Meteoritic dust from the atmospheric disintegration of a large meteoroid

Much of the mass of most meteoroids entering the Earth's atmosphere is consumed in the process of ablation. Larger meteoroids (> 10 cm), which in some cases reach the ground as meteorites, typically have survival fractions near 1-25 per cent of their initial mass. The fate of the remaining ablated material is unclear, but theory suggests that much of it should recondense through coagulation as nanometre-sized particles. No direct measurements of such meteoric 'smoke' have hitherto been made. Here we report the disintegration of one of the largest meteoroids to have entered the Earth's atmosphere during the past decade, and show that the dominant contribution to the mass of the residual atmospheric aerosol was in the form of micrometre-sized particles. This result is contrary to the usual view that most of the material in large meteoroids is efficiently converted to particles of much smaller size through ablation. Assuming that our observations are of a typical event, we suggest that large meteoroids provide the dominant source of micrometre-sized meteoritic dust at the Earth's surface over long timescales.     

Dendrite growth increased by visual activity requires NMDA receptor and Rho GTPases

Previous studies suggest that neuronal activity may guide the development of synaptic connections in the central nervous system through mechanisms involving glutamate receptors and GTPase-dependent modulation of the actin cytoskeleton. Here we demonstrate by in vivo time-lapse imaging of optic tectal cells in Xenopus laevis tadpoles that enhanced visual activity driven by a light stimulus promotes dendritic arbor growth. The stimulus-induced dendritic arbor growth requires glutamate-receptor-mediated synaptic transmission, decreased RhoA activity and increased Rac and Cdc42 activity. The results delineate a role for Rho GTPases in the structural plasticity driven by visual stimulation in vivo.     

Changing potency by spontaneous fusion

Recent reports have suggested that mammalian stem cells residing in one tissue may have the capacity to produce differentiated cell types for other tissues and organs 1-9. Here we define a mechanism by which progenitor cells of the central nervous system can give rise to non-neural derivatives. Cells taken from mouse brain were co-cultured with pluripotent embryonic stem cells. Following selection for a transgenic marker carried only by the brain cells, undifferentiated stem cells are recovered in which the brain cell genome has undergone epigenetic reprogramming. However, these cells also carry a transgenic marker and chromosomes derived from the embryonic stem cells. Therefore the altered phenotype does not arise by direct conversion of brain to embryonic stem cell but rather through spontaneous generation of hybrid cells. The tetraploid hybrids exhibit full pluripotent character, including multilineage contribution to chimaeras. We propose that transdetermination consequent to cell fusion 10 could underlie many observations otherwise attributed to an intrinsic plasticity of tissue stem cells 9.     

Sequence and analysis of chromosome 2 of Dictyostelium discoideum

The genome of the lower eukaryote Dictyostelium discoideum comprises six chromosomes. Here we report the sequence of the largest, chromosome 2, which at 8 megabases (Mb) represents about 25% of the genome. Despite an A + T content of nearly 80%, the chromosome codes for 2,799 predicted protein coding genes and 73 transfer RNA genes. This gene density, about 1 gene per 2.6 kilobases (kb), is surpassed only by Saccharomyces cerevisiae (one per 2 kb) and is similar to that of Schizosaccharomyces pombe (one per 2.5 kb). If we assume that the other chromosomes have a similar gene density, we can expect around 11,000 genes in the D. discoideum genome. A significant number of the genes show higher similarities to genes of vertebrates than to those of other fully sequenced eukaryotes. This analysis strengthens the view that the evolutionary position of D. discoideum is located before the branching of metazoa and fungi but after the divergence of the plant kingdom, placing it close to the base of metazoan evolution.     

Laboratory fattening and dietary-fat effects on Meadow voles ( Microtus pennsylvanicus )

When removed from the field and maintained under laboratory conditions, meadow voles exhibited significant change in body composition. Voles increased body mass due primarily to large gains in lipid mass combined with small losses in fat-free mass. Lipid deposition amounts increased as dietary fat was increased, and animals demonstrated a leveling of body mass instead of continuous unregulated obesity. When dietary fat content was changed, lipid deposition or utilization responded directly. Thus, meadow voles regulate overall body mass and body composition (lipid and fat-free mass) at levels that correspond to dietary quality (fat) and abundance in the laboratory, and they deposit considerably more lipid than do animals in the field. Our experiments demonstrate that food quality has a substantial effect on the body composition of wild-caught animals maintained in the laboratory.     

New records and species of Tetranychidae and Tenuipalpidae (Acarina) from Utah and Idaho

Twenty-three species of spider mites (Tetranychidae) are recognized for Utah and Idaho; three of these are described as new: Bryobia neoribis, Pseudobryobia knowltoni, and Schizotetranychus agropyron. Eleven species of Tenuipalpidae are recorded.     

RIP3 mediates the embryonic lethality of caspase-8-deficient mice

Apoptosis and necroptosis are complementary pathways controlled by common signalling adaptors, kinases and proteases; among these, caspase-8 (Casp8) is critical for death receptor-induced apoptosis. This caspase has also been implicated in non-apoptotic pathways that regulate Fas-associated via death domain (FADD)-dependent signalling and other less defined biological processes as diverse as innate immune signalling and myeloid or lymphoid differentiation patterns. Casp8 suppresses RIP3-RIP1 (also known as RIPK3-RIPK1) kinase complex-dependent necroptosis that follows death receptor activation as well as a RIP3-dependent, RIP1-independent necrotic pathway that has emerged as a host defence mechanism against murine cytomegalovirus. Disruption of Casp8 expression leads to embryonic lethality in mice between embryonic days 10.5 and 11.5 (ref. 7). Thus, Casp8 may naturally hold alternative RIP3-dependent death pathways in check in addition to promoting apoptosis. We find that RIP3 is responsible for the mid-gestational death of Casp8-deficient embryos. Remarkably, Casp8(-/-)Rip3(-/-) double mutant mice are viable and mature into fertile adults with a full immune complement of myeloid and lymphoid cell types. These mice seem immunocompetent but develop lymphadenopathy by four months of age marked by accumulation of abnormal T cells in the periphery, a phenotype reminiscent of mice with Fas-deficiency (lpr/lpr; also known as Fas). Thus, Casp8 contributes to homeostatic control in the adult immune system; however, RIP3 and Casp8 are together completely dispensable for mammalian development.