Biology subjects

Moore, K. J.

Publications and source records attributed to Moore, K. J..

5 recordsLinked to original sources

bioRxiv2025

Trends in stomatal density and size in maize hybrids representing 100 years of long-term breeding for yield

Maize hybrid breeding started over 100 years ago, has increased yield and vigor through improved genetics in conjunction with increased fertilizer and pesticide use, planting density, and agricultural mechanization. Stomata are expected to change in response to rising atmospheric CO2 concentration and average temperature anomalies ({degrees}C). Yet, the impact of long-term maize breeding over the past century on stomatal traits and their responses to climate factors remains poorly understood. We evaluated stomatal traits at the seedling stage in 27 maize hybrids released from 1920 to 2022, grown under controlled conditions. Modern hybrids (2013 - 2022) had a smaller total stomatal pore area (9.17 x 108 m2) than (1920 - 2012) historical ERA hybrids (9.94 x 108 m2; p[≤] 0.001), a higher stomatal density (47.2 per mm-2) vs. historical ERA hybrids (44.5), and a smaller leaf area (17.9 cm2 vs. 20.5 cm2). No significant differences were found in the size (m2), length (m), or width (m) of stomata between the two groups. Stomatal density increased, while all other traits decreased in modern hybrids. Stomatal density was negatively correlated with stomatal size (r = -0.62), length (r = -0.57), width (r = - 0.54), and leaf area (r = -0.54). Stomatal size had a negative correlation with atmospheric CO2 concentration (r = -0.22) and average temperature anomalies ({degrees}C) (r = -0.35) in the hybrids year of release and climate proxies. In contrast, stomatal density had a positive correlation with both atmospheric CO2 concentration and average temperature anomalies ({degrees}C) (r = 0.44) in year of release. Total stomatal pore area negatively correlated with atmospheric CO2 concentration (r = -0.45) and average temperature anomalies ({degrees}C) (r = -0.36). Our study indicates that maize stomatal traits suggest inadvertent selection for key stomatal traits (density and size), total stomatal pore area (per year decline of about 0.02%) associated with yield stability and environmental adaptation. HighlightsMaize stomatal traits changed through environmental (CO2 and {degrees}C) adaptation but total stomatal pore area, effects indirectly by decreased leaf area in maize hybrids representing 100 years of long-term breeding for yield. A negative correlation was observed across 27 ERA hybrids between stomatal density and stomatal size, length, width and leaf area. Stomatal density increases while stomata size, length width and leaf area decrease per se. Over the past 100 years, the total stomatal pore area on leaves decreased, while stomatal density increased as leaf area declined, revealing a connection between these two patterns. A negative correlation was found between total stomatal pore area and atmospheric CO2 concentrations, and temperature over the past century.

genetics↗

bioRxiv2025

Sex and reproductive condition shape thermal acclimation strategy in a plethodontid salamander

The question of whether males and females differ in their responses to temperature is essential to understanding adaptive capacities in a warming world. However, sex has traditionally been neglected in the field of thermal ecology, and our understanding of the factors that promote sex differences in thermal plasticity is underdeveloped. Here, we investigate the independent and interactive effects of sex and reproductive condition on thermal acclimation capacity in a plethodontid salamander (Plethodon cinereus). We carried out two stop-flow respirometry experiments, with salamanders acclimated to one of two thermal environments designed to simulate a Cool or Warm breeding season. In the first experiment, we compared the thermal acclimation responses of males and gravid females across a gradient of three ecologically relevant test temperatures and observed distinct patterns of sexual dimorphism of standardized metabolic rate (SMR) between thermal treatments that were not attributable to differences in body size. Specifically, gravid females in the warm treatment showed reduced SMR relative to gravid females in the cool treatment, particularly at higher test temperatures. In the second experiment, we expanded on our initial findings by directly testing the contribution of reproductive condition to observed sex differences in thermal acclimation capacity. By repeating the experiment of the early breeding season but including a third group of non-gravid females, we: (1) recapitulated our original finding - that gravid females exhibit a pronounced response to thermal acclimation relative to males; and (2) showed that female thermal acclimation responses are absent in nongravid females, and therefore we concluded that responses are contingent on reproductive condition. Taken together, our results provide a first glimpse into how sex and reproductive condition contribute to intraspecific variation in thermal acclimation capacity in an amphibian and underscore the need for more hypothesis-driven studies to directly test when, where, and how such patterns arise.

physiology↗

bioRxiv2025

Ischemic Injury Drives Tumor Growth via Accelerated Hematopoietic Aging

BackgroundPatients with peripheral artery disease have increased risk of cancer development. Aging-associated changes in hematopoietic stem and progenitor cells (HSPCs), including inflammation and increased myelopoiesis, are implicated in both cardiovascular disease (CVD) and cancer, but their contributions to CVD-driven tumor progression are unclear. ObjectivesTo study cancer growth following peripheral ischemia and consequent changes within the HSPC bone marrow compartment to uncover mechanisms through which altered hematopoiesis promotes oncogenesis. MethodsMammary cancer cell (E0771) growth was monitored in C57BL/6J mice after hind limb ischemia (HLI) or sham surgery. The tumor immune microenvironment, circulatory immune cells, and HSPC compartment were assessed by flow cytometry. Next-generation single-cell RNA and ATAC sequencing of HSPCs was performed to assess transcriptomic and epigenetic changes. The functional impact on tumor progression and persistence of ischemia-induced epigenetic reprogramming of HSPCs and their myeloid progeny was examined by bone marrow transplantation. ResultsPeripheral ischemia increased monocyte and neutrophil output at the expense of lymphocytes, driven by a shift toward CD150hi myeloid-biased hematopoietic stem cells (HSCs). This was associated with accelerated breast cancer growth and increased accumulation of tumoral immunosuppressive regulatory T cells and monocytes. Increased myelopoiesis was also supported by multiomic analyses showing HLI-induced transcriptional and epigenetic enrichment for inflammatory (NLRP3 inflammasome) and aging-associated (Neogenin-1, Thrombospondin-1) signatures in subsets of monocyte/dendritic progenitors. HLI-accelerated tumor growth and myeloid-skewing was transmissible via bone marrow transplantation, indicating long-term reprogramming of innate immune responses. ConclusionsPeripheral ischemia promotes inflammaging of HSCs and long-lasting alterations to anti-tumoral immunity, accelerating breast tumor growth.

immunology↗

bioRxiv2023

SARS-CoV-2 infection triggers pro-atherogenic inflammatory 1 responses in human coronary vessels

COVID-19 patients present higher risk for myocardial infarction (MI), acute coronary syndrome, and stroke for up to 1 year after SARS-CoV-2 infection. While the systemic inflammatory response to SARS-CoV-2 infection likely contributes to this increased cardiovascular risk, whether SARS-CoV-2 directly infects the coronary vasculature and attendant atherosclerotic plaques to locally promote inflammation remains unknown. Here, we report that SARS-CoV-2 viral RNA (vRNA) is detectable and replicates in coronary atherosclerotic lesions taken at autopsy from patients with severe COVID-19. SARS-CoV-2 localizes to plaque macrophages and shows a stronger tropism for arterial lesions compared to corresponding perivascular fat, correlating with the degree of macrophage infiltration. In vitro infection of human primary macrophages highlights that SARS-CoV-2 entry is increased in cholesterol-loaded macrophages (foam cells) and is dependent, in part, on neuropilin-1 (NRP-1). Furthermore, although viral replication is abortive, SARS-CoV-2 induces a robust inflammatory response that includes interleukins IL-6 and IL-1{beta}, key cytokines known to trigger ischemic cardiovascular events. SARS-CoV-2 infection of human atherosclerotic vascular explants recapitulates the immune response seen in cultured macrophages, including pro-atherogenic cytokine secretion. Collectively, our data establish that SARS-CoV-2 infects macrophages in coronary atherosclerotic lesions, resulting in plaque inflammation that may promote acute CV complications and long-term risk for CV events.

immunology↗

bioRxiv2019

Fatty acid oxidation impairs macrophage effector functions that control Mycobacterium tuberculosis

Macrophage activation involves metabolic reprogramming to support antimicrobial cellular functions. How these metabolic shifts influence the outcome of infection by intracellular pathogens remains incompletely understood. M. tuberculosis (Mtb) modulates host metabolic pathways and utilizes host nutrients, including cholesterol and fatty acids, to survive within macrophages. We found that intracellular growth of Mtb depends on host fatty acid catabolism: when host fatty acid {beta}-oxidation (FAO) was blocked chemically with trimetazidine, a compound in clinical use, or genetically by deletion of the mitochondrial fatty acid transporter carnitine palmitoyltransferase 2 (CPT2), Mtb failed to grow in macrophages and its growth was attenuated in mice. Global metabolic profiling and mechanistic studies support a model in which inhibition of FAO generates mitochondrial reactive oxygen species, which enhance macrophage NADPH oxidase and xenophagy activity to better control Mtb infection. Thus, FAO inhibition promotes key antimicrobial functions of macrophages and overcomes immune evasion mechanisms of Mtb.

microbiology↗