Alpine grassland plants grow earlier and faster but biomass remains unchanged over 35 years of climate change

Satellite data indicate significant advancement in alpine spring phenology over decades of climate warming, but corresponding field evidence is scarce. It is also unknown whether this advancement results from an earlier shift of phenological events, or enhancement of plant growth under unchanged phenological pattern. By analyzing a 35‐year dataset of seasonal biomass dynamics of a Tibetan alpine grassland, we show that climate change promoted both earlier phenology and faster growth, without changing annual biomass production. Biomass production increased in spring due to a warming‐induced earlier onset of plant growth, but decreased in autumn due mainly to increased water stress. Plants grew faster but the fast‐growing period shortened during the mid‐growing season. These findings provide the first in situ evidence of long‐term changes in growth patterns in alpine grassland plant communities, and suggest that earlier phenology and faster growth will jointly contribute to plant growth in a warming climate.     

Three proline rotamases involved in calcium homeostasis play differential roles in stress tolerance,virulence and calcineurin regulation of Beauveria bassiana

FK506‐sensitive proline rotamases (FPRs), also known as FK506‐binding proteins (FKBPs), can mediate immunosuppressive drug resistance in budding yeast but their physiological roles in filamentous fungi remain opaque. Here, we report that three FPRs (cytosolic/nuclear 12.15‐kD Fpr1, membrane‐associated 14.78‐kD Fpr2 and nuclear 50.43‐kD Fpr3) are all equally essential for cellular Ca²⁺ homeostasis and contribute significantly to calcineurin activity at different levels in the insect‐pathogenic fungus Beauveria bassiana although the deletion of fpr1 alone conferred resistance to FK506. Radial growth, conidiation, conidial viability and virulence were less compromised in the absence of fpr1 or fpr2 than in the absence of fpr3, which abolished almost all growth on scant media and reduced growth moderately on rich media. The Δfpr3 mutant was more sensitive to Na⁺, K⁺, Mn²⁺, Ca²⁺, Cu²⁺, metal chelate, heat shock and UVB irradiation than was Δfpr2 while both mutants were equally sensitive to Zn²⁺, Mg²⁺, Fe²⁺, H₂O₂ and cell wall‐perturbing agents. In contrast, the Δfpr1 mutant was less sensitive to fewer stress cues. Most of 32 examined genes involved in DNA damage repair, Na⁺/K⁺ detoxification or osmotolerance and Ca²⁺ homeostasis were downregulated sharply in Δfpr2 and Δfpr3 but rarely so affected in Δfpr1, coinciding well with their phenotypic changes. These findings uncover important, but differential, roles of three FPRs in the fungal adaptation to insect host and environment and provide novel insight into their essential roles in calcium signalling pathway.     

Lifespan of long‐lived growth hormone receptor knockout mice was not normalized by housing at 30°C since weaning

Growth hormone receptor knockout (GHRKO) mice are remarkably long‐lived and have improved glucose homeostasis along with altered energy metabolism which manifests through decreased respiratory quotient (RQ) and increased oxygen consumption (VO₂). Short‐term exposure of these animals to increased environmental temperature (eT) at 30°C can normalize their VO₂ and RQ. We hypothesized that increased heat loss in the diminutive GHRKO mice housed at 23°C and the consequent metabolic adjustments to meet the increased energy demand for thermogenesis may promote extension of longevity, and preventing these adjustments by chronic exposure to increased eT will reduce or eliminate their longevity advantage. To test these hypotheses, GHRKO mice were housed at increased eT (30°C) since weaning. Here, we report that contrasting with the effects of short‐term exposure of adult GHRKO mice to 30°C, transferring juvenile GHRKO mice to chronic housing at 30°C did not normalize the examined parameters of energy metabolism and glucose homeostasis. Moreover, despite decreased expression levels of thermogenic genes in brown adipose tissue (BAT) and elevated core body temperature, the lifespan of male GHRKO mice was not reduced, while the lifespan of female GHRKO mice was increased, along with improved glucose homeostasis. The results indicate that GHRKO mice have intrinsic features that help maintain their delayed, healthy aging, and extended longevity at both 23°C and 30°C.     

Climate sensitivity of conifer growth doesn’t reveal distinct low–high dipole along the elevation gradient in the Wolong National Natural Reserve,SW China

Recent climate warming is usually hypothesized to cause tree growth decline in the semi-arid regions where forests are particularly vulnerable to warming induced increases of water deficit. But there is still a large knowledge gap of climate warming effects on tree growth of cold temperate forest in the sub-humid region. Here we assess how climate warming has affected tree growth in the Wolong National Natural Reserve, Southwestern China, where recent warming might not cause tree growth decline because of the cold-humid climatic conditions. Tree-ring data from four co-dominant coniferous species (Larix potaninii var. macrocarpa, Tsuga chinensis, Abies faxoniana and Juniperus saltuaria) along an elevation gradient (from 2700 m to 3700 m) all imprinted temperature signals, and were both positively and significantly correlated with instrumental record of temperature data during the analyzed period of 1954–2010. Furthermore, the rising temperature since 1980 induced pervasive tree growth increases and stronger temperature signals for the coniferous species along the elevation gradient. The tree-ring chronology recorded a strong coherence with instrumental temperature since 1980 and was successful to keep up with the pace of climate warming rate. If climate warming continues, further increases in forest growth could be expected, and the terrestrial carbon sink will be strengthened for the local forest ecosystem in the future.     

An on-lattice agent-based Monte Carlo model simulating the growth kinetics of multicellular tumor spheroids

PurposeTo develop an on-lattice agent-based model describing the growth of multicellular tumor spheroids using simple Monte Carlo tools.MethodsCells are situated on the vertices of a cubic grid. Different cell states (proliferative, hypoxic or dead) and cell evolution rules, driven by 10 parameters, and the effects of the culture medium are included. About twenty spheroids of MCF-7 human breast cancer were cultivated and the experimental data were used for tuning the model parameters.ResultsSimulated spheroids showed adequate sizes of the necrotic nuclei and of the hypoxic and proliferative cell phases as a function of the growth time, mimicking the overall characteristics of the experimental spheroids. The relation between the radii of the necrotic nucleus and the whole spheroid obtained in the simulations was similar to the experimental one and the number of cells, as a function of the spheroid volume, was well reproduced. The statistical variability of the Monte Carlo model described the whole volume range observed for the experimental spheroids. Assuming that the model parameters vary within Gaussian distributions it was obtained a sample of spheroids that reproduced much better the experimental findings.ConclusionsThe model developed allows describing the growth of in vitro multicellular spheroids and the experimental variability can be well reproduced. Its flexibility permits to vary both the agents involved and the rules that govern the spheroid growth. More general situations, such as, e. g., tumor vascularization, radiotherapy effects on solid tumors, or the validity of the tumor growth mathematical models can be studied.     

Expanding the evolutionary explanations for sex differences in the human skeleton

While the anatomy and physiology of human reproduction differ between the sexes, the effects of hormones on skeletal growth do not. Human bone growth depends on estrogen. Greater estrogen produced by ovaries causes bones in female bodies to fuse before males' resulting in sex differences in adult height and mass. Female pelves expand more than males' due to estrogen and relaxin produced and employed by the tissues of the pelvic region and potentially also due to greater internal space occupied by female gonads and genitals. Evolutionary explanations for skeletal sex differences (aka sexual dimorphism) that focus too narrowly on big competitive men and broad birthing women must account for the adaptive biology of skeletal growth and its dependence on the developmental physiology of reproduction. In this case, dichotomizing evolution into proximate‐ultimate categories may be impeding the progress of human evolutionary science, as well as enabling the popular misunderstanding and abuse of it.