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End of 21st‐century hydroclimate projections suggest an expansion of subtropical dry zones, with Mediterranean and Sahel regions becoming much drier. However, paleobotanical assemblage evidence from the middle Miocene (17‐12 Ma), suggests both regions were instead humid environments. Here we show that by modifying regional sea surface temperatures (SST) in an Earth System Model (CESM1.2) simulation of the middle Miocene, the increased ocean evaporation and integrated water vapor flux overrides any drying effects associated with warming‐induced land‐surface evaporation driven by atmospheric CO2 concentrations. These modifications markedly reduce the bias in the model‐data comparison for this period. A vegetation model (BIOME4) forced with simulated climatologies predicts both regions were dominated by mixed forest, which is largely consistent with the paleobotanical record. This study unveils the potential for wetter subtropical Mediterranean climates associated with warming, presenting an alternative scenario from future drying projections with localized SST warming governing regional climate change. Plain Language Summary: Climate models project drier conditions over Europe and Northern Africa due to global warming. However, evidence from a past warm climate period, the middle Miocene (∼15 million years ago), finds wetter rather than drier environments. We refine climate model boundary conditions by reconstructing warmer ocean waters in the North Atlantic based on proxy evidence. The warmer ocean produces wetter environments by enhancing North Atlantic precipitation events and the North African monsoon. The increased rainfall and surface temperature cause a vegetation model to predict more forest coverage over Europe and Northern Africa, which is consistent with fossil evidence from ∼15 million years ago. This study unveils the potential for wetter climates associated with warming, presenting an alternative scenario from future drying projections, with localized sea surface warming governing regional climate. Key Points: Middle Miocene Europe rainfall discrepancy between herpetological (dry) and paleobotanical (wet) records complicate climate model validationSimulations that produce dry environments also produce cool North Atlantic sea surface temperatures which are inconsistent with proxiesSSTs informed by North Atlantic proxies produce wetter environments consistent with paleobotanical evidence [ABSTRACT FROM AUTHOR]

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The Miocene (23.03–5.33 Ma) is recognized as a period with close to modern‐day paleogeography, yet a much warmer climate. With large uncertainties in future hydroclimate projections, Miocene conditions illustrate a potential future analog for the Earth system. A recent opportunistic Miocene Model Intercomparison Project 1 (MioMIP1) focused on synthesizing published Miocene climate simulations and comparing them with available temperature reconstructions. Here, we build on this effort by analyzing the hydrological cycle response to Miocene forcings across early‐to‐middle (E2MMIO; 20.03–11.6 Ma) and middle‐to‐late Miocene (M2LMIO; 11.5–5.33 Ma) simulations with CO2 concentrations ranging from 200 to 850 ppm and providing a model‐data comparison against available precipitation reconstructions. We find global precipitation increases by ∼2.1 and 2.3% per degree of warming for E2MMIO and M2LMIO simulations, respectively. Models generally agree on a wetter than modern‐day tropics; mid and high‐latitude, however, do not agree on the sign of subtropical precipitation changes with warming. Global monsoon analysis suggests most monsoon regions, except the North American Monsoon, experience higher precipitation rates under warmer conditions. Model‐data comparison shows that mean annual precipitation is underestimated by the models regardless of CO2 concentration, particularly in the mid‐ to high‐latitudes. This suggests that the models may not be (a) resolving key processes driving the hydrological cycle response to Miocene boundary conditions and/or (b) other boundary conditions or processes not considered here are critical to reproducing Miocene hydroclimate. This study highlights the challenges in modeling and reconstructing the Miocene hydrological cycle and serves as a baseline for future coordinated MioMIP efforts. Plain Language Summary: This study looks at Earth's hydrological cycle during the Miocene (23–5 million years ago). During this period, the Earth's climate was 3–7°C warmer than today, with carbon dioxide (CO2) estimates ranging between 400 and 850 ppm. Understanding how the hydrological cycle responded during warmer climate conditions can give us insight into what might happen as the Earth gets warmer. We analyzed a suite of Miocene paleoclimate simulations with different CO2 concentrations in the atmosphere and compared them against fossil plant data, which gives an estimate of the average annual rainfall during the period. We found that during the Miocene global rainfall increased by about 2.1%–2.3% for each degree of warming. The models agree that the tropics, mid‐ and high‐latitude, became wetter than they are today but have lower agreement on whether subtropical areas got wetter or drier as they warmed. Compared to proxies, models consistently underestimated how much rain fell in a year, especially in the mid‐ to high‐latitude. This illustrates the challenges in reconstructing the Miocene's hydrological cycle and suggests that the models might not fully capture the range of uncertainties associated with changes in the hydrological cycle due to warming or other factors that differentiated the Miocene. Key Points: A multi‐model comparison of the hydrological cycle in early‐to‐middle and middle‐to‐late Miocene simulations is conductedModels generally agree on wetter than modern tropics, middle and high latitudes, but not on the sign of subtropical precipitation changesModel‐data comparison shows mean annual precipitation is underestimated by the models, particularly in the mid‐ to high‐latitudes [ABSTRACT FROM AUTHOR]

The Miocene epoch, spanning 23.03–5.33 Ma, was a dynamic climate of sustained, polar amplified warmth. Miocene atmospheric CO2 concentrations are typically reconstructed between 300 and 600 ppm and were potentially higher during the Miocene Climatic Optimum (16.75–14.5 Ma). With surface temperature reconstructions pointing to substantial midlatitude and polar warmth, it is unclear what processes maintained the much weaker‐than‐modern equator‐to‐pole temperature difference. Here, we synthesize several Miocene climate modeling efforts together with available terrestrial and ocean surface temperature reconstructions. We evaluate the range of model‐data agreement, highlight robust mechanisms operating across Miocene modeling efforts and regions where differences across experiments result in a large spread in warming responses. Prescribed CO2 is the primary factor controlling global warming across the ensemble. On average, elements other than CO2, such as Miocene paleogeography and ice sheets, raise global mean temperature by ∼2°C, with the spread in warming under a given CO2 concentration (due to a combination of the spread in imposed boundary conditions and climate feedback strengths) equivalent to ∼1.2 times a CO2 doubling. This study uses an ensemble of opportunity: models, boundary conditions, and reference data sets represent the state‐of‐art for the Miocene, but are inhomogeneous and not ideal for a formal intermodel comparison effort. Acknowledging this caveat, this study is nevertheless the first Miocene multi‐model, multi‐proxy comparison attempted so far. This study serves to take stock of the current progress toward simulating Miocene warmth while isolating remaining challenges that may be well served by community‐led efforts to coordinate modeling and data activities within a common analytical framework. Plain Language Summary: As human activity continues to increase atmospheric carbon dioxide concentrations, scientists turn to warm intervals in Earth's history to develop insight into the behavior of the climate system under elevated carbon dioxide and temperature. One such interval is the Miocene epoch which has become increasingly relevant as reconstructions of Miocene atmospheric CO2 concentrations point to values ranging between current concentrations of ∼400 ppm and those projected for the end of this century under Shared Socioeconomic Pathways 3 and 4. In this study, we evaluate the surface warming patterns simulated by a range of different climate models configured with Miocene paleogeography and CO2 concentrations spanning 200–850 ppm. We also synthesize available Miocene surface temperature reconstructions. The primary factor controlling the amount of global warming seen across the Miocene simulations analyzed is the CO2 concentration that was prescribed within a given simulation. On average, Miocene elements other than CO2, such as Miocene paleogeography and ice sheets, raise global mean temperature by ∼2°C. While some Miocene simulations with high CO2 forcing overlap with the reconstructed global mean surface temperature estimates for their target Miocene interval, they still generally fail to capture the reconstructed pattern of warming. Key Points: A synthesis of Miocene modeling efforts, and surface temperature reconstructions, is presented within a single analysis frameworkMiocene global mean surface temperature estimates span ∼5.3°C–11.5°C higher than preindustrial, only ∼2°C is explained by non–CO2 boundary conditions in climate modelsSome simulations overlap with reconstructed global mean surface temperature estimates but fail to capture the weak temperature gradient [ABSTRACT FROM AUTHOR]

The Miocene epoch (23.03–5.33 Ma) was a time interval of global warmth, relative to today. Continental configurations and mountain topography transitioned toward modern conditions, and many flora and fauna evolved into the same taxa that exist today. Miocene climate was dynamic: long periods of early and late glaciation bracketed a ∼2 Myr greenhouse interval—the Miocene Climatic Optimum (MCO). Floras, faunas, ice sheets, precipitation, pCO2, and ocean and atmospheric circulation mostly (but not ubiquitously) covaried with these large changes in climate. With higher temperatures and moderately higher pCO2 (∼400–600 ppm), the MCO has been suggested as a particularly appropriate analog for future climate scenarios, and for assessing the predictive accuracy of numerical climate models—the same models that are used to simulate future climate. Yet, Miocene conditions have proved difficult to reconcile with models. This implies either missing positive feedbacks in the models, a lack of knowledge of past climate forcings, or the need for re‐interpretation of proxies, which might mitigate the model‐data discrepancy. Our understanding of Miocene climatic, biogeochemical, and oceanic changes on broad spatial and temporal scales is still developing. New records documenting the physical, chemical, and biotic aspects of the Earth system are emerging, and together provide a more comprehensive understanding of this important time interval. Here, we review the state‐of‐the‐art in Miocene climate, ocean circulation, biogeochemical cycling, ice sheet dynamics, and biotic adaptation research as inferred through proxy observations and modeling studies. Plain Language Summary: During the Miocene time period (∼23–5 million years ago), Planet Earth looked similar to today, with some important differences: the climate was generally warmer and highly variable, while atmospheric CO2 was not much higher. Continental‐sized ice sheets were only present on Antarctica, but not in the northern hemisphere. The continents drifted to near their modern‐day positions, and plants and animals evolved into the many (near) modern species. Scientists study the Miocene because present‐day and projected future CO2 levels are in the same range as those reconstructed for the Miocene. Therefore, if we can understand climate changes and their biotic responses from the Miocene past, we are able to better predict current and future global changes. By comparing Miocene climate reconstructions from fossil and chemical data to climate simulations produced by computer models, scientists are able to test their understanding of the Earth system under higher CO2 and warmer conditions than those of today. This helps in constraining future warming scenarios for the coming decades. In this study, we summarize the current understanding of the Miocene world from data and models. We also identify gaps in our understanding that need further research attention in the future. Key Points: Miocene floras, faunas, and paleogeography were similar to today and provide plausible analogs for future climatic warmingThe Miocene saw great dynamism in biotic and climate systems, but the reasons for these shifts are still not well understoodThe pCO2‐temperature‐ice relationships during major Miocene climate oscillations and transitions warrant further research [ABSTRACT FROM AUTHOR]

The Late Miocene (~11.6-5.3 Ma) palaeorecord provides evidence for a warmer and wetter climate than that of today and there is uncertainty in the palaeo-CO2 record of at least 150 ppmv. We present results from fully coupled atmosphere-ocean-vegetation simulations for the Late Miocene that examine the relative roles of palaeogeography (topography and ice sheet geometry) and CO2 concentration in the determination of Late Miocene climate through comprehensive terrestrial model-data comparisons. Assuming that the data accurately reflects the Late Miocene climate, and that the Late Miocene palaeogeographic reconstruction used in the model is robust, then results indicate that the proxy-derived precipitation differences between the Late Miocene and modern can be largely accounted for by the palaeogeographic changes alone. However, the proxy-derived temperatures differences between the Late Miocene and modern can only begin to be accounted for if we assume a palaeo-CO2 concentration towards the higher end of the range of estimates. [ABSTRACT FROM AUTHOR]

High doses of propranolol inhibit phosphatidate phosphohydrolase (PAP) activity in intact cells, thus blocking metabolism of phosphatidic acid (PA), product of the phospholipase D (PLD) reaction. Vasopressin and phorbol ester activate PLD and ERK (extracellular signal-regulated protein kinase) mitogen-activated protein kinases in A7r5, a rat vascular smooth muscle cell line. Propranolol increased PA levels in intact A7r5 cells and inhibited cytosolic PAP and membrane calcium-independent phospholipase A2 but did not activate PLD or enhance agonist-induced PA accumulation. Incubation of cells with 200 microM propranolol for 10-45 min markedly elevated PA but caused only partial activation of ERKs. Propranolol and other lipophilic amines caused a time- and dose-dependent detachment of cells from their substrate. These results confirm that elevation of PA is not a strong signal for ERK activation and emphasize that caution should be exercised in using propranolol as a PAP inhibitor in intact cells.

Phospholipase D (PLD) is activated in mammalian cells in response to a variety of growth factors and may play a role in cell proliferation. Lysophosphatidic acid (LPA) is a bioactive metabolite potentially generated as a result of PLD activation. Two human prostate cancer cell lines, PC-3 and LNCaP, express membrane PLD activity. The effects of LPA on PLD activity and proliferation were examined in PC-3 cells, which express hPLD1a/1b. Phorbol 12-myristate 13-acetate (PMA) induced a prolonged activation of PLD, as detected in both intact cells and membranes. LPA induced a transient activation of PLD that was maximal by 10 minutes. The EC50 for LPA-induced PLD activation was approximately 1 microM. Pertussis toxin did not inhibit activation of PLD by LPA or PMA. Ro-31-8220 and bisindolylmaleimide I, inhibitors of protein kinase C, blocked activation by PLD by both PMA and LPA. PMA-induced activation of PLD did not appear to require translocation of PLDs from cytosol to membrane. LPA stimulated proliferation of PC-3 cells with an EC50 of approximately 0.2 microM; this response was not inhibited by pertussis toxin. Perillyl alcohol, an anti-cancer drug, reversibly inhibited proliferation in response to either serum or LPA but did not inhibit activation of PLD by PMA or LPA. These data establish that LPA activates PLD and stimulates proliferation via Gi-independent pathways in a human prostate cancer cell line.

Neutral sphingomyelinase (SMase) can be activated by extracellular signals to produce ceramide, which may affect mitogen-activated protein kinase (MAPK) activities. Neutral SMase activity was assessed in membranes from Jurkat, a human T-cell line, and EL4, a murine T-cell line. Ara-C activated SMase with 10 minutes in both Jurkat and EL4 cells, while phorbol ester (PMA) had no effect. PMA, but not Ara-C or ceramides, activated ERK MAPKS, in Jurkat and EL4. PMA acted synergistically with ionomycin to activate JNK MAPKs in Jurkat and EL4 within 10 minutes. Ara-C activated JNKs only after prolonged incubation (90-120 minutes). Thus, ceramide is not a positive signal for ERK activation in T-cell lines. The effects of Ara-C on JNK activity may be mediated through secondary response pathways.

The effects of phorbol 12-myristate 13-acetate (PMA) on the activities of phospholipase D (PLD3), mitogen-activated protein kinase (ERK), and c-Jun N-terminal kinase (JNK) were studied in Jurkat, a human T cell line, and EL4, a murine T-cell line. PMA treatment rapidly activated PLD in Jurkat, as detected either in intact or broken cells. In contrast, PMA did not stimulate PLD activity in EL4 cells. PLD activity was not detected in membranes prepared from EL4 cells. Jurkat, but not EL4, expresses a 120-kDa protein recognized by an anti-PLD antibody. In both Jurkat and EL4 cells, PMA caused activation of ERKs. Incubation of EL4 cells with bacterial PLD increased phosphatidic acid levels, but did not activate ERK. In both EL4 and Jurkat cells, co-stimulation with PMA and ionomycin stimulated JNK activity. These results show that activation of PLD is not required for activation of ERKs or JNKs by PMA in T-cell lines. Thus, while PLD activity is expressed in some T-cell lines, the role of this enzyme and its products in T-cell activation remain to be elucidated.

Regulation of the activity of the extracellular signal regulated kinase (ERK) mitogen-activated protein kinases was examined in Rat-1 HIR, a fibroblast cell line overexpressing the human insulin receptor. Insulin or phorbol ester induced partial activations of ERKs, while a combination of insulin and phorbol ester resulted in a synergistic activation. Preincubation with phorbol ester increased the subsequent response to insulin. Phorbol ester did not enhance tyrosine phosphorylation of the insulin receptor. Insulin did not enhance activation of phospholipase D in response to phorbol ester. Lysophosphatidic acid also acted synergistically with insulin to induce ERK activation. Lysophosphatidic acid alone had little effect on ERK, and did not activate phospholipase D. The combination of phorbol ester and insulin maintained tyrosine phosphorylation of focal adhesion kinase, while insulin alone decreased its tyrosine phosphorylation. Phorbol ester induced phosphorylation of She on serine/threonine, while insulin induced tyrosine phosphorylation of She and She-Grb2 binding. These results suggest that full activation of ERKs in fibroblasts can require the cooperation of at least two signaling pathways, one of which may result from a protein kinase C-dependent phosphorylation of effectors regulating ERK activation. In this manner, phorbol esters may enhance mitogenic signals initiated by growth factor receptors.

Activation of mitogen-activated protein kinases (MAPKs) was examined in the A7r5 rat vascular smooth muscle cell line. Treatment of A7r5 cells with vasopressin, phorbol ester (PMA), or serum resulted in activation of two MAPKs, Erk-1 and Erk-2. Phosphatidylinositol-specific phospholipase C was activated in response to vasopressin but not to PMA. Vasopressin and PMA both caused maximal activation of PLD within 5 minutes. Application of bacterial phospholipase D (PLD) to A7r5 cells increased phosphatidic acid to levels similar to those seen with vasopressin or PMA. Acute exposure of the cells to vasopressin, PMA, or PLD increased phosphorylation of many of the same cytosolic and membrane proteins. However, bacterial PLD did not promote significant activation of Erk-1 and Erk-2. Phosphatidic acid and lysophosphatidic acid (LPA) likewise did not stimulate MAPK activity in A7r5 cells. Serum and vasopressin stimulated DNA synthesis when present for more than 30 min, while PLD, PMA, phosphatidic acid, and LPA were not mitogenic. These data suggest that activations of MAPKs and PLD are concurrent but independent responses to vasopressin in A7r5 cells. Acute activation of these enzymes is not sufficient to simulate DNA synthesis.

Phospholipase D (PLD) is activated in mammalian cells in response to a wide variety of stimuli. A rapid assay for agonist-activated PLD activity in cell extracts was developed, utilizing a fluorescent derivative of phosphatidylcholine as substrate. Utilization of the substrate was assessed following thin-layer chromatography of the reaction mixture. Hydrolysis products generated by phospholipases D, C, and A2 could be visualized in the same reaction. Phorbol ester and vasopressin increased PLD activity in intact A7r5 vascular smooth muscle cells, as measured by an isotopic labeling method. Using the in vitro fluorescent assay, enhanced PLD activity was detected in membranes prepared from A7r5 cells that had been treated with phorbol ester or vasopressin. The agonist-activated activity was independent of phosphorylation occurring during the course of the assay. PLD activity was detected, in varying amounts, in membranes prepared from a variety of different mouse tissues. These results show that a fluorescent assay can be used to rapidly assess the activity of PLD and other phosphatidylcholine-utilizing phospholipases in cell and tissue extracts. The effects of agonists on PLD activity can be retained and quantitated in a broken cell preparation, permitting characterization of the agonist-activated form of the enzyme.