Persistence of soil organic matter as an ecosystem property

Globally, soil organic matter (SOM) contains more than three times as much carbon as either the atmosphere or terrestrial vegetation. Yet it remains largely unknown why some SOM persists for millennia whereas other SOM decomposes readily--and this limits our ability to predict how soils will respond to climate change. Recent analytical and experimental advances have demonstrated that molecular structure alone does not control SOM stability: in fact, environmental and biological controls predominate. Here we propose ways to include this understanding in a new generation of experiments and soil carbon models, thereby improving predictions of the SOM response to global warming.     

Sialic acid-specific lectins: occurrence, specificity and function

Sialic acids consist of a family of acidic ninecarbon sugars that are typically located at the terminal positions of a variety of glycoconjugates. Naturally occurring sialic acids show an immense diversity of structure, and this reflects their involvement in a variety of biologically important processes. One such process involves the direct participation of sialic acids in recognition events through specific interactions with lectins, a family of proteins that recognise and bind sugars. This review will present a detailed overview of our current knowledge regarding the occurrence, specificity and function of sialic acid-specific lectins, particularly those that occur in viruses, bacteria and non-vertebrate eukaryotes. Received 13 December 2005; received after revision 9 February 2006; accepted 15 February 2006     

Tetraspanin15 regulates cellular trafficking and activity of the ectodomain sheddase ADAM10

A disintegrin and metalloproteinase10 (ADAM10) has been implicated as a major sheddase responsible for the ectodomain shedding of a number of important surface molecules including the amyloid precursor protein and cadherins. Despite a well-documented role of ADAM10 in health and disease, little is known about the regulation of this protease. To address this issue we conducted a split-ubiquitin yeast two-hybrid screen to identify membrane proteins that interact with ADAM10. The yeast experiments and co-immunoprecipitation studies in mammalian cell lines revealed tetraspanin15 (TSPAN15) to specifically associate with ADAM10. Overexpression of TSPAN15 or RNAi-mediated knockdown of TSPAN15 led to significant changes in the maturation process and surface expression of ADAM10. Expression of an endoplasmic reticulum (ER) retention mutant of TSPAN15 demonstrated an interaction with ADAM10 already in the ER. Pulse-chase experiments confirmed that TSPAN15 accelerates the ER-exit of the ADAM10-TSPAN15 complex and stabilizes the active form of ADAM10 at the cell surface. Importantly, TSPAN15 also showed the ability to mediate the regulation of ADAM10 protease activity exemplified by an increased shedding of N-cadherin and the amyloid precursor protein. In conclusion, our data show that TSPAN15 is a central modulator of ADAM10-mediated ectodomain shedding. Therapeutic manipulation of its expression levels may be an additional approach to specifically regulate the activity of the amyloid precursor protein alpha-secretase ADAM10.     

The Drosophila posterior-group gene nanos functions by repressing hunchback activity

The development of the body plan in the Drosophila embryo depends on the activity of maternal determinants localized at the anterior and posterior of the egg. These activities define both the polarity of the anterior-posterior (AP) axis and the spatial domains of expression of the zygotic gap genes, which in turn control the subsequent steps in segmentation. The nature and mode of action of one anterior determinant, the bicoid(bcd) gene product, has recently been defined, but the posterior determinants are less well characterized. At least seven maternally acting genes are required for posterior development. Mutations in these maternal posterior-group genes result in embryos lacking all abdominal segments. Cytoplasmic transplantation studies indicate that the maternally encoded product of the nanos(nos) gene may act as an abdominal determinant, whereas the other maternal posterior-group genes appear to be required for the appropriate localization and stabilization of this signal. Here we show that the lack of the nos gene product can be compensated for by eliminating the maternal activity of the gap gene hunchback (hb). Embryos lacking both of these maternally derived gene products are viable and can survive as fertile adults. These results suggest that the nos gene product functions by repressing the activity of the maternal hb products in the posterior of the egg.     

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