Stability of organic carbon in deep soil layers controlled by fresh carbon supply

The world's soils store more carbon than is present in biomass and in the atmosphere. Little is known, however, about the factors controlling the stability of soil organic carbon stocks and the response of the soil carbon pool to climate change remains uncertain. We investigated the stability of carbon in deep soil layers in one soil profile by combining physical and chemical characterization of organic carbon, soil incubations and radiocarbon dating. Here we show that the supply of fresh plant-derived carbon to the subsoil (0.6-0.8 m depth) stimulated the microbial mineralization of 2,567 +/- 226-year-old carbon. Our results support the previously suggested idea that in the absence of fresh organic carbon, an essential source of energy for soil microbes, the stability of organic carbon in deep soil layers is maintained. We propose that a lack of supply of fresh carbon may prevent the decomposition of the organic carbon pool in deep soil layers in response to future changes in temperature. Any change in land use and agricultural practice that increases the distribution of fresh carbon along the soil profile could however stimulate the loss of ancient buried carbon.     

A biophysical signature of network affiliation and sensory processing in mitral cells

One defining characteristic of the mammalian brain is its neuronal diversity. For a given region, substructure, layer or even cell type, variability in neuronal morphology and connectivity persists. Although it is well known that such cellular properties vary considerably according to neuronal type, the substantial biophysical diversity of neurons of the same morphological class is typically averaged out and ignored. Here we show that the amplitude of hyperpolarization-evoked sag of membrane potential recorded in olfactory bulb mitral cells is an emergent, homotypic property of local networks and sensory information processing. Simultaneous whole-cell recordings from pairs of cells show that the amount of hyperpolarization-evoked sag potential and current (Ih) is stereotypic for mitral cells belonging to the same glomerular circuit. This is corroborated by a mosaic, glomerulus-based pattern of expression of the HCN2 (hyperpolarization-activated cyclic nucleotide-gated channel 2) subunit of the Ih channel. Furthermore, inter-glomerular differences in both membrane potential sag and HCN2 protein are diminished when sensory input to glomeruli is genetically and globally altered so that only one type of odorant receptor is universally expressed. Population diversity in this intrinsic property therefore reflects differential expression between local mitral cell networks processing distinct odour-related information.     

Espaliers: A generalization of dendrograms

Dendrograms are widely used to represent graphically the clusters and partitions obtained with hierarchical clustering schemes. Espaliers are generalized dendrograms in which the length of horizontal lines is used in addition to their level in order to display the values of two characteristics of each cluster (e.g., the split and the diameter) instead of only one. An algorithm is first presented to transform a dendrogram into an espalier without rotation of any part of the former. This is done by stretching some of the horizontal lines to obtain a diagram with vertical and horizontal lines only, the cutting off by diagonal lines the parts of the horizontal lines exceeding their prescribed length. The problem of finding if, allowing rotations, no diagonal lines are needed is solved by anO(N ²) algorithm whereN is the number of entities to be classified. This algorithm is the generalized to obtain espaliers with minimum width and, possibly, some diagonal lines.Work of the first and second authors has been supported by FCAR (Fonds pour la Formation de Chercheurs et l'Aide à la Recherche) grant 92EQ1048, and grant N00014-92-J-1194 from the Office of Naval Research. Work of the first author has also been supported by NSERC (Natural Sciences and Engineering Research Council of Canada) grant to École des Hautes Études Commerciales, Montréal and by NSERC grant GP0105574. Work of the second author has been supported by NSERC grant GP0036426, by FCAR grant 90NC0305, and by an NSF Professorship for Women in Science at Princeton University from September 1990 until December 1991. Work of the third author was done in part during a visit to GERAD, Montréal.     

Endothelial signaling and the molecular basis of arteriovenous malformation

Arteriovenous malformations occur when abnormalities of vascular patterning result in the flow of blood from arteries to veins without an intervening capillary bed. Recent work has revealed the importance of the Notch and TGF-β signaling pathways in vascular patterning. Specifically, Notch signaling has an increasingly apparent role in arterial specification and suppression of branching, whereas TGF-β is implicated in vascular smooth muscle development and remodeling under angiogenic stimuli. These physiologic roles, consequently, have implicated both pathways in the pathogenesis of arteriovenous malformation. In this review, we summarize the studies of endothelial signaling that contribute to arteriovenous malformation and the roles of genes implicated in their pathogenesis. We further discuss how endothelial signaling may contribute to vascular smooth muscle development and how knowledge of signaling pathways may provide us targets for medical therapy in these vascular lesions.     

Multiple self-healing squamous epithelioma is caused by a disease-specific spectrum of mutations in TGFBR1

Multiple self-healing squamous epithelioma (MSSE), also known as Ferguson-Smith disease (FSD), is an autosomal-dominant skin cancer condition characterized by multiple squamous-carcinoma-like locally invasive skin tumors that grow rapidly for a few weeks before spontaneously regressing, leaving scars. High-throughput genomic sequencing of a conservative estimate (24.2 Mb) of the disease locus on chromosome 9 using exon array capture identified independent mutations in TGFBR1 in three unrelated families. Subsequent dideoxy sequencing of TGFBR1 identified 11 distinct monoallelic mutations in 18 affected families, firmly establishing TGFBR1 as the causative gene. The nature of the sequence variants, which include mutations in the extracellular ligand-binding domain and a series of truncating mutations in the kinase domain, indicates a clear genotype-phenotype correlation between loss-of-function TGFBR1 mutations and MSSE. This distinguishes MSSE from the Marfan syndrome-related disorders in which missense mutations in TGFBR1 lead to developmental defects with vascular involvement but no reported predisposition to cancer.     

Searching for “signal 2”: costimulation requirements of γδ T cells

T cell activation requires the integration of signals that arise from various types of receptors. Although TCR triggering is a necessary condition, it is often not sufficient to induce full T-cell activation, as reflected in cell proliferation and cytokine secretion. This has been firmly demonstrated for conventional αβ T cells, for which a large panel of costimulatory receptors has been identified. By contrast, the area remains more obscure for unconventional, innate-like γδ T cells, as the literature has been scarce and at times contradictory. Here we review the current state of the art on the costimulatory requirements of γδ T cell activation. We highlight the roles of members of the immunoglobulin (like CD28 or JAML) or tumour necrosis factor receptor (like CD27) superfamilies of coreceptors, but also of more atypical costimulatory molecules, such as NKG2D or CD46. Finally, we identify various areas where our knowledge is still markedly insufficient, hoping to provoke future research on γδ T cell costimulation.     

Mutations in CEP290, which encodes a centrosomal protein, cause pleiotropic forms of Joubert syndrome

Joubert syndrome-related disorders (JSRD) are a group of syndromes sharing the neuroradiological features of cerebellar vermis hypoplasia and a peculiar brainstem malformation known as the 'molar tooth sign'. We identified mutations in the CEP290 gene in five families with variable neurological, retinal and renal manifestations. CEP290 expression was detected mostly in proliferating cerebellar granule neuron populations and showed centrosome and ciliary localization, linking JSRDs to other human ciliopathies.