Cenozoic evolution of the steppe-desert biome in Central Asia

The origins and development of the arid and highly seasonal steppe-desert biome in Central Asia, the largest of its kind in the world, remain largely unconstrained by existing records. It is unclear how Cenozoic climatic, geological, and biological forces, acting at diverse spatial and temporal scales, shaped Central Asian ecosystems through time. Our synthesis shows that the Central Asian steppe-desert has existed since at least Eocene times but experienced no less than two regime shifts, one at the Eocene–Oligocene Transition and one in the mid-Miocene. These shifts separated three successive “stable states,” each characterized by unique floral and faunal structures. Past responses to disturbance in the Asian steppe-desert imply that modern ecosystems are unlikely to recover their present structures and diversity if forced into a new regime. This is of concern for Asian steppes today, which are being modified for human use and lost to desertification at unprecedented rates

Adenylate Cyclase Toxin Promotes Internalisation of Integrins and Raft Components and Decreases Macrophage Adhesion Capacity

Bordetella pertussis, the bacterium that causes whooping cough, secretes an adenylate cyclase toxin (ACT) that must be post-translationally palmitoylated in the bacterium cytosol to be active. The toxin targets phagocytes expressing the CD11b/CD18 integrin receptor. It delivers a catalytic adenylate cyclase domain into the target cell cytosol producing a rapid increase of intracellular cAMP concentration that suppresses bactericidal functions of the phagocyte. ACT also induces calcium fluxes into target cells. Biochemical, biophysical and cell biology approaches have been applied here to show evidence that ACT and integrin molecules, along with other raft components, are rapidly internalized by the macrophages in a toxin-induced calcium rise-dependent process. The toxin-triggered internalisation events occur through two different routes of entry, chlorpromazine-sensitive receptor-mediated endocytosis and clathrin-independent internalisation, maybe acting in parallel. ACT locates into raft-like domains, and is internalised, also in cells devoid of receptor. Altogether our results suggest that adenylate cyclase toxin, and maybe other homologous pathogenic toxins from the RTX (Repeats in Toxin) family to which ACT belongs, may be endowed with an intrinsic capacity to, directly and efficiently, insert into raft-like domains, promoting there its multiple activities. One direct consequence of the integrin removal from the cell surface of the macrophages is the hampering of their adhesion ability, a fundamental property in the immune response of the leukocytes that could be instrumental in the pathogenesis of Bordetella pertussis

Bordetella Adenylate Cyclase Toxin Mobilizes Its β2 Integrin Receptor into Lipid Rafts to Accomplish Translocation across Target Cell Membrane in Two Steps

Bordetella adenylate cyclase toxin (CyaA) binds the αMβ2 integrin (CD11b/CD18, Mac-1, or CR3) of myeloid phagocytes and delivers into their cytosol an adenylate cyclase (AC) enzyme that converts ATP into the key signaling molecule cAMP. We show that penetration of the AC domain across cell membrane proceeds in two steps. It starts by membrane insertion of a toxin ‘translocation intermediate’, which can be ‘locked’ in the membrane by the 3D1 antibody blocking AC domain translocation. Insertion of the ‘intermediate’ permeabilizes cells for influx of extracellular calcium ions and thus activates calpain-mediated cleavage of the talin tether. Recruitment of the integrin-CyaA complex into lipid rafts follows and the cholesterol-rich lipid environment promotes translocation of the AC domain across cell membrane. AC translocation into cells was inhibited upon raft disruption by cholesterol depletion, or when CyaA mobilization into rafts was blocked by inhibition of talin processing. Furthermore, CyaA mutants unable to mobilize calcium into cells failed to relocate into lipid rafts, and failed to translocate the AC domain across cell membrane, unless rescued by Ca2+ influx promoted in trans by ionomycin or another CyaA protein. Hence, by mobilizing calcium ions into phagocytes, the ‘translocation intermediate’ promotes toxin piggybacking on integrin into lipid rafts and enables AC enzyme delivery into host cytosol

Genome-Wide Identification of HrpL-Regulated Genes in the Necrotrophic Phytopathogen Dickeya dadantii 3937

BACKGROUND: Dickeya dadantii is a necrotrophic pathogen causing disease in many plants. Previous studies have demonstrated that the type III secretion system (T3SS) of D. dadantii is required for full virulence. HrpL is an alternative sigma factor that binds to the hrp box promoter sequence of T3SS genes to up-regulate their expression. METHODOLOGY/PRINCIPAL FINDINGS: To explore the inventory of HrpL-regulated genes of D. dadantii 3937 (3937), transcriptome profiles of wild-type 3937 and a hrpL mutant grown in a T3SS-inducing medium were examined. Using a cut-off value of 1.5, significant differential expression was observed in sixty-three genes, which are involved in various cellular functions such as type III secretion, chemotaxis, metabolism, regulation, and stress response. A hidden Markov model (HMM) was used to predict candidate hrp box binding sites in the intergenic regions of 3937, including the promoter regions of HrpL-regulated genes identified in the microarray assay. In contrast to biotrophic phytopathgens such as Pseudomonas syringae, among the HrpL up-regulated genes in 3937 only those within the T3SS were found to contain a hrp box sequence. Moreover, direct binding of purified HrpL protein to the hrp box was demonstrated for hrp box-containing DNA fragments of hrpA and hrpN using the electrophoretic mobility shift assay (EMSA). In this study, a putative T3SS effector DspA/E was also identified as a HrpL-upregulated gene, and shown to be translocated into plant cells in a T3SS-dependent manner. CONCLUSION/SIGNIFICANCES: We provide the genome-wide study of HrpL-regulated genes in a necrotrophic phytopathogen (D. dadantii 3937) through a combination of transcriptomics and bioinformatics, which led to identification of several effectors. Our study indicates the extent of differences for T3SS effector protein inventory requirements between necrotrophic and biotrophic pathogens, and may allow the development of different strategies for disease control for these different groups of pathogens

Changes in CO2 during ocean anoxic event 1d indicate similarities to other carbon cycle perturbations

Past greenhouse intervals of the Mesozoic were repeatedly punctuated by Ocean Anoxic Events (OAEs), major perturbations to the global carbon cycle and abrupt climate changes that may serve as relevant analogs for Earth’s greenhouse gas-forced climate future. The key to better understanding these transient climate disruptions and possible CO2 forced tipping-points resides in high-resolution, precise, and accurate estimates of atmospheric CO2 for individual OAEs. Here we present a high-temporal resolution, multi-proxy pCO2 reconstruction for the onset of mid-Cretaceous (Albian-Cenomanian Boundary) OAE1d. Coupling of pCO2 estimates with carbon isotopic compositions (δ13C) of charcoal, vitrain, and cuticle from the Rose Creek Pit (RCP), Nebraska, reveals complex phasing, including a lag between the well-documented negative δ13C excursion defining the onset of OAE1d and the CO2 increase. This lag indicates that increased CO2 or other C-based greenhouse gases may not have been the primary cause of the negative excursion. Our study reveals a pCO2 increase within the interval of the negative δ13C excursion, reaching a maximum of up to ~840 ppm (95% confidence interval -307 ppm/+167 ppm) toward its end. The reconstructed magnitude of CO2 increase (~357 ppm) is similar to that of Late Cretaceous OAE2 but of smaller magnitude than that of other major carbon cycle perturbations of the Mesozoic assessed via stomatal methods (e.g., the Toarcian OAE [TOAE], Triassic-Jurassic boundary event, Cretaceous-Paleogene Boundary event). Furthermore, our results indicate a possible shared causal or developmental mechanism with OAE1a and the TOAE

Links between CO2 glaciation and water flow: reconciling the Cenozoic history of the Antarctic Circumpolar Current

International audienceThe timing of the onset of the Antarctic Circum-polar Current (ACC) is a crucial event of the Cenozoic because of its cooling and isolating effect over Antarctica. It is intimately related to the glaciations occurring throughout the Cenozoic from the Eocene-Oligocene (EO) transition (≈ 34 Ma) to the middle Miocene glaciations (≈ 13.9 Ma). However, the exact timing of the onset remains debated, with evidence for a late Eocene setup contradicting other data pointing to an occurrence closer to the Oligocene-Miocene (OM) boundary. In this study, we show the potential impact of the Antarctic ice sheet on the initiation of a strong proto-ACC at the EO boundary. Our results reveal that the regional cooling effect of the ice sheet increases sea ice formation, which disrupts the meridional density gradient in the Southern Ocean and leads to the onset of a circumpolar current and its progressive strengthening. We also suggest that subsequent variations in atmospheric CO 2 , ice sheet volumes and tectonic reorganizations may have affected the ACC intensity after the Eocene-Oligocene transition. This allows us to build a hypothesis for the Cenozoic evolution of the Antarctic Circumpolar Current that may provide an explanation for the second initiation of the ACC at the Oligocene-Miocene boundary while reconciling evidence supporting both early Oligocene and early Miocene onset of the ACC

Evolution of Ocean circulation in the North Atlantic Ocean during the Miocene: impact of the Greenland ice sheet and the Eastern Tethys Seaway

International audienceThe Atlantic Meridional Overturning Circulation (AMOC) is today the central feature of the Global ocean circulation (Talley, 2013). It is dominated by two overturning cells usually referred to as the Antarctic Bottom Water (AABW) and the North Atlantic Deep Water (NADW). The NADW forms mainly in the Norwegian Sea by winter open-ocean cooling of salt-rich water advected northward by the Gulf Stream. The cooling increases the density of surface waters, which results in vertical convection and the formation of deep water. The newly formed deep and dense waters flow southward to the Southern Ocean, where they are upwelled under the action of the Antarctic Circumpolar Current (ACC). They are then dragged either into the AABW overturning branch and redistributed in the Pacific and Indian basins via the ACC or into the formation area of the Antarctic Intermediate Water (AAIW), thereby flowing northward as (sub)surface currents and closing the AMOC cell (Talley, 2013). The structure of the modern AMOC results from the particular configuration of the Atlantic basin geometry with a closed Central American Seaway and an open Drake Passage (Ferreira et al., 2018). During Cenozoic times (66-0 Ma) and, in particular, the Miocene period (23-5 Ma), the physical structure of the AMOC was probably different compared to the present-day because the configuration of major gateways and submarine topographic barriers in the Atlantic and Pacific basins differ substantially (Hutchinson et al., 2019). From the early Miocene (∼23 Ma) to today, these changes include the deepening of the Greenland-Scotland Ridge (Stärz et al., 2017), the opening of Fram Strait (Ehlers & Jokat, 2013) and Bering Strait (Gladenkov & Gladenkov, 2004) in the northern high latitudes; the closure of Central American Seaway (Montes et al., 2015) and Eastern Tethys Seaway (ETS, Bialik et al., 2019) in the tropics; and the potential narrowing of Drake Passage (Lagabrielle et al., 2009) in the southern high latitudes. Apart from those change in the seaways and the Eurasiatic landsea mask, the continental configuration during the Miocene period was close to the modern one with however some substantial changes in the topography worldwide such as lower elevation in major mountain belts (Andes, Himalayas, East Africa, and European ranges); see Poblete et al. (2021) for review

Extinction intensity during Ordovician and Cenozoic glaciations explained by cooling and palaeogeography

A striking feature of the marine fossil record is the variable intensity of extinction during superficially similar climate transitions. Here we combine climate models and species trait simulations to explore the degree to which differing paleogeographic boundary conditions and differing magnitudes of cooling and glaciation can explain the relative intensity of marine extinction during greenhouse-icehouse transitions in the Late Ordovician and the Cenozoic. Simulations modelled the response of virtual species to cooling climate using a spatially explicit cellular automaton algorithm. We find that paleogeography alone may be a minor contributing factor, as identical changes in meridional sea surface temperature gradients caused greater extinction in Late Ordovician simulations than in Cenozoic simulations. Differences in extinction from paleogeography are significant but by themselves insufficient to explain observed differences in extinction intensity. However, when simulations included inferred changes in continental flooding and interval-specific models of sea surface temperature, predicted differences in relative extinction intensity were more consistent with observations from the fossil record. Our results support the hypothesis that intense extinction in the Late Ordovician is partially attributable to exceptionally rapid and severe cooling compared to Cenozoic events