Response of the Hadley Circulation to Climate Change in an Aquaplanet GCM Coupled to a Simple Representation of Ocean Heat Transport

It is unclear how the width and strength of the Hadley circulation are controlled and how they respond to climate changes. Simulations of global warming scenarios with comprehensive climate models suggest the Hadley circulation may widen and weaken as the climate warms. But these changes are not quantitatively consistent among models, and how they come about is not understood. Here, a wide range of climates is simulated with an idealized moist general circulation model (GCM) coupled to a simple representation of ocean heat transport, in order to place past and possible future changes in the Hadley circulation into a broader context and to investigate the mechanisms responsible for them. By comparison of simulations with and without ocean heat transport, it is shown that it is essential to take low-latitude ocean heat transport and its coupling to wind stress into account to obtain Hadley circulations in a dynamical regime resembling Earth’s, particularly in climates resembling present-day Earth’s and colder. As the optical thickness of an idealized longwave absorber in the simulations is increased and the climate warms, the Hadley circulation strengthens in colder climates and weakens in warmer climates; it has maximum strength in a climate close to present-day Earth’s. In climates resembling present-day Earth’s and colder, the Hadley circulation strength is largely controlled by the divergence of angular momentum fluxes associated with eddies of midlatitude origin; the latter scale with the mean available potential energy in midlatitudes. The importance of these eddy momentum fluxes for the Hadley circulation strength gradually diminishes as the climate warms. The Hadley circulation generally widens as the climate warms, but at a modest rate that depends sensitively on how it is determined

Baroclinic Eddies and the Extent of the Hadley Circulation: An Idealized GCM Study

The Hadley circulation has widened over the past 30 years. This widening has been qualitatively reproduced in general circulation model (GCM) simulations of a warming climate. Comprehensive GCM studies suggest this widening may be caused by a poleward shift in baroclinic eddy activity. Yet the limited amplitude of the climate change signals analyzed so far precludes a quantitative comparison with theories. This study uses two idealized GCMs, one with and one without an active hydrologic cycle, to investigate changes in the extent of the Hadley circulation over a wide range of climates. The climates span global-mean temperatures from 243 to 385 K and equator-to-pole temperature contrasts from 12 to 100 K. Baroclinic eddies control the extent of the Hadley circulation across most of these climates. A supercriticality criterion that quantifies the depth of baroclinic eddies relative to that of the troposphere turns out to be a good indicator of where baroclinic eddies become deep enough to terminate the Hadley circulation. The supercriticality depends on meridional temperature gradients and an effective stability that accounts for the effect of convective heating on baroclinic eddies. As the equator-to-pole temperature contrast weakens or the convective static stability increases, convective heating increasingly influences the thermal stratification of the troposphere and the supercriticality. Consistent with the supercriticality criterion, the Hadley circulation contracts as meridional temperature gradients increase, and it widens as the effective static stability increases. The former occurs during El Niño and may account for the observed Hadley circulation contraction then; the latter occurs during global warming

Local Energetic Constraints on Walker Circulation Strength

The weakening of tropical overturning circulations is a robust response to global warming in climate models and observations. However, there remain open questions on the causes of this change and the extent to which this weakening affects individual circulation features such as the Walker circulation. The study presents idealized GCM simulations of a Walker circulation forced by prescribed ocean heat flux convergence in a slab ocean, where the longwave opacity of the atmosphere is varied to simulate a wide range of climates. The weakening of the Walker circulation with warming results from an increase in gross moist stability (GMS), a measure of the tropospheric moist static energy (MSE) stratification, which provides an effective static stability for tropical circulations. Baroclinic mode theory is used to determine changes in GMS in terms of the tropical-mean profiles of temperature and MSE. The GMS increases with warming, owing primarily to the rise in tropopause height, decreasing the sensitivity of the Walker circulation to zonally anomalous net energy input. In the absence of large changes in net energy input, this results in a rapid weakening of the Walker circulation with global warming

Northern hemisphere stationary waves in a changing climate

AbstractPurpose of ReviewStationary waves are planetary-scale longitudinal variations in the time-averaged atmospheric circulation.Here, we consider the projected response of Northern Hemisphere stationary waves to climate change in winter and summer. Wediscuss how the response varies across different metrics, identify robust responses, and review proposed mechanisms.Recent FindingsClimate models project shifts in the prevailing wind patterns, with corresponding impacts on regional precip-itation, temperature, and extreme events. Recent work has improved our understanding of the links between stationary waves andregional climate and identified robust stationary wave responses to climate change, which include an increased zonal lengthscalein winter, a poleward shift of the wintertime circulation over the Pacific, a weakening of monsoonal circulations, and an overallweakening of stationary wave circulations, particularly their divergent component and quasi-stationary disturbances.SummaryNumerous factors influence Northern Hemisphere stationary waves, and mechanistic theories exist for only a fewaspects of the stationary wave response to climate change. Idealized studies have proven useful for understanding the climateresponses of particular atmospheric circulation features and should be a continued focus of future research.R.C.J.W. received funding from the TamakiFoundation, NSF (Grant AGS-1929775), and NASA (GrantNNX17AH56G). R.H.W. received funding from the European UnionHorizon 2020 research and innovation programme under the MarieSkłodowska-Curie grant agreement No. 797961. XJL received fundingfrom the European Union Horizon 2020 research and innovation pro-gramme under the Marie Skłodowska-Curie grant agreement No.754433.Peer ReviewedPostprint (published version

A noncanonical autophagy pathway restricts Toxoplasma gondii growth in a strain-specific manner in IFN-γ-activated human cells

ABSTRACT A core set of autophagy proteins is required for gamma interferon (IFN-γ)-mediated clearance of Toxoplasma gondii in the mouse because of their control of several downstream effectors, including immunity-related GTPases (IRGs) and guanylate-binding proteins (GBPs). However, these effectors are absent (i.e., IRGs) from or nonessential (i.e., GBPs) in IFN-γ-activated human cells, raising the question of how these cells control parasite replication. Here, we define a novel role for ubiquitination and recruitment of autophagy adaptors in the strain-specific control of T. gondii replication in IFN-γ-activated human cells. Vacuoles containing susceptible strains of T. gondii became ubiquitinated, recruited the adaptors p62 and NDP52, and were decorated with LC3. Parasites within LC3-positive vacuoles became enclosed in multiple layers of host membranes, resulting in stunting of parasite replication. However, LC3-positive T. gondii-containing vacuoles did not fuse with endosomes and lysosomes, indicating that this process is fundamentally different from xenophagy, a form of autophagy involved in the control of intracellular bacterial pathogens. Genetic knockout of ATG16L or ATG7 reverted the membrane encapsulation and restored parasite replication, indicating that core autophagy proteins involved in LC3 conjugation are important in the control of parasite growth. Despite a role for the core autophagy machinery in this process, upstream activation through Beclin 1 was not sufficient to enhance the ubiquitination of T. gondii-containing vacuoles, suggesting a lack of reliance on canonical autophagy. These findings demonstrate a new mechanism for IFN-γ-dependent control of T. gondii in human cells that depends on ubiquitination and core autophagy proteins that mediate membrane engulfment and restricted growth

Autosis is a Na+,K+-ATPase-regulated form of cell death triggered by autophagy-inducing peptides, starvation, and hypoxia-ischemia.

A long-standing controversy is whether autophagy is a bona fide cause of mammalian cell death. We used a cell-penetrating autophagy-inducing peptide, Tat-Beclin 1, derived from the autophagy protein Beclin 1, to investigate whether high levels of autophagy result in cell death by autophagy. Here we show that Tat-Beclin 1 induces dose-dependent death that is blocked by pharmacological or genetic inhibition of autophagy, but not of apoptosis or necroptosis. This death, termed "autosis," has unique morphological features, including increased autophagosomes/autolysosomes and nuclear convolution at early stages, and focal swelling of the perinuclear space at late stages. We also observed autotic death in cells during stress conditions, including in a subpopulation of nutrient-starved cells in vitro and in hippocampal neurons of neonatal rats subjected to cerebral hypoxia-ischemia in vivo. A chemical screen of ~5,000 known bioactive compounds revealed that cardiac glycosides, antagonists of Na(+),K(+)-ATPase, inhibit autotic cell death in vitro and in vivo. Furthermore, genetic knockdown of the Na(+),K(+)-ATPase α1 subunit blocks peptide and starvation-induced autosis in vitro. Thus, we have identified a unique form of autophagy-dependent cell death, a Food and Drug Administration-approved class of compounds that inhibit such death, and a crucial role for Na(+),K(+)-ATPase in its regulation. These findings have implications for understanding how cells die during certain stress conditions and how such cell death might be prevented

Three red suns in the sky: A transiting, terrestrial planet in a triple M-dwarf system at 6.9 pc

We present the discovery from Transiting Exoplanet Survey Satellite (TESS) data of LTT 1445Ab. At a distance of 6.9 pc, it is the second nearest transiting exoplanet system found to date, and the closest one known for which the primary is an M dwarf. The host stellar system consists of three mid-to-late M dwarfs in a hierarchical configuration, which are blended in one TESS pixel. We use MEarth data and results from the Science Processing Operations Center data validation report to determine that the planet transits the primary star in the system. The planet has a radius of ${1.38}_{-0.12}^{+0.13}$ ${R}_{\oplus }$, an orbital period of ${5.35882}_{-0.00031}^{+0.00030}$ days, and an equilibrium temperature of ${433}_{-27}^{+28}$ K. With radial velocities from the High Accuracy Radial Velocity Planet Searcher, we place a 3σ upper mass limit of 8.4 ${M}_{\oplus }$ on the planet. LTT 1445Ab provides one of the best opportunities to date for the spectroscopic study of the atmosphere of a terrestrial world. We also present a detailed characterization of the host stellar system. We use high-resolution spectroscopy and imaging to rule out the presence of any other close stellar or brown dwarf companions. Nineteen years of photometric monitoring of A and BC indicate a moderate amount of variability, in agreement with that observed in the TESS light-curve data. We derive a preliminary astrometric orbit for the BC pair that reveals an edge-on and eccentric configuration. The presence of a transiting planet in this system hints that the entire system may be co-planar, implying that the system may have formed from the early fragmentation of an individual protostellar core.Accepted manuscrip

Impaired Autophagy of an Intracellular Pathogen Induced by a Crohn's Disease Associated ATG16L1 Variant

The genetic risk factors predisposing individuals to the development of inflammatory bowel disease are beginning to be deciphered by genome-wide association studies. Surprisingly, these new data point towards a critical role of autophagy in the pathogenesis of Crohn's disease. A single common coding variant in the autophagy protein ATG16L1 predisposes individuals to the development of Crohn's disease: while ATG16L1 encoding threonine at amino acid position 300 (ATG16L1*300T) confers protection, ATG16L1 encoding for alanine instead of threonine (ATG16L1*300A, also known as T300A) mediates risk towards the development of Crohn's disease. Here we report that, in human epithelial cells, the Crohn's disease-associated ATG16L1 coding variant shows impairment in the capture of internalized Salmonella within autophagosomes. Thus, we propose that the association of ATG16L1*300A with increased risk of Crohn's disease is due to impaired bacterial handling and lowered rates of bacterial capture by autophagy