Land plants and DNA barcodes: short-term and long-term goals

Land plants have had the reputation of being problematic for DNA barcoding for two general reasons: (i) the standard DNA regions used in algae, animals and fungi have exceedingly low levels of variability and (ii) the typically used land plant plastid phylogenetic markers (e.g. rbcL, trnL-F, etc.) appear to have too little variation. However, no one has assessed how well current phylogenetic resources might work in the context of identification (versus phylogeny reconstruction). In this paper, we make such an assessment, particularly with two of the markers commonly sequenced in land plant phylogenetic studies, plastid rbcL and internal transcribed spacers of the large subunits of nuclear ribosomal DNA (ITS), and find that both of these DNA regions perform well even though the data currently available in GenBank/EBI were not produced to be used as barcodes and BLAST searches are not an ideal tool for this purpose. These results bode well for the use of even more variable regions of plastid DNA (such as, for example, psbA-trnH) as barcodes, once they have been widely sequenced. In the short term, efforts to bring land plant barcoding up to the standards being used now in other organisms should make swift progress. There are two categories of DNA barcode users, scientists in fields other than taxonomy and taxonomists. For the former, the use of mitochondrial and plastid DNA, the two most easily assessed genomes, is at least in the short term a useful tool that permits them to get on with their studies, which depend on knowing roughly which species or species groups they are dealing with, but these same DNA regions have important drawbacks for use in taxonomic studies (i.e. studies designed to elucidate species limits). For these purposes, DNA markers from uniparentally (usually maternally) inherited genomes can only provide half of the story required to improve taxonomic standards being used in DNA barcoding. In the long term, we will need to develop more sophisticated barcoding tools, which would be multiple, low-copy nuclear markers with sufficient genetic variability and PCR-reliability; these would permit the detection of hybrids and permit researchers to identify the 'genetic gaps' that are useful in assessing species limits.

Oxygen/Glucose deprivation induces a reduction in synaptic AMPA receptors on hippocampal CA3 neurons mediated by mGluR1 and adenosine A3 receptors

Hippocampal CA1 pyramidal neurons are highly sensitive to ischemic damage, whereas neighboring CA3 pyramidal neurons are less susceptible. It is proposed that switching of AMPA receptor (AMPAR) subunits on CA1 neurons during an in vitro model of ischemia, oxygen/glucose deprivation (OGD), leads to an enhanced permeability of AMPARs to Ca2+, resulting in delayed cell death. However, it is unclear whether the same mechanisms exist in CA3 neurons and whether this underlies the differential sensitivity to ischemia. Here, we investigated the consequences of OGD for AMPAR function in CA3 neurons using electrophysiological recordings in rat hippocampal slices. Following a 15 min OGD protocol, a substantial depression of AMPAR-mediated synaptic transmission was observed at CA3 associational/commissural and mossy fiber synapses but not CA1 Schaffer collateral synapses. The depression of synaptic transmission following OGD was prevented by metabotropic glutamate receptor 1 (mGluR1) or A3 receptor antagonists, indicating a role for both glutamate and adenosine release. Inhibition of PLC, PKC, or chelation of intracellular Ca2+ also prevented the depression of synaptic transmission. Inclusion of peptides to interrupt the interaction between GluA2 and PICK1 or dynamin and amphiphysin prevented the depression of transmission, suggesting a dynamin and PICK1-dependent internalization of AMPARs after OGD. We also show that a reduction in surface and total AMPAR protein levels after OGD was prevented by mGluR1 or A3 receptor antagonists, indicating that AMPARs are degraded following internalization. Thus, we describe a novel mechanism for the removal of AMPARs in CA3 pyramidal neurons following OGD that has the potential to reduce excitotoxicity and promote neuroprotection

Playing with history: negotiating subjectivity in contemporary lens based work

Contemporary artists exploring Jewish identity in the UK are caught between two exclusions, broadly speaking: an art community that that sees itself as ‘post –identity’ and a ‘black’ art scene that revolves around the organizations that emerged out of the Identity debates of the 1980s and 1990s, namely Iniva, Third Text, Autograph. These organizations and those debates, don’t usually include Jewish identity within their remit as Jewish artists are considered to be well represented in the British art scene and, in any case, white. Out of these assumptions, questions arise in relation to the position of Jews in Britain and what is at stake for an artist in exploring Jewish Identity in their work. There is considerable scholarship, relatively speaking on art and Jewish Identity in the US (such as Lisa Bloom; Norman Kleeblatt; Catherine Sousslouf), which inform the debates on visual culture and Jews. In this chapter, I will be drawing out some of the distinctions between the US and the UK debates within my analysis, building on my own writing over the last ten years as well as the work of Juliet Steyn, Jon Stratton and Griselda Pollock. In short, this chapter aims to explore the problematic of what Jewish Identity can offer the viewer as art; what place such art inhabits within a wider artistic context and how, if at all, it is received. There is a predominance of lens based work that explores Identity arising out of the provenance of feminist practices and the politics of documentary that will be important in the framing of the work. I do not aim to consider what constitutes a Jewish artist, that has been done elsewhere and is an inadequate and somewhat spurious conversation . I will also not be focusing on artists whose intention is to celebrate an unproblematised Jewishness (however that is constituted in any given work). Recent artworks and scholarship has in any case rendered the trumpeting of attachment to any singular identity anachronistic at best. I will focus on artists working in the UK who incorporate questions of Jewishness into a larger visual enquiry that build on Judith Butler’s notion of identity as process or performative as well as the more recent debates and artwork that consider the intersectionality of identifications that co-constitute provisional identities (Jones, Modood, Sara Ahmed, Braidotti/Nikki S Lee, Glenn Ligon). The case studies to think through these questions of identity, will be artworks by Susan Hiller, Doug Fishbone and Suzanne Triester. In thinking through works by these artists, I will also serve to contextualise them, situating them briefly within the history of the landmark exhibition in the UK, Rubies and Rebels and the work of Ruth Novaczek, Lily Markewitz, Oreet Ashery and myself.

A central role for heme iron in colon carcinogenesis associated with red meat intake

Epidemiology shows that red and processed meat intake is associated with an increased risk of colorectal cancer. Heme iron, heterocyclic amines and endogenous N-nitroso compounds (NOC) are proposed to explain this effect, but their relative contribution is unknown. Our study aimed at determining, at nutritional doses, which is the main factor involved and proposing a mechanism of cancer promotion by red meat. The relative part of heme iron (1% in diet), heterocyclic amines (PhIP+MeIQx, 50+25 μg/kg in diet) and NOC (induced by NaNO2+NaNO3 0.17+0.23 g/l of drinking water) was determined by a factorial design and preneoplastic endpoints in chemically-induced rats and validated on tumors in Min mice. The molecular mechanisms (genotoxicity, cytotoxicity) were analyzed in vitro in normal and Apc- deficient cell lines and confirmed on colon mucosa. Heme iron increased the number of preneoplastic lesions but dietary heterocyclic amines and NOC had no effect on carcinogenesis in rats. Dietary hemoglobin increased tumor load in Min mice (control diet: 67±39 mm2; 2,5% hemoglobin diet: 114±47 mm2, p=0.004). In vitro, fecal water from rats given hemoglobin was rich in aldehydes and was cytotoxic to normal cells, but not to premalignant cells. The aldehydes 4-hydroxynonenal and 4-hydroxyhexenal were more toxic to normal versus mutated cells and were only genotoxic to normal cells. Genotoxicity was also observed in colon mucosa of mice given hemoglobin. These results highlight the role of heme iron in the promotion of colon cancer by red meat and suggest that heme iron could initiate carcinogenesis through lipid peroxidation.