No supernovae associated with two long-duration gamma-ray bursts

It is now accepted that long-duration gamma-ray bursts (GRBs) are produced during the collapse of a massive star. The standard 'collapsar' model predicts that a broad-lined and luminous type Ic core-collapse supernova accompanies every long-duration GRB. This association has been confirmed in observations of several nearby GRBs. Here we report that GRB 060505 (ref. 10) and GRB 060614 (ref. 11) were not accompanied by supernova emission down to limits hundreds of times fainter than the archetypal supernova SN 1998bw that accompanied GRB 980425, and fainter than any type Ic supernova ever observed. Multi-band observations of the early afterglows, as well as spectroscopy of the host galaxies, exclude the possibility of significant dust obscuration and show that the bursts originated in actively star-forming regions. The absence of a supernova to such deep limits is qualitatively different from all previous nearby long-duration GRBs and suggests a new phenomenological type of massive stellar death.     

Retinopathy and attenuated circadian entrainment in Crx-deficient mice

Crx, an Otx-like homeobox gene, is expressed specifically in the photoreceptors of the retina and the pinealocytes of the pineal gland. Crx has been proposed to have a role in the regulation of photoreceptor-specific genes in the eye and of pineal-specific genes in the pineal gland. Mutations in human CRX are associated with the retinal diseases, cone-rod dystrophy-2 (adCRD2; refs 3, 4, 5), retinitis pigmentosa (RP) and Leber congenital amaurosis (LCA), which all lead to loss of vision. We generated mice carrying a targeted disruption of Crx. Crx-/- mice do not elaborate photoreceptor outer segments and lacked rod and cone activity as assayed by electroretinogram (ERG). Expression of several photoreceptor- and pineal-specific genes was reduced in Crx mutants. Circadian entrainment was also affected in Crx-/- mice.     

Comparative genomes of Chlamydia pneumoniae and C. trachomatis

Chlamydia are obligate intracellular eubacteria that are phylogenetically separated from other bacterial divisions. C. trachomatis and C. pneumoniae are both pathogens of humans but differ in their tissue tropism and spectrum of diseases. C. pneumoniae is a newly recognized species of Chlamydia that is a natural pathogen of humans, and causes pneumonia and bronchitis. In the United States, approximately 10% of pneumonia cases and 5% of bronchitis cases are attributed to C. pneumoniae infection. Chronic disease may result following respiratory-acquired infection, such as reactive airway disease, adult-onset asthma and potentially lung cancer. In addition, C. pneumoniae infection has been associated with atherosclerosis. C. trachomatis infection causes trachoma, an ocular infection that leads to blindness, and sexually transmitted diseases such as pelvic inflammatory disease, chronic pelvic pain, ectopic pregnancy and epididymitis. Although relatively little is known about C. trachomatis biology, even less is known concerning C. pneumoniae. Comparison of the C. pneumoniae genome with the C. trachomatis genome will provide an understanding of the common biological processes required for infection and survival in mammalian cells. Genomic differences are implicated in the unique properties that differentiate the two species in disease spectrum. Analysis of the 1,230,230-nt C. pneumoniae genome revealed 214 protein-coding sequences not found in C. trachomatis, most without homologues to other known sequences. Prominent comparative findings include expansion of a novel family of 21 sequence-variant outer-membrane proteins, conservation of a type-III secretion virulence system, three serine/threonine protein kinases and a pair of parologous phospholipase-D-like proteins, additional purine and biotin biosynthetic capability, a homologue for aromatic amino acid (tryptophan) hydroxylase and the loss of tryptophan biosynthesis genes.     

Hydrological response to a seafloor spreading episode on the Juan de Fuca ridge

Seafloor hydrothermal systems are known to respond to seismic and magmatic activity along mid-ocean ridges, often resulting in locally positive changes in hydrothermal discharge rate, temperature and microbial activity, and shifts in composition occurring at the time of earthquake swarms and axial crustal dike injections. Corresponding regional effects have also been observed. Here we present observations of a hydrological response to seafloor spreading activity, which resulted in a negative formation-fluid pressure transient during and after an earthquake swarm in the sediment-sealed igneous crust of the Middle Valley rift of the northernmost Juan de Fuca ridge. The observations were made with a borehole seal and hydrologic observatory originally established in 1991 to study the steady-state pressure and temperature conditions in this hydrothermally active area. The magnitude of the co-seismic response is consistent with the elastic strain that would be expected from the associated earthquakes, but the prolonged negative pressure transient after the swarm is surprising and suggests net co-seismic dilatation of the upper, permeable igneous crust. The rift valley was visited four weeks after the onset of the seismic activity, but no signature of increased hydrothermal activity was detected in the water column. It appears that water, not magma, filled the void left by this spreading episode.     

Regulation of innate and adaptive immune responses by MAP kinase phosphatase 5

Mitogen-activated protein (MAP) kinases are essential regulators in immune responses, and their activities are modulated by kinases and phosphatases. MAP kinase phosphatase (MKP) is a family of dual-specificity phosphatases whose function is evolutionarily conserved. A number of mammalian MKPs have been identified so far, but their specific physiological functions in negative regulation of MAP kinases have not been genetically defined. Here we examine innate and adaptive immune responses in the absence of MKP5. JNK activity was selectively increased in Mkp5 (also known as Dusp10)-deficient mouse cells. Mkp5-deficient cells produced greatly enhanced levels of pro-inflammatory cytokines during innate immune responses and exhibited greater T-cell activation than their wild-type counterparts. However, Mkp5-deficient T cells proliferated poorly upon activation, which resulted in increased resistance to experimental autoimmune encephalomyelitis. By contrast, Mkp5-deficient CD4(+) and CD8(+) effector T cells produced significantly increased levels of cytokines compared with wild-type cells, which led to much more robust and rapidly fatal immune responses to secondary infection with lymphocytic choriomeningitis virus. Therefore, MKP5 has a principal function in both innate and adaptive immune responses, and represents a novel target for therapeutic intervention of immune diseases.     

Cenozoic climate change as a possible cause for the rise of the Andes

Causal links between the rise of a large mountain range and climate have often been considered to work in one direction, with significant uplift provoking climate change. Here we propose a mechanism by which Cenozoic climate change could have caused the rise of the Andes. Based on considerations of the force balance in the South American lithosphere, we suggest that the height of, and tectonics in, the Andes are strongly controlled both by shear stresses along the plate interface in the subduction zone and by buoyancy stress contrasts between the trench and highlands, and shear stresses in the subduction zone depend on the amount of subducted sediments. We propose that the dynamics of subduction and mountain-building in this region are controlled by the processes of erosion and sediment deposition, and ultimately climate. In central South America, climate-controlled sediment starvation would then cause high shear stress, focusing the plate boundary stresses that support the high Andes.     

Comparative analysis of the genome sequences of Bordetella pertussis,Bordetella parapertussis and Bordetella bronchiseptica

Bordetella pertussis, Bordetella parapertussis and Bordetella bronchiseptica are closely related Gram-negative beta-proteobacteria that colonize the respiratory tracts of mammals. B. pertussis is a strict human pathogen of recent evolutionary origin and is the primary etiologic agent of whooping cough. B. parapertussis can also cause whooping cough, and B. bronchiseptica causes chronic respiratory infections in a wide range of animals. We sequenced the genomes of B. bronchiseptica RB50 (5,338,400 bp; 5,007 predicted genes), B. parapertussis 12822 (4,773,551 bp; 4,404 genes) and B. pertussis Tohama I (4,086,186 bp; 3,816 genes). Our analysis indicates that B. parapertussis and B. pertussis are independent derivatives of B. bronchiseptica-like ancestors. During the evolution of these two host-restricted species there was large-scale gene loss and inactivation; host adaptation seems to be a consequence of loss, not gain, of function, and differences in virulence may be related to loss of regulatory or control functions.     

Evidence for cold events in the early Holocene from the Guliya ice core, Tibetan Plateau, China

Evidence for the “8.2 ka cold event” has been provided mostly from the circum-North Atlantic area. However, whether this cold event occurred in other places is a key to understanding its cause. Here, we provide the evidence for the “8.2 ka cold event” from the Guliya ice core in the northwest Tibetan Plateau, and it was found that the peak cooling (~8.3—8.2 ka) in this ice core was about 7.8—10℃, which was larger than the cooling in the North Atlantic region. The primary causes for this episode were diminished solar activity and weakened thermohaline circulation. Moreover, another weak cold event, centered about 9.4 ka, was also recorded in the Guliya ice core record. These two cold events were concurrent with the ice-rafting episodes in the North Atlantic during the early Holocene, which implies that the millennial-scale climatic cyclicity might exist in the Tibetan Plateau as well as in the North Atlantic.