ER co-regulatory protein expression may facilitate resistance to therapy and be involved in breast cancer progression. To date, a small number of enzymes that control methylation status of histones have been identified as co-regulators of ER signalling. We have identified the histone H3 lysine 9 mono- and di-methyl demethylase enzyme KDM3A as a positive regulator of ER activity. Here, we demonstrate that depletion of KDM3A by RNAi abrogates the recruitment of the ER to cis-regulatory elements within target gene promoters, thereby inhibiting estrogen-induced gene expression changes. Global gene expression analysis of KDM3A-depleted cells identified gene clusters associated with cell growth. Consistent with this, we show that knockdown of KDM3A reduces ER-positive cell proliferation and demonstrate that KDM3A is required for growth in a model of endocrine therapy-resistant disease. Crucially, we show that KDM3A catalytic activity is required for both ER-target gene expression and cell growth, demonstrating that developing compounds which target demethylase enzymatic activity may be efficacious in treating both ER-positive and endocrine therapy-resistant disease