The pace of past climate change vs. potential bird distributions and land use in the United States

Climate change may drastically alter patterns of species distributions and richness, but predicting future species patterns in occurrence is challenging. Significant shifts in distributions have already been observed, and understanding these recent changes can improve our understanding of potential future changes. We assessed how past climate change affected potential breeding distributions for landbird species in the conterminous United States. We quantified the bioclimatic velocity of potential breeding distributions, that is, the pace and direction of change for each species’ suitable climate space over the past 60 years. We found that potential breeding distributions for landbirds have shifted substantially with an average velocity of 1.27 km yr^?1, about double the pace of prior distribution shift estimates across terrestrial systems globally (0.61 km yr^?1). The direction of shifts was not uniform. The majority of species’ distributions shifted west, northwest, and north. Multidirectional shifts suggest that changes in climate conditions beyond mean temperature were influencing distributional changes. Indeed, precipitation variables that were proxies for extreme conditions were important variables across all models. There were winners and losers in terms of the area of distributions; many species experienced contractions along west and east distribution edges, and expansions along northern distribution edges. Changes were also reflected in the potential species richness, with some regions potentially gaining species (Midwest, East) and other areas potentially losing species (Southwest). However, the degree to which changes in potential breeding distributions are manifested in actual species richness depends on landcover. Areas that have become increasingly suitable for breeding birds due to changing climate are often those attractive to humans for agriculture and development. This suggests that many areas might have supported more breeding bird species had the landscape not been altered. Our study illustrates that climate change is not only a future threat, but something birds are already experiencing.     

Ephemeral ecological speciation and the latitudinal biodiversity gradient

The richness of biodiversity in the tropics compared to high‐latitude parts of the world forms one of the most globally conspicuous patterns in biology, and yet few hypotheses aim to explain this phenomenon in terms of explicit microevolutionary mechanisms of speciation and extinction. We link population genetic processes of selection and adaptation to speciation and extinction by way of their interaction with environmental factors to drive global scale macroecological patterns. High‐latitude regions are both cradle and grave with respect to species diversification. In particular, we point to a conceptual equivalence of “environmental harshness” and “hard selection” as eco‐evolutionary drivers of local adaptation and ecological speciation. By describing how ecological speciation likely occurs more readily at high latitudes, with such nascent species especially prone to extinction by fusion, we derive the ephemeral ecological speciation hypothesis as an integrative mechanistic explanation for latitudinal gradients in species turnover and the net accumulation of biodiversity.     

Assembly,molecular organization,and membrane-binding properties of development-specific septins

Septin complexes display remarkable plasticity in subunit composition, yet how a new subunit assembled into higher-order structures confers different functions is not fully understood. Here, this question is addressed in budding yeast, where during meiosis Spr3 and Spr28 replace the mitotic septin subunits Cdc12 and Cdc11 (and Shs1), respectively. In vitro, the sole stable complex that contains both meiosis-specific septins is a linear Spr28–Spr3–Cdc3–Cdc10–Cdc10–Cdc3–Spr3–Spr28 hetero-octamer. Only coexpressed Spr3 and Spr28 colocalize with Cdc3 and Cdc10 in mitotic cells, indicating that incorporation requires a Spr28-Spr3 protomer. Unlike their mitotic counterparts, Spr28-Spr3–capped rods are unable to form higher-order structures in solution but assemble to form long paired filaments on lipid monolayers containing phosphatidylinositol-4,5-bisphosphate, mimicking presence of this phosphoinositide in the prospore membrane. Spr28 and Spr3 fail to rescue the lethality of a cdc11Δ cdc12Δ mutant, and Cdc11 and Cdc12 fail to restore sporulation proficiency to spr3Δ/spr3Δ spr28Δ/spr28Δ diploids. Thus, specific meiotic and mitotic subunits endow septin complexes with functionally distinct properties.     

Marker Exchange Mutagenesis of mxaF,Encoding the Large Subunit of the Mxa Methanol Dehydrogenase,in Methylosinus trichosporium OB3b

Methanotrophs have remarkable redundancy in multiple steps of the central pathway of methane oxidation to carbon dioxide. For example, it has been known for over 30 years that two forms of methane monooxygenase, responsible for oxidizing methane to methanol, exist in methanotrophs, i.e., soluble methane monooxygenase (sMMO) and particulate methane monooxygenase (pMMO), and that expression of these two forms is controlled by the availability of copper. Specifically, sMMO expression occurs in the absence of copper, while pMMO expression increases with increasing copper concentrations. More recently, it was discovered that multiple forms of methanol dehydrogenase (MeDH), Mxa MeDH and Xox MeDH, also exist in methanotrophs and that the expression of these alternative forms is regulated by the availability of cerium. That is, expression of Xox MeDH increases in the presence of cerium, while Mxa MeDH expression decreases in the presence of cerium. As it had been earlier concluded that pMMO and Mxa MeDH form a supercomplex in which electrons from Mxa MeDH are back donated to pMMO to drive the initial oxidation of methane, we speculated that Mxa MeDH could be rendered inactive through marker-exchange mutagenesis but growth on methane could still be possible if cerium was added to increase the expression of Xox MeDH under sMMO-expressing conditions. Here we report that mxaF, encoding the large subunit of Mxa MeDH, could indeed be knocked out in Methylosinus trichosporium OB3b, yet growth on methane was still possible, so long as cerium was added. Interestingly, growth of this mutant occurred in both the presence and the absence of copper, suggesting that Xox MeDH can replace Mxa MeDH regardless of the form of MMO expressed.     

Differences in measures of boldness even when underlying behavioral syndromes are present in two populations of the song sparrow (<Emphasis Type="Italic">Melospiza melodia</Emphasis>)

One commonly studied behavioral syndrome is the correlation between aggression and boldness. Studies in song sparrows (M. melodia) have found greater aggression and boldness in urban populations and a correlation between aggression and boldness in rural populations, but not within urban populations. In previous studies, boldness was measured as flight initiation distance (FID), which may reflect habituation by urban birds to human presence. In this study, we measured boldness using playbacks of heterospecific alarm calls and investigated whether higher boldness is a general trait of urban birds and whether the same pattern of correlations between aggression and boldness would be seen. We conducted trials involving FID, alarm call playbacks and conspecific song playbacks on 25 birds from both an urban and a rural site. The results showed that urban birds were bolder, as measured by FID and response to alarm calls. Boldness and aggression were correlated in rural birds with each method of measuring boldness but were correlated in urban birds only when using alarm call playbacks. Our results suggest that a behavioral syndrome exists in both urban and rural populations but that urban birds are able to decrease their response to human disturbance.     

Function and regulation in MAPK signaling pathways: lessons learned from the yeast Saccharomyces cerevisiae

Signaling pathways that activate different mitogen-activated protein kinases (MAPKs) elicit many of the responses that are evoked in cells by changes in certain environmental conditions and upon exposure to a variety of hormonal and other stimuli. These pathways were first elucidated in the unicellular eukaryote Saccharomyces cerevisiae (budding yeast). Studies of MAPK pathways in this organism continue to be especially informative in revealing the molecular mechanisms by which MAPK cascades operate, propagate signals, modulate cellular processes, and are controlled by regulatory factors both internal to and external to the pathways. Here we highlight recent advances and new insights about MAPK-based signaling that have been made through studies in yeast, which provide lessons directly applicable to, and that enhance our understanding of, MAPK-mediated signaling in mammalian cells.     

Sphingosine kinase 1 expression is regulated by signaling through PI3K, AKT2, and mTOR in human coronary artery smooth muscle cells

Sphingosine kinase 1 (SphK1) is a lipid kinase implicated in mitogenic signaling pathways in vascular smooth muscle cells. We demonstrate that human coronary artery smooth muscle (HCASM) cells require SphK1 for growth and that SphK1 mRNA and protein levels are elevated in PDGF stimulated HCASM cells. To determine the mechanism of PDGF-induced SphK1 expression, we used pharmacological inhibitors of the PI3K/AKT/mTOR signaling pathway. Wortmannin, SH-5, and rapamycin significantly blocked PDGF-stimulated induction of SphK1 mRNA and protein expression, indicating a regulatory role of the PI3K/AKT/mTOR pathway in SphK1 expression. To determine which isoform of AKT regulates SphK1 mRNA and protein levels, siRNAs specific for AKT1, AKT2, and AKT3 were used. We show that AKT2 siRNA significantly blocked PDGF-stimulated increases in SphK1 mRNA and protein expression levels as well as SphK1 enzymatic activity levels. In contrast, AKT1 or AKT3 siRNA did not have an effect. Together, these results demonstrate that the PI3K/AKT/mTOR signaling pathway is involved in regulation of SphK1, with AKT2 playing a key role in PDGF-induced SphK1 expression in HCASM cells.