Biology subjects

Ta, K.

Publications and source records attributed to Ta, K..

3 recordsLinked to original sources

bioRxiv2026

Eleven deep-sea coral genome assemblies unveil insights into evolution, adaptation, and coral biodiversity

Deep-sea corals are vital in maintaining coral ecosystem biodiversity, yet their genetic characteristics remain largely unexplored. Here, we present 11 deep-sea coral genome assemblies, including four Hexacorallia and seven Octocorallia species, significantly contributing new genomic information across two orders. Our analysis reveals the historical dynamics of coral speciation and the influence of environmental factors on the evolution of coral reef ecosystems.Total of 126 horizontal gene transfer (HGT) events were detected, among which genes from the ancestor of symbiodiniaceae indicate that the ancestors of deep-sea corals may have inhabited shallow-sea environments. Notably, several of these HGTs are involved in phosphorus (PhnX/PhnW) and cholesterol (DHCR7) metabolisms within corals, indicating that HGTs may serve as an adaptive survival strategy for the coral holobionts. Deep-sea corals also rely on symbiotic bacteria to synthesize 10 essential amino acids (such as valine and tyrosine), retaining only partial amino acid synthesis capacity. In addition, we investigated the evolution of key biological rhythm genes and temperature adaptation in corals. The loss of key rhythm genes (e.g., clock and cry) in deep-sea corals and copy number difference of genes related to heat stress (e.g., Cbl-b and Rchy) revealed genetic difference between deep-sea and shallow-sea corals. Our new genome assemblies enhance the understanding of deep-sea coral evolution, biodiversity, and adaptation, providing a genetic foundation for coral conservation.

genomics↗

bioRxiv2026

A Long-lived Avatar for Modeling Age-Related Vascular Disease

BackgroundCurrent microphysiological models do not support long-term investigations into the chronic effects of vascular risk factors and the development of vascular diseases. Prolonged culture frequently leads to cellular senescence and loss of functional integrity, resulting in variability and inconsistency in modeling chronic vascular responses. Here we aimed to develop and sustain a long-term multicellular human vascular avatar, addressing the critical need for long-term disease modeling and drug testing. MethodsTo identify the optimal media for longevity, cell identity and function were assessed by morphology, qPCR, beta-gal staining, ELISA, bulk RNA-seq and single cell RNA-seq analysis. After optimizing the culture media, iPSCs-derived ECs and VSMCs from unaffected and Hutchinson-Gilford Progeria Syndrome (HGPS) donors were grown in Gravitational Lumen Patterning (GLP) Vessel- Chips for 1-6 months to generate a long-lived vascular avatar for the study of vascular aging. ResultsGuided by quantitative morphological analyses and bulk RNAseq profiling, we generated a novel optimized culture media VSL (VEGF, SB431542 as a TGF-{beta} inhibitor, low fetal bovine serum) that enhances the long-term health of vascular endothelial cells (ECs). Furthermore, we modified the VSL formulation (mVSL) by modulating 8Br-cAMP, FGF, PDGF, and a cell viability enhancer HMH1015 levels to enhance EC-VSMC (vascular smooth muscle cell) crosstalk and support long-term cellular viability. Subsequently, we maintained and characterized a human vascular avatar with a three-dimensional extracellular matrix environment and 3D vascular architecture for over 180 days. Finally, we demonstrated that this long-lived human vascular avatar enabled modeling vascular aging using iPSC-derived vascular cells from patients with Hutchinson-Gilford Progeria Syndrome (HGPS). ConclusionsWe have successfully engineered and maintained a human vascular avatar for over 180 days. The vascular avatar provides a robust platform for modeling disease-associated vascular aging and for evaluating therapeutic strategies targeting chronic vascular disorders.

bioengineering↗

bioRxiv2020

Molecular and physiological responses predict acclimation limits in juvenile brook trout ( Salvelinus fontinalis )

Brook trout (Salvelinus fontinalis) populations are at risk of exposure to high water temperatures in the species native range in eastern North America. We quantified the physiological and molecular responses of juvenile brook trout to six acclimation temperatures that span the thermal distribution of the species (5, 10, 15, 20, 23, and 25{degrees}C). Using quantitative PCR (qPCR), we measured the mRNA transcript abundance of temperature-induced cellular stress genes to identify a potential sub-lethal temperature threshold for brook trout between 20-23{degrees}C. Brook trout exhibited an upregulation of stress-related genes (heat shock protein 90-beta; heat shock cognate 71 kDa protein; glutathione peroxidase 1) and a downregulation of transcription factors and osmoregulation-related genes (Na+/K+/2Cl- co-transporter-1-a; nuclear protein 1) at temperatures [≥]20{degrees}C. We also used respirometry to assess the effects of the acclimation temperatures on oxygen consumption. Standard metabolic rate results indicated that energy expenditure was higher at temperatures [≥]20{degrees}C. We then examined the effects of acclimation temperature on metabolic rate and blood plasma parameters in fish exposed to an acute exhaustive exercise and air exposure stress. Fish acclimated to temperatures [≥]20{degrees}C exhibited elevated levels of plasma cortisol, muscle lactate, and plasma glucose after exposure to the acute stressors. After 24 h of recovery, fish showed longer metabolic recovery times at 15 and 20{degrees}C and cortisol levels remaining elevated at temperatures [≥]20{degrees}C. Our findings suggest that brook trout may have a limited ability to acclimate to temperatures >20{degrees}C and increases in temperatures beyond 20{degrees}C may impact brook trout populations.

physiology↗