About

John Asher Johnson is a Professor of Astronomy at the Center for Astrophysics | Harvard & Smithsonian. His research interests include the detection and characterization of exoplanets. He received his Ph.D. and M.S. in Astronomy from the University of California, Berkeley, and his B.S. in Physics from the University of Missouri-Rolla (now known as the Missouri University of Science and Technology).

Research topics

• Medicine
• Internal medicine
• Biology
• Astrophysics
• Cell biology
• Cardiology
• Physics
• Astronomy
• Environmental health
• Demography
• Immunology
• Cancer research

Selected publications

• Smooth Muscle Cell-Specific TGFβ2 Protects Against Thoracic Aortic Aneurysm and Dissection in Mice

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-10-03

  preprintOpen access

  Abstract Objective Thoracic aortic aneurysm and dissection (TAAD) are major complications of Loeys- Dietz syndrome caused by heterozygous TGFB2 mutations. While Tgfb2 knockout mice die at birth and adult heterozygotes develop late, non-dissecting or non-rupturing aneurysms, the role of vascular smooth muscle cell (SMC)–derived TGFβ2 in postnatal aortic homeostasis and disease remains undefined. Approach and Results We generated tamoxifen-inducible, SMC-specific Tgfb2 conditional knockout mice ( Tgfb2 cKO) by crossing Tgfb2 flox alleles with Myh11CreER T2 and ROSA mT/mG lineage reporter mice. Tgfb2 deletion was induced at 4 weeks of age. Tgfb2 cKO mice developed rapidly progressive aneurysms involving both ascending and descending aortas, with intramural dissection and/or rupture at the proximal descending aorta. Lineage tracing confirmed loss of Tgfb2 -deficient SMCs during disease progression. Histological and morphometric analyses revealed elastic fiber fragmentation, SMC loss and de-differentiation, medial thickening, adventitial fibrosis, and accumulation of collagen and proteoglycans. Molecular profiling demonstrated reduced expression of SMC contractile genes ( Acta2, Myh11 ), increased fibrillar collagen ( Col1a1 ) expression, early suppression of SMAD2/3 phosphorylation and increased non-canonical TGFβ signaling via p38 and pERK1/2 MAPK pathways. Conclusions These findings demonstrate that TGFβ2 derived from vascular SMCs is essential for postnatal aortic wall homeostasis by preserving SMC differentiation, maintaining extracellular matrix integrity, and supporting and preserving a proper balance of both canonical and non-canonical TGFβ signaling. Loss of SMC-specific Tgfb2 precipitates medial degeneration, aneurysm formation, dissection, and rupture, providing direct mechanistic insight into TGFB2 -associated aortopathy and establishing a robust novel genetic mouse model for evaluating targeted therapies in TAAD. Highlights Postnatal, SMC-specific Tgfb2 deletion in mice caused rapidly progressive thoracic aortic aneurysms, dissections, and fatal rupture. Loss of Tgfb2 disrupts SMC contractile phenotype and ECM homeostasis, leading to medial degeneration, elastin fragmentation, and abnormal collagen/proteoglycan accumulation. Canonical TGFβ–SMAD signaling is suppressed, while MAPK pathways are activated, indicating ligand-specific signaling imbalance. Findings highlight TGFβ2 as a central regulator of postnatal aortic homeostasis and suggest that targeted ligand-specific therapeutic strategies may better preserve aortic wall stability. Significance This study identifies smooth muscle cell–derived TGFβ2 as a critical, nonredundant regulator of postnatal aortic wall integrity, linking its loss to thoracic aortic aneurysm, dissection, and rupture, and highlighting TGFβ2 ligand-specific signaling as a targeted therapeutic target. Graphical Abstract Smooth muscle cell–derived TGFβ2 maintains postnatal aortic wall homeostasis by preserving contractile gene expression, elastin architecture, and balanced ECM remodeling. Conditional deletion of Tgfb2 in SMCs shifts signaling from canonical SMAD2/3 to MAPK pathways, leading to medial degeneration, progressive aneurysm, dissection, and rupture—highlighting TGFβ2 as a nonredundant, ligand-specific regulator and potential therapeutic target in thoracic aortopathy.

  PublisherOA PDFDOI

• Revisiting Physical Parameters of the Benchmark Brown Dwarf LHS 6343 C through a Hubble Space Telescope/WFC3 Secondary-eclipse Observation

  The Astrophysical Journal · 2024-09-01 · 2 citations

  articleOpen access

  Abstract The LHS 6343 system consists of a resolved M-dwarf binary with an evolved, negligibly irradiated brown dwarf (BD), LHS 6343 C, orbiting the primary star. Such BD eclipsing binaries present rare and unique opportunities to calibrate substellar evolutionary and atmosphere models since mass, radius, temperature, and luminosity can be directly measured. We update this BD’s mass (62.6 ± 2.2 M Jup ) and radius (0.788 ± 0.043 R Jup ) using empirical stellar relations and a Gaia Data Release 3 distance. We use Hubble Space Telescope/Wide Field Camera 3 (WFC3) observations of an LHS 6343 C secondary eclipse to obtain a near-IR emission spectrum, which matches to a spectral type of T1.5 ± 1. We combine this spectrum with existing Kepler and Spitzer/IRAC secondary-eclipse photometry to perform atmospheric characterization using the ATMO-2020, Sonora-Bobcat, and BT-Settl model grids. ATMO-2020 models with strong nonequilibrium chemistry yield the best fit to observations across all modeled bandpasses while predicting physical parameters consistent with Gaia-dependent analogs. BT-Settl predicts values slightly more consistent with such analogs but offers a significantly poorer fit to the WFC3 spectrum. Finally, we obtain a semi-empirical measurement of LHS 6343 C’s apparent luminosity by integrating its observed and modeled spectral energy distribution. Applying knowledge of the system’s distance yields a bolometric luminosity of log( L bol / L ☉ ) = −4.77 ± 0.03 and, applying the Stefan–Boltzmann law for the known radius, an effective temperature of 1303 ± 29 K. We also use the ATMO-2020 and Sonora-Bobcat evolutionary model grids to infer an age for LHS 6343 C of <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" overflow="scroll"> <mml:mn>2.86</mml:mn> <mml:mspace width="0.08cm"/> <mml:msubsup> <mml:mrow/> <mml:mrow> <mml:mo>−</mml:mo> <mml:mn>0.33</mml:mn> </mml:mrow> <mml:mrow> <mml:mo>+</mml:mo> <mml:mn>0.40</mml:mn> </mml:mrow> </mml:msubsup> <mml:mspace width="0.25em"/> <mml:mi>Gyr</mml:mi> </mml:math> and <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" overflow="scroll"> <mml:mn>3.11</mml:mn> <mml:mspace width="0.08cm"/> <mml:msubsup> <mml:mrow/> <mml:mrow> <mml:mo>−</mml:mo> <mml:mn>0.38</mml:mn> </mml:mrow> <mml:mrow> <mml:mo>+</mml:mo> <mml:mn>0.50</mml:mn> </mml:mrow> </mml:msubsup> <mml:mspace width="0.25em"/> <mml:mi>Gyr</mml:mi> </mml:math> respectively.

  PublisherDOI

• Trials and Tribulations in the Reanalysis of KELT-24 b: a Case Study for the Importance of Stellar Modeling

  arXiv (Cornell University) · 2024-06-06

  preprintOpen access

  We present a new analysis of the KELT-24 system, comprising a well-aligned hot Jupiter, KELT-24~b, and a bright ($V=8.3$), nearby ($d=96.9~\mathrm{pc}$) F-type host star. KELT-24~b was independently discovered by two groups in 2019, with each reporting best-fit stellar parameters that were notably inconsistent. Here, we present three independent analyses of the KELT-24 system, each incorporating a broad range of photometric and spectroscopic data, including eight sectors of TESS photometry and more than 200 new radial velocities (RVs) from MINERVA. Two of these analyses use KELT-24's observed spectral energy distribution (SED) through a direct comparison to stellar evolutionary models, while our third analysis assumes an unknown additional body contributing to the observed broadband photometry and excludes the SED. Ultimately, we find that the models that include the SED are a poor fit to the available data, so we adopt the system parameters derived without it. We also highlight a single transit-like event observed by TESS, deemed likely to be an eclipsing binary bound to KELT-24, that will require follow-up observations to confirm. We discuss the potential of these additional bodies in the KELT-24 system as a possible explanation for the discrepancies between the results of the different modeling approaches, and explore the system for longer-period planets that may be weakly evident in the RV observations. The comprehensive investigations that we present not only increase the fidelity of our understanding of the KELT-24 system, but also serve as a blueprint for future stellar modeling in global analyses of exoplanet systems.

  PublisherOA PDFDOI

• Clinical and Demographic Factors Associated With COVID-19, Severe COVID-19, and SARS-CoV-2 Infection in Adults

  JAMA Network Open · 2023 · 23 citations

  • Medicine
  • Demography
  • Internal medicine

  Importance: Current data identifying COVID-19 risk factors lack standardized outcomes and insufficiently control for confounders. Objective: To identify risk factors associated with COVID-19, severe COVID-19, and SARS-CoV-2 infection. Design, Setting, and Participants: This secondary cross-protocol analysis included 4 multicenter, international, randomized, blinded, placebo-controlled, COVID-19 vaccine efficacy trials with harmonized protocols established by the COVID-19 Prevention Network. Individual-level data from participants randomized to receive placebo within each trial were combined and analyzed. Enrollment began July 2020 and the last data cutoff was in July 2021. Participants included adults in stable health, at risk for SARS-CoV-2, and assigned to the placebo group within each vaccine trial. Data were analyzed from April 2022 to February 2023. Exposures: Comorbid conditions, demographic factors, and SARS-CoV-2 exposure risk at the time of enrollment. Main Outcomes and Measures: Coprimary outcomes were COVID-19 and severe COVID-19. Multivariate Cox proportional regression models estimated adjusted hazard ratios (aHRs) and 95% CIs for baseline covariates, accounting for trial, region, and calendar time. Secondary outcomes included severe COVID-19 among people with COVID-19, subclinical SARS-CoV-2 infection, and SARS-CoV-2 infection. Results: A total of 57 692 participants (median [range] age, 51 [18-95] years; 11 720 participants [20.3%] aged ≥65 years; 31 058 participants [53.8%] assigned male at birth) were included. The analysis population included 3270 American Indian or Alaska Native participants (5.7%), 7849 Black or African American participants (13.6%), 17 678 Hispanic or Latino participants (30.6%), and 40 745 White participants (70.6%). Annualized incidence was 13.9% (95% CI, 13.3%-14.4%) for COVID-19 and 2.0% (95% CI, 1.8%-2.2%) for severe COVID-19. Factors associated with increased rates of COVID-19 included workplace exposure (high vs low: aHR, 1.35 [95% CI, 1.16-1.58]; medium vs low: aHR, 1.41 [95% CI, 1.21-1.65]; P < .001) and living condition risk (very high vs low risk: aHR, 1.41 [95% CI, 1.21-1.66]; medium vs low risk: aHR, 1.19 [95% CI, 1.08-1.32]; P < .001). Factors associated with decreased rates of COVID-19 included previous SARS-CoV-2 infection (aHR, 0.13 [95% CI, 0.09-0.19]; P < .001), age 65 years or older (aHR vs age <65 years, 0.57 [95% CI, 0.50-0.64]; P < .001) and Black or African American race (aHR vs White race, 0.78 [95% CI, 0.67-0.91]; P = .002). Factors associated with increased rates of severe COVID-19 included race (American Indian or Alaska Native vs White: aHR, 2.61 [95% CI, 1.85-3.69]; multiracial vs White: aHR, 2.19 [95% CI, 1.50-3.20]; P < .001), diabetes (aHR, 1.54 [95% CI, 1.14-2.08]; P = .005) and at least 2 comorbidities (aHR vs none, 1.39 [95% CI, 1.09-1.76]; P = .008). In analyses restricted to participants who contracted COVID-19, increased severe COVID-19 rates were associated with age 65 years or older (aHR vs <65 years, 1.75 [95% CI, 1.32-2.31]; P < .001), race (American Indian or Alaska Native vs White: aHR, 1.98 [95% CI, 1.38-2.83]; Black or African American vs White: aHR, 1.49 [95% CI, 1.03-2.14]; multiracial: aHR, 1.81 [95% CI, 1.21-2.69]; overall P = .001), body mass index (aHR per 1-unit increase, 1.03 [95% CI, 1.01-1.04]; P = .001), and diabetes (aHR, 1.85 [95% CI, 1.37-2.49]; P < .001). Previous SARS-CoV-2 infection was associated with decreased severe COVID-19 rates (aHR, 0.04 [95% CI, 0.01-0.14]; P < .001). Conclusions and Relevance: In this secondary cross-protocol analysis of 4 randomized clinical trials, exposure and demographic factors had the strongest associations with outcomes; results could inform mitigation strategies for SARS-CoV-2 and viruses with comparable epidemiological characteristics.

  PublisherOA PDFDOI

• The Metallicity Distribution and Hot Jupiter Rate of the Kepler Field: Hectochelle High-resolution Spectroscopy for 776 Kepler Target Stars

  DSpace@MIT (Massachusetts Institute of Technology) · 2023-07-21

  articleOpen access

  The occurrence rate of hot Jupiters from the Kepler transit survey is roughly half that of radial velocity surveys targeting solar neighborhood stars. One hypothesis to explain this difference is that the two surveys target stars with different stellar metallicity distributions. To test this hypothesis, we measure the metallicity distribution of the Kepler targets using the Hectochelle multi-fiber, high-resolution spectrograph. Limiting our spectroscopic analysis to 610 dwarf stars in our sample with &gt; 3.5, we measure a metallicity distribution characterized by a mean of [M H]mean = -0.045 ± 0.009, in agreement with previous studies of the Kepler field target stars. In comparison, the metallicity distribution of the California Planet Search radial velocity sample has a mean of [M H]CPS,mean = -0.005 ± 0.006, and the samples come from different parent populations according to a Kolmogorov-Smirnov test. We refit the exponential relation between the fraction of stars hosting a close-in giant planet and the host star metallicity using a sample of dwarf stars from the California Planet Search with updated metallicities. The best-fit relation tells us that the difference in metallicity between the two samples is insufficient to explain the discrepant hot Jupiter occurrence rates; the metallicity difference would need to be ≃0.2-0.3 dex for perfect agreement. We also show that (sub)giant contamination in the Kepler sample cannot reconcile the two occurrence calculations. We conclude that other factors, such as binary contamination and imperfect stellar properties, must also be at play.

  PublisherDOI

• Speedy downloads: Why NASA is turning to lasers for next-gen space comms

  Knowable Magazine · 2023-11-13

  article1st authorCorresponding
  PublisherDOI

• Increased TGFβ1 and SMAD3 Contribute to Age-Related Aortic Valve Calcification

  Frontiers in Cardiovascular Medicine · 2022-07-19 · 17 citations

  articleOpen access

  Aims Calcific aortic valve disease (CAVD) is a progressive heart disease that is particularly prevalent in elderly patients. The current treatment of CAVD is surgical valve replacement, but this is not a permanent solution, and it is very challenging for elderly patients. Thus, a pharmacological intervention for CAVD may be beneficial. In this study, we intended to rescue aortic valve (AV) calcification through inhibition of TGFβ1 and SMAD3 signaling pathways. Methods and Results The klotho gene, which was discovered as an aging-suppressor gene, has been observed to play a crucial role in AV calcification. The klotho knockout ( Kl –/– ) mice have shorter life span (8–12 weeks) and develop severe AV calcification. Here, we showed that increased TGFβ1 and TGFβ-dependent SMAD3 signaling were associated with AV calcification in Kl –/– mice. Next, we generated Tgfb1 - and Smad3 -haploinsufficient Kl –/– mice to determine the contribution of TGFβ1 and SMAD3 to the AV calcification in Kl –/– mice. The histological and morphometric evaluation suggested a significant reduction of AV calcification in Kl –/– ; Tgfb1 ± mice compared to Kl –/– mice. Smad3 heterozygous deletion was observed to be more potent in reducing AV calcification in Kl –/– mice compared to the Kl –/– ; Tgfb1 ± mice. We observed significant inhibition of Tgfb1 , Pai1 , Bmp2, Alk2 , Spp1 , and Runx2 mRNA expression in Kl –/– ; Tgfb1 ± and Kl –/– ; Smad3 ± mice compared to Kl –/– mice. Western blot analysis confirmed that the inhibition of TGFβ canonical and non-canonical signaling pathways were associated with the rescue of AV calcification of both Kl –/– ; Tgfb1 ± and Kl –/– ; Smad3 ± mice. Conclusion Overall, inhibition of the TGFβ1-dependent SMAD3 signaling pathway significantly blocks the development of AV calcification in Kl –/– mice. This information is useful in understanding the signaling mechanisms involved in CAVD.

  PublisherDOI

• PLANETS AROUND LOW-MASS STARS (PALMS). V. AGE-DATING LOW-MASS COMPANIONS TO MEMBERS AND INTERLOPERS OF YOUNG MOVING GROUPS

  UNC Libraries · 2021-07-03

  articleOpen access

  We present optical and near-infrared adaptive optics (AO) imaging and spectroscopy of 13 ultracool (>M6) companions to late-type stars (K7-M4.5), most of which have recently been identified as candidate members of nearby young moving groups (YMGs; 8-120 Myr) in the literature. The inferred masses of the companions (~10-100 Mjup) are highly sensitive to the ages of the primary stars so we critically examine the kinematic and spectroscopic properties of each system to distinguish bona fide YMG members from old field interlopers. 2MASS J02155892-0929121 C is a new M7 substellar companion (40-60 Mjup) with clear spectroscopic signs of low gravity and hence youth. The primary, possibly a member of the ~40 Myr Tuc-Hor moving group, is visually resolved into three components, making it a young low-mass quadruple system in a compact (1 Gyr) tidally-locked spectroscopic binaries without convincing kinematic associations with any known moving group. The high rate of false positives in the form of old active stars with YMG-like kinematics underscores the importance of radial velocity and parallax measurements to validate candidate young stars identified via proper motion and activity selection alone. Finally, we spectroscopically confirm the cool temperature and substellar nature of HD 23514 B, a recently discovered M8 benchmark brown dwarf orbiting the dustiest-known member of the Pleiades.

  PublisherDOI

• Myocardial TGFβ2 Is Required for Atrioventricular Cushion Remodeling and Myocardial Development

  Journal of Cardiovascular Development and Disease · 2021-03-02 · 7 citations

  articleOpen access

  Among the three transforming growth factor beta (TGFβ) ligands, TGFβ2 is essential for heart development and is produced by multiple cell types, including myocardium. Heterozygous mutations in TGFB2 in patients of connective tissue disorders result in congenital heart defects and adult valve malformations, including mitral valve prolapse (MVP) with or without regurgitation. Tgfb2 germline knockout fetuses exhibit multiple cardiac defects but the role of myocardial-TGFβ2 in heart development is yet to be elucidated. Here, myocardial Tgfb2 conditional knockout (CKO) embryos were generated by crossing Tgfb2flox mice with Tgfb2+/−; cTntCre mice. Tgfb2flox/− embryos were normal, viable. Cell fate mapping was done using dual-fluorescent mT/mG+/− mice. Cre-mediated Tgfb2 deletion was assessed by genomic PCR. RNAscope in situ hybridization was used to detect the loss of myocardial Tgfb2 expression. Histological, morphometric, immunohistochemical, and in situ hybridization analyses of CKOs and littermate controls at different stages of heart development (E12.5–E18.5) were used to determine the role of myocardium-derived TGFβ2 in atrioventricular (AV) cushion remodeling and myocardial development. CKOs exhibit a thin ventricular myocardium, AV cushion remodeling defects and developed incomplete AV septation defects. The loss of myocardial Tgfb2 resulted in impaired cushion maturation and dysregulated cell death. Phosphorylated SMAD2, a surrogate for TGFβ signaling, was “paradoxically” increased in both AV cushion mesenchyme and ventricular myocardium in the CKOs. Our results indicate that TGFβ2 produced by cardiomyocytes acting as cells autonomously on myocardium and via paracrine signaling on AV cushions are required for heart development.

  PublisherOA PDFDOI

• CHARACTERIZING THE COOL KOIs. VII. REFINED PHYSICAL PROPERTIES OF THE TRANSITING BROWN DWARF LHS 6343 C

  UNC Libraries · 2021-07-02

  articleOpen access

  We present an updated analysis of LHS 6343, a triple system in the Kepler field which consists of a brown dwarf eclipsing one member of a widely-separated M+M binary system. By analyzing the full Kepler dataset and 34 Keck/HIRES radial velocity observations, we measure both the observed eclipse depth and Doppler semiamplitude to 0.5% precision. With Robo-AO and Palomar/PHARO adaptive optics imaging as well as TripleSpec spectroscopy, we measure a model-dependent mass for LHS 6343 C of 62.1 +/- 1.2 M_Jup and a radius of 0.783 +/- 0.011 R_Jup. We detect the secondary eclipse in the Kepler data at 3.5 sigma, measuring e cos omega = 0.0228 +/- 0.0008. We also derive a method to measure the mass and radius of a star and transiting/eclipsing companion directly, without any reliance on stellar models. The mass and radius of both objects depend only on the orbital period, stellar density, reduced semimajor axis, Doppler semiamplitude, eccentricity, and inclination. With this method, we calculate a model-independent mass and radius for LHS 6343 C to a precision of 3% and 2%, respectively.

  PublisherDOI

Recent grants

• MINERVA: Purchase of Kiwispec, a Robotic Precision Spectrograph to Detect Earth-Like Planets Around Nearby Stars

  NSF · $1.1M · 2016–2020

• MINERVA: A dedicated observatory for exoplanet science

  NSF · $469k · 2015–2019

• Exploring the Relationship Between Stellar Mass and Planet Occurrence

  NSF · $139k · 2007–2009

Frequent coauthors

• Andrew W. Howard

  California Institute of Technology

  176 shared

• Geoffrey W. Marcy

  Health Awareness (United States)

  167 shared

• R. Paul Butler

  Carnegie Institution for Science

  136 shared

• Debra A. Fischer

  132 shared

• Robert A. Wittenmyer

  108 shared

• Lars A. Buchhave

  106 shared

• David W. Latham

  102 shared

• Howard Isaacson

  96 shared

Education

• Ph.D., Astronomy

  Harvard University

  2008

• B.A., Physics

  Harvard University

  2003