SummaryThere is considerable concern over declines in insect pollinator communities and potential impacts on the pollination of crops and wildflowers [1][2][3][4] . Among the multiple pressures facing pollinators [2][3][4] , decreasing floral resources due to habitat loss and degradation has been suggested as a key contributing factor 2-8 . However, a lack of quantitative data has hampered testing for historical changes in floral resources. Here we show that overall floral rewards can be estimated at a national scale by combining vegetation surveys and direct nectar measurements. We find evidence for substantial losses in nectar resources in England and Wales between the 1930s and 1970s; however, total nectar provision in Great Britain as a whole had stabilised by 1978, and increased from 1998 to 2007. These findings concur with trends in pollinator diversity, which declined in the mid-20th century 9 but stabilised more recently 10 . The diversity of nectar sources declined from 1978 to 1990 but stabilised thereafter at low levels, with four plant species accounting for over 50% of national nectar provision in 2007. Calcareous grassland, broadleaved woodland and neutral grassland are the habitats that produce the greatest amount of nectar per unit area from the most diverse sources, whereas arable land is the poorest in both respects. While agrienvironment schemes add resources to arable landscapes, their national contribution is low. Due to

Muscle satellite cells have been shown to be a heterogeneous population of committed myogenic progenitors and noncommitted stem cells. This hierarchical composition of differentiating progenitors and self-renewable stem cells assures the extraordinary regenerative capacity of skeletal muscles. Recent studies have revealed a role for asymmetric division in satellite cell maintenance and offer novel insights into the regulation of satellite cell function by the niche. A thorough understanding of the molecular regulation and cell fate determination of satellite cells and other potential stem cells resident in muscle is essential for successful stem cell-based therapies to treat muscular diseases.

No abstract

Perturbations to mammalian SWI/SNF (BAF) complexes contribute to over 20% of human cancers, with driving roles first identified in malignant rhabdoid tumor (MRT), an aggressive pediatric cancer characterized by biallelic inactivation of the core BAF complex subunit SMARCB1 (BAF47). However, the mechanism by which this alteration contributes to tumorigenesis remains poorly understood. We find that BAF47 loss destabilizes BAF complexes on chromatin, absent significant changes in intra-complex integrity. Rescue of BAF47 in BAF47-deficient sarcoma cell lines results in increased genome-wide BAF complex occupancy, facilitating widespread enhancer activation and opposition of polycomb-mediated repression at bivalent promoters. We demonstrate differential regulation by BAF and PBAF complexes at enhancers and promoters, respectively, suggesting distinct functions of each complex which are perturbed upon BAF47 loss. Our results demonstrate collaborative mechanisms of mSWI/SNF-mediated gene activation, identifying functions that are coopted or abated to drive human cancers and developmental disorders.

The Rb family, Rb, p107, and p130, play important roles in cell cycle control and cellular differentiation, and Rb has been suggested to regulate adipocyte differentiation. We report here that mice lacking p107 displayed a uniform replacement of white adipose tissue (WAT) with brown adipose tissue (BAT). Mutant WAT depots contained mutilocular adipocytes that expressed elevated levels of PGC-1alpha and UCP-1 typical of BAT. WAT from p107-/- mice contained markedly elevated numbers of adipogenic precursors that displayed downregulated expression of pRb. Consistent with the hypothesis that pRb is required for adult adipocyte differentiation, Cre-mediated deletion of Rb in adult primary preadipocytes blocked their differentiation into white adipocytes. Importantly, pRb was observed to bind the PGC-1alpha promoter and repress transcription. Therefore, p107 and pRb regulate PGC-1alpha expression to control the switch between white and brown adipocyte differentiation from a common pool of presumptive adult progenitors in fat tissue.

The duration of specific periods within a plant's life cycle are critical for plant growth and performance. In the High Arctic, the start of many of these phenological periods is determined by snowmelt date, which may change in a changing climate. It has been suggested that the end of these periods during late-season are triggered by external cues, such as day length, light quality or temperature, leading to the hypothesis that earlier or later snowmelt dates will lengthen or shorten the duration of these periods, respectively, and thereby affect plant performance. We tested whether snowmelt date controls phenology and phenological period duration in High Arctic Svalbard using a melt timing gradient from natural and experimentally altered snow depths. We investigated the response of early-and late-season phenophases from both vegetative and reproductive phenological periods of eight common species. We found that all phenophases follow snowmelt patterns, irrespective of timing of occurrence, vegetative or reproductive nature. Three of four phenological period durations based on these phenophases were fixed for most species, defining the studied species as periodic. Periodicity can thus be considered an evolutionary trait leading to disadvantages compared with aperiodic species and we conclude that the mesic and heath vegetation types in Svalbard are at risk of being outcompeted by invading, aperiodic species from milder biomes.

The regenerative capacity of muscle is regulated by p38-γ, which phosphorylates MyoD and leads to formation of a complex that represses myogenin transcription.

SUMMARY Hematopoiesis provides an accessible system for studying the principles underlying cell-fate decisions in stem cells. Proposed models of hematopoiesis suggest that quantitative changes in lineage-specific transcription factors (LS-TFs) underlie cell-fate decisions. However, evidence for such models is lacking as TF levels are typically measured via RNA expression rather than by analyzing temporal changes in protein abundance. Here, we used single-cell mass cytometry and absolute quantification by mass spectrometry to capture the temporal dynamics of TF protein expression in individual cells during human erythropoiesis. We found that LS-TFs from alternate lineages are co-expressed, as proteins, in individual early progenitor cells and quantitative changes of LS-TFs occur gradually rather than abruptly to direct cell-fate decisions. Importantly, upregulation of a megakaryocytic TF in early progenitors is sufficient to deviate cells from an erythroid to a megakaryocyte trajectory, showing that quantitative changes in protein abundance of LS-TFs in progenitors can determine alternate cell fates.