What determines cell size?

AbstractFirst paragraph (this article has no abstract) For well over 100 years, cell biologists have been wondering what determines the size of cells. In modern times, we know all of the molecules that control the cell cycle and cell division, but we still do not understand how cell size is determined. To check whether modern cell biology has made any inroads on this age-old question, BMC Biology asked several heavyweights in the field to tell us how they think cell size is controlled, drawing on a range of different cell types. The essays in this collection address two related questions - why does cell size matter, and how do cells control it

The National Microbiome Data Collaborative Data Portal: An integrated multi-omics microbiome data resource

The National Microbiome Data Collaborative (NMDC) Data Portal (https://data.microbiomedata.org) supports microbiome multi-omics data exploration and access through an integrated, distributed data framework aligned with the FAIR (Findable, Accessible, Interoperable and Reusable) data principles (1). The NMDC Data Portal currently hosts 10.2 terabytes of multi-omics microbiome data, spanning five data types (metagenomes, metatranscriptomes, metaproteomes, metabolomes, and natural organic matter characterizations), generated at two Department of Energy User Facilities, the Joint Genome Institute (JGI) at Lawrence Berkeley National Laboratory (LBNL) and the Environmental Molecular Systems Laboratory (EMSL) at Pacific Northwest National Laboratory (PNNL). A flexible data schema (https://github.com/microbiomedata/nmdc-schema) leveraging community-driven standards underpins how data is managed and integrated. Annotated multi-omic data products are produced by the NMDC workflows and linked through common biosamples to enable search capabilities based on environmental context, instrumentation, and functional attributes. As a pilot system, the NMDC Data Portal offers download capabilities and several search components, including interactive geographic visualization of samples; environmental classification distribution visualized through an interactive Sankey diagram; time-series slider to select longitudinal samples of interest; and an upset plot displaying the number of multi-omics data generated from the same biosample within a study

Contrasting response of European forest and grassland energy exchange to heatwaves

Recent European heatwaves have raised interest in the impact of land cover conditions on temperature extremes. At present, it is believed that such extremes are enhanced by stronger surface heating of the atmosphere, when soil moisture content is below average. However, the impact of land cover on the exchange of water and energy and the interaction of this exchange with the soil water balance during heatwaves is largely unknown. Here we analyse observations from an extensive network of flux towers in Europe that reveal a difference between the temporal responses of forest and grassland ecosystems during heatwaves. We find that initially, surface heating is twice as high over forest than over grassland. Over grass, heating is suppressed by increased evaporation in response to increased solar radiation and temperature. Ultimately, however, this process accelerates soil moisture depletion and induces a critical shift in the regional climate system that leads to increased heating. We propose that this mechanism may explain the extreme temperatures in August 2003. We conclude that the conservative water use of forest contributes to increased temperatures in the short term, but mitigates the impact of the most extreme heat and/or long-lasting events

LUBAC is essential for embryogenesis by preventing cell death and enabling haematopoiesis

The Linear Ubiquitin chain Assembly Complex (LUBAC) is required for optimal gene activation and prevention of cell death upon activation of immune receptors, including TNFR1. Deficiency in the LUBAC components SHARPIN or HOIP in mice results in severe inflammation in adulthood or embryonic lethality, respectively, due to deregulation of TNFR1-mediated cell death. In humans, deficiency in the third LUBAC component, HOIL-1, causes autoimmunity and inflammatory disease, similar to HOIP deficiency, whereas HOIL-1 deficiency in mice was reported to cause no overt phenotype. By creating HOIL-1-deficient mice, we here show that HOIL-1 is, however, as essential for LUBAC function as HOIP, albeit for different reasons: whereas HOIP is LUBAC's catalytically active component, HOIL-1 is required for LUBAC assembly, stability and optimal retention in the TNFR1-signalling complex (TNFR1-SC), thereby preventing aberrant cell death. Both, HOIL-1 and HOIP prevent embryonic lethality at mid-gestation by interfering with aberrant TNFR1-mediated endothelial cell death, which only partially depends on RIPK1 kinase activity. Co-deletion of Caspase-8 with RIPK3 or MLKL prevents cell death in Hoil-1-/- embryos, yet only combined loss of Caspase-8 with MLKL results in viable HOIL-1-deficient mice. Interestingly, Ripk3-/-Caspase-8-/-Hoil-1-/- embryos die at late-gestation due to haematopoietic defects that are rescued by co-deletion of RIPK1 but not MLKL. Collectively, these results demonstrate that both, HOIP and HOIL-1 are essential LUBAC components and are required for embryogenesis by preventingaberrant cell death. Furthermore, they unveil that, when LUBAC and Caspase-8 are absent, RIPK3 prevents RIPK1 from inducing embryonic lethality by causing defects in foetal haematopoiesis