Why scientific societies should involve more early-career researchers.

Early-career researchers (ECRs) make up a large portion of the academic workforce. Yet, most leadership positions in scientific societies are held by senior scientists, and ECRs have little to no say over the decisions that will shape the future of research. This article looks at the level of influence ECRs have in 20 scientific societies based in the US and UK, and provides guidelines on how societies can successfully include ECRs in leadership roles.

Actionable recommendations from trainees to improve science training.

Over the past 20 years, a series of reports written by groups of senior researchers and administrators have recommended changes to improve the training environments for graduate students and postdoctoral researchers in the United States. However, academic institutions and departments have largely failed to implement these recommendations, which has exacerbated the problems faced by these trainees. Here, based on input from trainees at different career stages, we outline seven practical changes that academic institutions and departments can make to improve their training environments.

Effective Self-Management for Early Career Researchers in the Natural and Life Sciences.

Early career researchers (ECRs) are faced with a range of competing pressures in academia, making self-management key to building a successful career. The Organization for Human Brain Mapping undertook a group effort to gather helpful advice for ECRs in self-management.

Changing the Culture of Science Communication Training for Junior Scientists.

Being successful in an academic environment places many demands on junior scientists. Science communication currently may not be adequately valued and rewarded, and yet communication to multiple audiences is critical for ensuring that it remains a priority in today's society. Due to the potential for science communication to produce better scientists, facilitate scientific progress, and influence decision-making at multiple levels, training junior scientists in both effective and ethical science communication practices is imperative, and can benefit scientists regardless of their chosen career path. However, many challenges exist in addressing specific aspects of this training. Principally, science communication training and resources should be made readily available to junior scientists at institutions, and there is a need to scale up existing science communication training programs and standardize core aspects of these programs across universities, while also allowing for experimentation with training. We propose a comprehensive core training program be adopted by universities, utilizing a centralized online resource with science communication information from multiple stakeholders. In addition, the culture of science must shift toward greater acceptance of science communication as an essential part of training. For this purpose, the science communication field itself needs to be developed, researched and better understood at multiple levels. Ultimately, this may result in a larger cultural change toward acceptance of professional development activities as valuable for training scientists.

MyD88 promotes myoblast fusion in a cell-autonomous manner.

Myoblast fusion is an indispensable step for skeletal muscle development, postnatal growth, and regeneration. Myeloid differentiation primary response gene 88 (MyD88) is an adaptor protein that mediates Toll-like receptors and interleukin-1 receptor signaling. Here we report a cell-autonomous role of MyD88 in the regulation of myoblast fusion. MyD88 protein levels are increased during in vitro myogenesis and in conditions that promote skeletal muscle growth in vivo. Deletion of MyD88 impairs fusion of myoblasts without affecting their survival, proliferation, or differentiation. MyD88 regulates non-canonical NF-κB and canonical Wnt signaling during myogenesis and promotes skeletal muscle growth and overload-induced myofiber hypertrophy in mice. Ablation of MyD88 reduces myofiber size during muscle regeneration, whereas its overexpression promotes fusion of exogenous myoblasts to injured myofibers. Our study shows that MyD88 modulates myoblast fusion and suggests that augmenting its levels may be a therapeutic approach to improve skeletal muscle formation in degenerative muscle disorders.

Noncoding RNAs in the regulation of skeletal muscle biology in health and disease.

Skeletal muscle is composed of multinucleated myofibers that arise from the fusion of myoblasts during development. Skeletal muscle is essential for various body functions such as maintaining posture, locomotion, breathing, and metabolism. Skeletal muscle undergoes remarkable adaptations in response to environmental stimuli leading to atrophy or hypertrophy. Moreover, degeneration of skeletal muscle is a common feature in a number of muscular disorders including muscular dystrophy. Emerging evidence suggests that noncoding RNAs, such as microRNAs (miRNAs) and long noncoding RNAs (lncRNAs), are critical for skeletal muscle physiology. Several miRNAs and lncRNAs have now been found to control skeletal muscle development and regeneration. Noncoding RNAs also play an important role in the regulation of skeletal muscle mass in adults. Furthermore, aberrant expression of miRNAs and lncRNAs has been observed in several muscular disorders. In this article, we discuss the mechanisms of action of miRNAs and lncRNAs in skeletal muscle formation, growth, regeneration, and disease. We further highlight potential therapeutic strategies for utilizing noncoding RNAs to improve skeletal muscle function.

Monitoring the compliance of the academic enterprise with the Fair Labor Standards Act.

Background: On December 1, 2016, the Fair Labor Standards Act (FLSA) was due to be updated by the U.S. Department of Labor. Key changes included an increase in the salary threshold for exemption from overtime for working more than 40 hours per week, and indexing the salary level so that it is updated automatically every 3 years. This was predicted to have a profound effect on academe as postdoctoral researchers were mostly paid at a salary below the new threshold. On November 22, 2016, an injunction was granted nationwide, delaying implementation of the updates, which were finally struck down entirely on August 31, 2017. Here we review the key changes to the FLSA, how they came about, and how the postdoctoral population was affected. Methods: We describe recent data collection efforts to uncover what institutions with postdocs were doing to comply with the FLSA. Results: Our data showed that 57% of institutions checked (containing 41% of the estimated postdoctoral workforce in science, engineering and health) had not decided or had no public decision available one month prior to implementation, and only 35.5% of institutions were planning to raise salaries to the new minimum. After the injunction, a number of institutions and the NIH continued with their plans to raise salaries. Overall, despite the removal of a federal mandate, approximately 60% of postdocs are at institutions whose policy is to raise salaries. Conclusions: Our data show uncertainty in postdoctoral salaries in the U.S. prior to implementation of the FLSA ruling. In addition, while some institutions did suspend plans to raise postdoctoral salaries after the injunction, many continued with the raise. The implementation of postdoctoral salary raises may be inconsistent, however, as the legal minimum is still $23,660.

Creatine kinase B is necessary to limit myoblast fusion during myogenesis.

Myoblast fusion is critical for proper muscle growth and regeneration. During myoblast fusion, the localization of some molecules is spatially restricted; however, the exact reason for such localization is unknown. Creatine kinase B (CKB), which replenishes local ATP pools, localizes near the ends of cultured primary mouse myotubes. To gain insights into the function of CKB, we performed a yeast two-hybrid screen to identify CKB-interacting proteins. We identified molecules with a broad diversity of roles, including actin polymerization, intracellular protein trafficking, and alternative splicing, as well as sarcomeric components. In-depth studies of α-skeletal actin and α-cardiac actin, two predominant muscle actin isoforms, demonstrated their biochemical interaction and partial colocalization with CKB near the ends of myotubes in vitro. In contrast to other cell types, specific knockdown of CKB did not grossly affect actin polymerization in myotubes, suggesting other muscle-specific roles for CKB. Interestingly, knockdown of CKB resulted in significantly increased myoblast fusion and myotube size in vitro, whereas knockdown of creatine kinase M had no effect on these myogenic parameters. Our results suggest that localized CKB plays a key role in myotube formation by limiting myoblast fusion during myogenesis.

The N-BAR domain protein, Bin3, regulates Rac1- and Cdc42-dependent processes in myogenesis.

Actin dynamics are necessary at multiple steps in the formation of multinucleated muscle cells. BAR domain proteins can regulate actin dynamics in several cell types, but have been little studied in skeletal muscle. Here, we identify novel functions for the N-BAR domain protein, Bridging integrator 3 (Bin3), during myogenesis in mice. Bin3 plays an important role in regulating myofiber size in vitro and in vivo. During early myogenesis, Bin3 promotes migration of differentiated muscle cells, where it colocalizes with F-actin in lamellipodia. In addition, Bin3 forms a complex with Rac1 and Cdc42, Rho GTPases involved in actin polymerization, which are known to be essential for myotube formation. Importantly, a Bin3-dependent pathway is a major regulator of Rac1 and Cdc42 activity in differentiated muscle cells. Overall, these data classify N-BAR domain proteins as novel regulators of actin-dependent processes in myogenesis, and further implicate BAR domain proteins in muscle growth and repair.