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Biology subjects

Arnold, K. M.

Publications and source records attributed to Arnold, K. M..

2 recordsLinked to original sources

The impact of temperature-induced vertebral anomalies on C-start swimming performance in Astyanax mexicanus (Teleostei: Characidae)

This study investigates the impact temperature-induced vertebral anomalies have on the C-start escape response of Astyanax mexicanus, a model species in evolutionary developmental biology. Employing three temperature treatments to induce varying degrees of skeletal anomalies, we assessed their effects on key swimming performance metrics including, C-start time, curvature coefficient, head displacement distance, and displacement velocity. Through the use of linear mixed models and generalized linear mixed models, our results reveal that specific anomalies such as vertebral fusions and anomalous haemal and neural spines affected the curving ability of C-start escape responses. However, these did not negatively impact other performance parameters, with velocity, distance, and response time showing no significant impacts from any anomaly types, when assessed individually. This suggests a complex interplay between structural deformities and compensatory physiological mechanisms that maintain functional performance. Other variables measured had a stronger and significant impact on swimming performance, including standard length, vertebral number, and temperature treatment, which influenced escape speed, curving ability, and overall locomotor performance. Our findings challenge conventional perceptions about the debilitating impact of vertebral anomalies, indicating that many affected fish can still effectively perform escape maneuvers critical for survival.

zoology↗

PH domain and leucine rich repeat phosphatase 1 (Phlpp1) suppresses parathyroid hormone receptor 1 (Pth1r) expression and signaling during bone growth

Endochondral ossification is tightly controlled by a coordinated network of signaling cascades including parathyroid hormone (PTH). PH domain and leucine rich repeat phosphatase (Phlpp1) affects endochondral ossification by suppressing chondrocyte proliferation in the growth plate, longitudinal bone growth, and bone mineralization. As such, Phlpp1-/- mice have shorter long bones, thicker growth plates, and proportionally larger growth plate proliferative zones. The goal of this study was to determine how Phlpp1 deficiency affects PTH signaling during bone growth. Transcriptomic analysis revealed greater Pth1r expression and H3K27ac enrichment at the Pth1r promoter in Phlpp1-deficient chondrocytes. PTH(1-34) enhanced and PTH(7-34) attenuated cell proliferation, cAMP signaling, CREB phosphorylation, and cell metabolic activity in Phlpp1-inhibited chondrocytes. To understand the role of Pth1r action in the endochondral phenotypes of Phlpp1-deficient mice, Phlpp1-/- mice were injected with Pth1r ligand PTH(7-34) daily for the first four weeks of life. PTH(7-34) reversed the abnormal growth plate and long bone growth phenotypes of Phlpp1-/- mice but did not rescue deficits in bone mineral density or trabecular number. These results demonstrate that elevated Pth1r expression and signaling contributes to increased proliferation in Phlpp1-/- chondrocytes and shorter bones in Phlpp1-deficient mice. Our data reveal a novel molecular relationship between Phlpp1 and Pth1r in chondrocytes during growth plate development and longitudinal bone growth.

molecular biology↗