Inequalities in the distribution of National Institutes of Health research project grant funding

  1. Michael S Lauer  Is a corresponding author
  2. Deepshikha Roychowdhury
  1. National Institutes of Health, United States

Abstract

Previous reports have described worsening inequalities of National Institutes of Health (NIH) funding. We analyzed Research Project Grant data through the end of Fiscal Year 2020, confirming worsening inequalities beginning at the time of the NIH budget doubling (1998-2003), while finding that trends in recent years have reversed for both investigators and institutions, but only to a modest degree. We also find that career-stage trends have stabilized, with equivalent proportions of early-, mid-, and late-career investigators funded from 2017 to 2020. The fraction of women among funded PIs continues to increase, but they are still not at parity. Analyses of funding inequalities show that inequalities for investigators, and to a lesser degree for institutions, have consistently been greater within groups (i.e., within groups by career stage, gender, race, and degree) than between groups.

Data availability

Source data have been provided in R format. R markdown source code corresponds with all numbers, tables, and figures.

Article and author information

Author details

  1. Michael S Lauer

    Office of the Director, National Institutes of Health, Bethesda, United States
    For correspondence
    Michael.Lauer@nih.gov
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-9217-8177
  2. Deepshikha Roychowdhury

    Office of Extramural Research, National Institutes of Health, Bethesda, United States
    Competing interests
    The authors declare that no competing interests exist.

Funding

National Institutes of Health

  • Michael S Lauer

National Institutes of Health

  • Deepshikha Roychowdhury

The authors are both full-time employees of the NIH and conducted this work as part of their official United States federal government duties.

Copyright

This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.

Metrics

  • 7,517
    views
  • 703
    downloads
  • 51
    citations

Views, downloads and citations are aggregated across all versions of this paper published by eLife.

Download links

A two-part list of links to download the article, or parts of the article, in various formats.

Downloads (link to download the article as PDF)

Open citations (links to open the citations from this article in various online reference manager services)

Cite this article (links to download the citations from this article in formats compatible with various reference manager tools)

  1. Michael S Lauer
  2. Deepshikha Roychowdhury
(2021)
Inequalities in the distribution of National Institutes of Health research project grant funding
eLife 10:e71712.
https://doi.org/10.7554/eLife.71712

Share this article

https://doi.org/10.7554/eLife.71712

Further reading

    1. Computational and Systems Biology
    George N Bendzunas, Dominic P Byrne ... Natarajan Kannan
    Research Article

    In eukaryotes, protein kinase signaling is regulated by a diverse array of post-translational modifications, including phosphorylation of Ser/Thr residues and oxidation of cysteine (Cys) residues. While regulation by activation segment phosphorylation of Ser/Thr residues is well understood, relatively little is known about how oxidation of cysteine residues modulate catalysis. In this study, we investigate redox regulation of the AMPK-related brain-selective kinases (BRSK) 1 and 2, and detail how broad catalytic activity is directly regulated through reversible oxidation and reduction of evolutionarily conserved Cys residues within the catalytic domain. We show that redox-dependent control of BRSKs is a dynamic and multilayered process involving oxidative modifications of several Cys residues, including the formation of intramolecular disulfide bonds involving a pair of Cys residues near the catalytic HRD motif and a highly conserved T-loop Cys with a BRSK-specific Cys within an unusual CPE motif at the end of the activation segment. Consistently, mutation of the CPE-Cys increases catalytic activity in vitro and drives phosphorylation of the BRSK substrate Tau in cells. Molecular modeling and molecular dynamics simulations indicate that oxidation of the CPE-Cys destabilizes a conserved salt bridge network critical for allosteric activation. The occurrence of spatially proximal Cys amino acids in diverse Ser/Thr protein kinase families suggests that disulfide-mediated control of catalytic activity may be a prevalent mechanism for regulation within the broader AMPK family.

    1. Computational and Systems Biology
    2. Genetics and Genomics
    Fangluo Chen, Dylan C Sarver ... G William Wong
    Research Article

    Obesity is a major risk factor for type 2 diabetes, dyslipidemia, cardiovascular disease, and hypertension. Intriguingly, there is a subset of metabolically healthy obese (MHO) individuals who are seemingly able to maintain a healthy metabolic profile free of metabolic syndrome. The molecular underpinnings of MHO, however, are not well understood. Here, we report that CTRP10/C1QL2-deficient mice represent a unique female model of MHO. CTRP10 modulates weight gain in a striking and sexually dimorphic manner. Female, but not male, mice lacking CTRP10 develop obesity with age on a low-fat diet while maintaining an otherwise healthy metabolic profile. When fed an obesogenic diet, female Ctrp10 knockout (KO) mice show rapid weight gain. Despite pronounced obesity, Ctrp10 KO female mice do not develop steatosis, dyslipidemia, glucose intolerance, insulin resistance, oxidative stress, or low-grade inflammation. Obesity is largely uncoupled from metabolic dysregulation in female KO mice. Multi-tissue transcriptomic analyses highlighted gene expression changes and pathways associated with insulin-sensitive obesity. Transcriptional correlation of the differentially expressed gene (DEG) orthologs in humans also shows sex differences in gene connectivity within and across metabolic tissues, underscoring the conserved sex-dependent function of CTRP10. Collectively, our findings suggest that CTRP10 negatively regulates body weight in females, and that loss of CTRP10 results in benign obesity with largely preserved insulin sensitivity and metabolic health. This female MHO mouse model is valuable for understanding sex-biased mechanisms that uncouple obesity from metabolic dysfunction.