Research careers are typically envisioned as a single path in which researchers start being one of a large number of researchers working under the guidance of one or more experienced scientists and, if they are successful, end with the individual leading their own research group and training future generations of scientists. Here we study the author contribution statements of published research papers in order to explore possible biases and disparities in career trajectories in science. We used Bayesian networks to train a prediction model based on a dataset of 70,694 publications from PLoS journals, which included 347,136 distinct authors and their associated contribution statements. This model was used to predict the contributions of 222,925 authors in 6,236,239 publications, and to apply a robust archetypal analysis to profile scientists across four career stages: junior, early-career, mid-career and late-career. All three of the archetypes we found - leader, specialized, and supporting - were encountered for early-career and mid-career researchers. Junior researchers displayed only two archetypes (specialized, and supporting), as did late-career researchers (leader and supporting). Scientists assigned to the leader and specialized archetypes tended to have longer careers than those assigned to the supporting archetype. We also observed consistent gender bias at all stages: the majority of male scientists belonged to the leader archetype, while the larger proportion of women belonged to the specialized archetype, especially for early-career and mid-career researchers.
All data is openly accessible at http://doi.org/10.5281/zenodo.3891055
Datasets on contributorship and bibliometric variables for the study 'Task specialization and its effects on research careersZenodo, 10.5281/zenodo.3891055.
- Nicolas Robinson-Garcia
- Rodrigo Costas
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
- Peter Rodgers, eLife, United Kingdom
© 2020, Robinson-Garcia et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
Mutations in the lever arm of β-cardiac myosin are a frequent cause of hypertrophic cardiomyopathy, a disease characterized by hypercontractility and eventual hypertrophy of the left ventricle. Here, we studied five such mutations: three in the pliant region of the lever arm (D778V, L781P, and S782N) and two in the light chain-binding region (A797T and F834L). We investigated their effects on both motor function and myosin subfragment 2 (S2) tail-based autoinhibition. The pliant region mutations had varying effects on the motor function of a myosin construct lacking the S2 tail: overall, D778V increased power output, L781P reduced power output, and S782N had little effect on power output, while all three reduced the external force sensitivity of the actin detachment rate. With a myosin containing the motor domain and the proximal S2 tail, the pliant region mutations also attenuated autoinhibition in the presence of filamentous actin but had no impact in the absence of actin. By contrast, the light chain-binding region mutations had little effect on motor activity but produced marked reductions in autoinhibition in both the presence and absence of actin. Thus, mutations in the lever arm of β-cardiac myosin have divergent allosteric effects on myosin function, depending on whether they are in the pliant or light chain-binding regions.
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