Haze optical depth in exoplanet atmospheres varies with rotation rate: Implications for observations

Transmission spectroscopy supports the presence of uncharacterised, light-scattering and -absorbing aerosols in the atmospheres of many exoplanets. The complexity of factors influencing the formation, 3-D transport, radiative impact, and removal of aerosols makes it challenging to match theoretical models to the existing data. Our study simplifies these factors to focus on the interaction between planetary general circulation and haze distribution at the planetary limb. We use an intermediate complexity general circulation model, ExoPlaSim, to simulate idealised organic haze particles as radiatively active tracers in the atmospheres of tidally locked terrestrial planets for 32 rotation rates. We find three distinct 3-D spatial haze distributions, corresponding to three circulation regimes, each with a different haze profile at the limb. All regimes display significant terminator asymmetry. In our parameter space, super-Earth-sized planets with rotation periods greater than 13 days have the lowest haze optical depths at the terminator, supporting the choice of slower rotators as observing targets.Comment: 25 pages, 15 figure

Asymmetric Ionospheric Jets in Jupiter's Aurora

Simultaneous infrared observations of (Formula presented.) and H2 emissions from Jupiter's northern aurora using the Near Infrared Spectrograph at Keck Observatory were used to measure the ionospheric and thermospheric wind velocities. (Formula presented.) ions supercorotate near the dawn auroral oval and subcorotate across the dusk sector and in the dawn polar region relative to the planetary rotation rate, broadly in agreement with past observations and models. An anticyclonic vortex is discovered in H2 flows, closely matching the mean magnetospheric subcorotation when the observed magnetospheric flows are averaged azimuthally. In comparing ion and neutral winds, we measure the line-of-sight effective ion drift in the neutral reference frame for the first time, revealing two blue-shifted sunward flows of ∼2 km/s. Observed (Formula presented.) and H2 emissions overlap with predictions of the Pedersen conductivity layer, suggesting two different regions of the ionosphere: (a) a deep layer, where neutral forces dominate the thermosphere and symmetric breakdown-in-corotation currents can close, and (b) a higher layer, where the observed effective ion drift allows dawn-to-dusk Pedersen currents within the upper atmosphere, in turn closing asymmetric currents within the magnetosphere. This ionospheric structure aligns well with recent Juno observations of Jupiter's aurora. The detected thermospheric vortex implies the driving of neutral flows by the momentum from the magnetosphere within the thermosphere and deeper in the atmosphere to potentially 20 mbar. Jovian neutral thermosphere might bridge the gap between current observations and modelings and perhaps be significant to the dynamics of aurora on Earth and other outer planets

How Do Human Cells React to the Absence of Mitochondrial DNA?

Mitochondrial biogenesis is under the control of two different genetic systems: the nuclear genome (nDNA) and the mitochondrial genome (mtDNA). The mtDNA is a circular genome of 16.6 kb encoding 13 of the approximately 90 subunits that form the respiratory chain, the remaining ones being encoded by the nDNA. Eukaryotic cells are able to monitor and respond to changes in mitochondrial function through alterations in nuclear gene expression, a phenomenon first defined in yeast and known as retrograde regulation. To investigate how the cellular transcriptome is modified in response to the absence of mtDNA, we used Affymetrix HG-U133A GeneChip arrays to study the gene expression profile of two human cell lines, 143BTK(-) and A549, which had been entirely depleted of mtDNA (rho(o) cells), and compared it with that of corresponding undepleted parental cells (rho(+) cells).Our data indicate that absence of mtDNA is associated with: i) a down-regulation of cell cycle control genes and a reduction of cell replication rate, ii) a down-regulation of nuclear-encoded subunits of complex III of the respiratory chain and iii) a down-regulation of a gene described as the human homolog of ELAC2 of E. coli, which encodes a protein that we show to also target to the mitochondrial compartment.Our results indicate a strong correlation between mitochondrial biogenesis and cell cycle control and suggest that some proteins could have a double role: for instance in controlling both cell cycle progression and mitochondrial functions. In addition, the finding that ELAC2 and maybe other transcripts that are located into mitochondria, are down-regulated in rho(o) cells, make them good candidates for human disorders associated with defective replication and expression of mtDNA

Morphologic evidence of diffuse vascular damage in human and in the experimental model of ethylmalonic encephalopathy

Ethylmalonic encephalopathy (EE) is a rare autosomal recessive disorder characterized by early onset encephalopathy, chronic diarrhoea, petechiae, orthostatic acrocyanosis and defective cytochrome c oxidase (COX) in muscle and brain. High levels of lactic, ethylmalonic and methylsuccinic acids are detected in body fluids. EE is caused by mutations in ETHE1, a mitochondrial sulphur dioxygenase. By studying a suitable mouse model, we found that loss of ETHE1 leads to accumulation of sulphide, which is a poison for COX and other enzymatic activities thus accounting for the main features of EE. We report here the first autopsy case of a child with a genetically confirmed diagnosis of EE, and compare the histological, histochemical and immunohistochemical findings with those of the constitutive Ethe1 -/- mice. In addition to COX depleted cells, widespread endothelial lesions of arterioles and capillaries of the brain and gastrointestinal tract were the pathologic hallmarks in both organisms. Our findings of diffuse vascular damage of target critical organs are in keeping with the hypothesis that the pathologic effects of ETHE1 deficiency may stem from high levels of circulating hydrogen sulphide rather than the inability of specific organs to detoxify its endogenous production. © SSIEM and Springer 2011

Coenzyme A corrects pathological defects in human neurons of PANK2-associated neurodegeneration

Pantothenate kinase-associated neurodegeneration (PKAN) is an early onset and severely disabling neurodegenerative disease for which no therapy is available. PKAN is caused by mutations in PANK2, which encodes for the mitochondrial enzyme pantothenate kinase 2. Its function is to catalyze the first limiting step of Coenzyme A (CoA) biosynthesis. We generated induced pluripotent stem cells from PKAN patients and showed that their derived neurons exhibited premature death, increased ROS production, mitochondrial dysfunctions—including impairment of mitochondrial iron-dependent biosynthesis—and major membrane excitability defects. CoA supplementation prevented neuronal death and ROS formation by restoring mitochondrial and neuronal functionality. Our findings provide direct evidence that PANK2 malfunctioning is responsible for abnormal phenotypes in human neuronal cells and indicate CoA treatment as a possible therapeutic intervention

Asymmetric Ionospheric Jets in Jupiter's Aurora

Simultaneous infrared observations of H 3 + ${\mathrm{H}}_{3}^{+}$ and H2 emissions from Jupiter's northern aurora using the Near Infrared Spectrograph at Keck Observatory were used to measure the ionospheric and thermospheric wind velocities. H 3 + ${\mathrm{H}}_{3}^{+}$ ions supercorotate near the dawn auroral oval and subcorotate across the dusk sector and in the dawn polar region relative to the planetary rotation rate, broadly in agreement with past observations and models. An anticyclonic vortex is discovered in H2 flows, closely matching the mean magnetospheric subcorotation when the observed magnetospheric flows are averaged azimuthally. In comparing ion and neutral winds, we measure the line‐of‐sight effective ion drift in the neutral reference frame for the first time, revealing two blue‐shifted sunward flows of ∼2 km/s. Observed H 3 + ${\mathrm{H}}_{3}^{+}$ and H2 emissions overlap with predictions of the Pedersen conductivity layer, suggesting two different regions of the ionosphere: (a) a deep layer, where neutral forces dominate the thermosphere and symmetric breakdown‐in‐corotation currents can close, and (b) a higher layer, where the observed effective ion drift allows dawn‐to‐dusk Pedersen currents within the upper atmosphere, in turn closing asymmetric currents within the magnetosphere. This ionospheric structure aligns well with recent Juno observations of Jupiter's aurora. The detected thermospheric vortex implies the driving of neutral flows by the momentum from the magnetosphere within the thermosphere and deeper in the atmosphere to potentially 20 mbar. Jovian neutral thermosphere might bridge the gap between current observations and modelings and perhaps be significant to the dynamics of aurora on Earth and other outer planets

Mutations in TTC19 cause mitochondrial complex III deficiency and neurological impairment in humans and flies.

Although mutations in CYTB (cytochrome b) or BCS1L have been reported in isolated defects of mitochondrial respiratory chain complex III (cIII), most cIII-defective individuals remain genetically undefined. We identified a homozygous nonsense mutation in the gene encoding tetratricopeptide 19 (TTC19) in individuals from two families affected by progressive encephalopathy associated with profound cIII deficiency and accumulation of cIII-specific assembly intermediates. We later found a second homozygous nonsense mutation in a fourth affected individual. We demonstrated that TTC19 is embedded in the inner mitochondrial membrane as part of two high-molecular-weight complexes, one of which coincides with cIII. We then showed a physical interaction between TTC19 and cIII by coimmunoprecipitation. We also investigated a Drosophila melanogaster knockout model for TTC19 that showed low fertility, adult-onset locomotor impairment and bang sensitivity, associated with cIII deficiency. TTC19 is a putative cIII assembly factor whose disruption is associated with severe neurological abnormalities in humans and flies