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Light microscopy enables researchers to observe cellular mechanisms with high spatial and temporal resolution. However, the increasing complexity of current imaging technologies, coupled with financial constraints of potential users, hampers the general accessibility and potential reach of cutting-edge microscopy. Open microscopy can address this issue by making well-designed and well-documented hardware and software solutions openly available to a broad audience. In this Comment, we provide a definition of open microscopy and present recent projects in the field. We discuss current and future challenges of open microscopy and their implications for funders, policymakers, researchers and scientists. We believe that open microscopy requires a holistic approach. Sample preparation, designing and building of hardware components, writing software, data acquisition and data interpretation must go hand in hand to enable interdisciplinary and reproducible science to the benefit of society.

Here we discuss barriers to reproducibility in regard to microscopes and related hardware, along with best practices for sharing novel designs created using computer-aided design (CAD). We hope to start a fruitful community discussion on how instrument development, especially in microscopy, can become more open and reproducible, ultimately leading to better, more trustworthy science.

Predicting responses of plankton to variations in essential nutrients is hampered by limited in situ measurements, a poor understanding of community composition, and the lack of reference gene catalogs for key taxa. Iron is a key driver of plankton dynamics and, therefore, of global biogeochemical cycles and climate. To assess the impact of iron availability on plankton communities, we explored the comprehensive bio‐oceanographic and bio‐omics data sets from TaraOceans in the context of the iron products from two state‐of‐the‐art global scale biogeochemical models. We obtained novel information about adaptation and acclimation toward iron in a range of phytoplankton, including picocyanobacteria and diatoms, and identified whole subcommunities covarying with iron. Many of the observed global patterns were recapitulated in the Marquesas archipelago, where frequent plankton blooms are believed to be caused by natural iron fertilization, although they are not captured in large‐scale biogeochemical models. This work provides a proof of concept that integrative analyses, spanning from genes to ecosystems and viruses to zooplankton, can disentangle the complexity of plankton communities and can lead to more accurate formulations of resource bioavailability in biogeochemical models, thus improving our understanding of plankton resilience in a changing environment. Marine phytoplankton require iron for their growth and proliferation. According to John Martin's iron hypothesis, fertilizing the ocean with iron could dramatically increase photosynthetic activity, thus representing a biological means to counteract global warming. However, while there is a constantly growing knowledge of how iron is distributed in the ocean and about its role in cellular processes in marine photosynthetic groups such as diatoms and cyanobacteria, less is known about how iron availability shapes plankton communities and how they respond to it. In the present work, we exploited recently published TaraOceans data sets to address these questions. We first defined specific subcommunities of co‐occurring organisms that co‐vary with iron availability in the oceans. We then identified specific patterns of adaptation and acclimation to iron in different groups of phytoplankton. Finally, we validated our global results at local scale, specifically in the Marquesas archipelago, where recurrent phytoplankton blooms are believed to be a result of iron fertilization. By integrating global data with a localized response, we provide a framework for understanding the resilience of plankton ecosystems in a changing environment. Coherent assemblages of taxa covarying with iron at global level are identified in plankton communitiesFunctional responses to iron availability involve both changes in copy numbers of iron‐responsive genes and their transcriptional regulationPlankton responses to local variations in iron concentrations recapitulate global patterns

Are the answers to biological questions obtained via live fluorescence microscopy substantially affected by phototoxicity? Although a single set of standards for assessing phototoxicity cannot exist owing to the breadth of samples and experimental questions associated with biological imaging, we need quantitative, practical assessments and reporting standards to ensure that imaging has a minimal impact on observed biological processes and sample health. Here we discuss the problem of phototoxicity in biology and suggest guidelines to improve its reporting and assessment.

La cellule est un univers dynamique et compartimenté où interagissent une multitude de sous composants à l’échelle nanométrique. Afin d’étudier l’organisation subcellulaire, il est devenu nécessaire de posséder des outils permettant une manipulation directe extrêmement précise et non invasive. L’avènement des lasers à impulsions, dès les années 60, a conduit à la naissance de la chirurgie au laser. Aujourd’hui, la réduction des impulsions laser en dessous de la nanoseconde permet de mieux comprendre leur interaction avec les tissus biologiques et de contrôler des interventions chirurgicales à une résolution de l’ordre de quelques centaines de nanomètres. Utilisant l’ionisation de la matière par la lumière, cette nanochirurgie laser permet d’effectuer des interventions chirurgicales intracellulaires telles que la découpe de microtubules ou de fibres de tension, sans endommager les structures environnantes ou compromettre la viabilité cellulaire. Ainsi, l’utilisation de lasers à impulsions ultra-courtes, plus précis et puissants, offre une nouvelle approche pour l’étude des forces en biologie ou pour la quantification de la dynamique du cytosquelette.

Recent data have demonstrated the role of Cdk1- and Cdk2-dependent phosphorylation of MyoDSer200in the regulation of MyoD activity and protein turnover. In the present study, we show that in presence of p57Kip2, MyoDAla200, a MyoD mutant that cannot be phosphorylated by cyclin-Cdk complexes, displayed activity 2–5-fold higher than of MyoDAla200alone in transactivation of muscle-specific genes myosin heavy chain, creatine kinase, and myosin light chain 1. Furthermore, p57Kip2increases the levels of MyoDAla200in cotransfected cells. This result implies that p57Kip2may regulate MyoD through a process distinct from its function as a cyclin-dependent kinase inhibitors. We report that overexpression of p57Kip2increased the half-life of MyoDAla200. This increased half-life of MyoD involves a physical interaction between MyoD and p57Kip2but not with p16Ink4a, as shown by cross-immunoprecipitation not only on overexpressed proteins from transfected cells, but also on endogenous MyoD and p57Kip2from C2C12 myogenic cells. Mutational and functional analyses of the two proteins show that the NH2domain of p57Kip2associates with basic region in the basic helix-loop-helix domain of MyoD. Competition/association assays and site-directed mutagenesis of the NH2terminus of p57Kip2identified the intermediate α-helix domain, located between the Cdk and the cyclin binding sites, as essential for MyoD interaction. These data show that the α-helix domain of p57Kip2, which is conserved in the Cip/Kip proteins, is implicated in protein-protein interaction and confers a specific regulatory mechanism, outside of their Cdk-inhibitory activity, by which the p57Kip2family members positively act on myogenic differentiation.

We show that expression of p57Kip2, a potent tight-binding inhibitor of several G1cyclin–cyclin-dependent kinase (Cdk) complexes, increases markedly during C2C12 myoblast differentiation. We examined the effect of p57Kip2on the activity of the transcription factor MyoD. In transient transfection assays, transcriptional transactivation of the mouse muscle creatine kinase promoter by MyoD was enhanced by the Cdk inhibitors. In addition, p57Kip2, p21Cip1, and p27Kip1but not p16Ink4ainduced an increased level of MyoD protein, and we show that MyoD, an unstable nuclear protein, was stabilized by p57Kip2. Forced expression of p57Kip2correlated with hypophosphorylation of MyoD in C2C12 myoblasts. A dominant-negative Cdk2 mutant arrested cells at the G1phase transition and induced hypophosphorylation of MyoD. Furthermore, phosphorylation of MyoD by purified cyclin E-Cdk2 complexes was inhibited by p57Kip2. In addition, the NH2 domain of p57Kip2necessary for inhibition of cyclin E-Cdk2 activity was sufficient to inhibit MyoD phosphorylation and to stabilize it, leading to its accumulation in proliferative myoblasts. Taken together, our data suggest that repression of cyclin E-Cdk2-mediated phosphorylation of MyoD by p57Kip2could play an important role in the accumulation of MyoD at the onset of myoblast differentiation.

ABSTRACTWe show that expression of p57Kip2, a potent tight-binding inhibitor of several G1cyclin–cyclin-dependent kinase (Cdk) complexes, increases markedly during C2C12 myoblast differentiation. We examined the effect of p57Kip2on the activity of the transcription factor MyoD. In transient transfection assays, transcriptional transactivation of the mouse muscle creatine kinase promoter by MyoD was enhanced by the Cdk inhibitors. In addition, p57Kip2, p21Cip1, and p27Kip1but not p16Ink4ainduced an increased level of MyoD protein, and we show that MyoD, an unstable nuclear protein, was stabilized by p57Kip2. Forced expression of p57Kip2correlated with hypophosphorylation of MyoD in C2C12 myoblasts. A dominant-negative Cdk2 mutant arrested cells at the G1phase transition and induced hypophosphorylation of MyoD. Furthermore, phosphorylation of MyoD by purified cyclin E-Cdk2 complexes was inhibited by p57Kip2. In addition, the NH2 domain of p57Kip2necessary for inhibition of cyclin E-Cdk2 activity was sufficient to inhibit MyoD phosphorylation and to stabilize it, leading to its accumulation in proliferative myoblasts. Taken together, our data suggest that repression of cyclin E-Cdk2-mediated phosphorylation of MyoD by p57Kip2could play an important role in the accumulation of MyoD at the onset of myoblast differentiation.