Single‐Cell Transcriptomics and Metabolomics Reveal Glutamate Dehydrogenase as a Central Regulator of Nitrogen Metabolic Remodeling During Alkalinity Adaptation in Crustaceans
5 affiliations
- 1Key Laboratory of Exploration and Utilization of Aquatic Genetic Resources, Ministry of Education Shanghai Ocean University Shanghai China
- 2Laboratory of Aquatic Genomics, College of Life Sciences and Oceanography Shenzhen University Shenzhen China
- 3Tropical Aquaculture Research and Development Center, South China Sea Fisheries Research Institute Chinese Academy of Fishery Sciences Sanya China
- 4School of Pharmacy, Laboratory of Drug Discovery from Natural Resources and Industrialization, State Key Laboratory of Mechanism and Quality of Chinese Medicine Macau University of Science and Technology Taipa Macau China
- 5College of Science and Engineering Flinders University Adelaide Australia
Abstract
Alkaline environments disrupt ammonia excretion and challenge nitrogen metabolism in aquatic invertebrates, but the underlying cellular mechanisms remain unclear. To elucidate the adaptive mechanisms of crustaceans in highly alkaline environments, the responses of Macrobrachium hainanense to acute carbonate alkalinity stress are characterized using single‐cell RNA sequencing. High alkalinity inhibits normal ammonia excretion, leading to ammonia accumulation in the hemolymph, gill injury, mitochondrial dysfunction, and elevated oxidative stress. Marked heterogeneous remodeling occurs across distinct cell populations; pillar cells, nephrocytes, and semi‐granulocytes play primary roles in nitrogen metabolic regulation, acid‐base homeostasis, and immune defense, respectively. Further analyses identify glutamate dehydrogenase (GDH) as a key regulator of alkalinity adaptation. Inhibition of GDH significantly reduces alkaline tolerance, exacerbating tissue damage and metabolic disturbances while impairing ATP maintenance and inducing mitochondrial dysfunction under alkaline stress. Furthermore, GDH suppression inhibits urea metabolism while enhancing purine catabolism, indicating an adaptive shift in nitrogen metabolic strategy. This study provides a single‐cell resolution of crustacean alkalinity adaptation and identifies GDH‐mediated metabolic remodeling as a determinant of the environmental stress response. These findings offer theoretical insights into the regulatory mechanisms underlying stress adaptation in invertebrates.
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BibTeX
@article{jin2026singlecell,
title = {{Single‐Cell Transcriptomics and Metabolomics Reveal Glutamate Dehydrogenase as a Central Regulator of Nitrogen Metabolic Remodeling During Alkalinity Adaptation in Crustaceans}},
author = {Yiting Jin and Zhimin Lv and Chao Bian and Qibin Yang and Na Zhou and Jianguang Qin and Shengming Sun},
journal = {Advanced Science},
year = {2026},
month = aug,
doi = {10.1002/advs.76978},
url = {https://doi.org/10.1002/advs.76978},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Single‐Cell Transcriptomics and Metabolomics Reveal Glutamate Dehydrogenase as a Central Regulator of Nitrogen Metabolic Remodeling During Alkalinity Adaptation in Crustaceans
AU - Yiting Jin
AU - Zhimin Lv
AU - Chao Bian
AU - Qibin Yang
AU - Na Zhou
AU - Jianguang Qin
AU - Shengming Sun
PY - 2026
DA - 2026/08/05
JO - Advanced Science
DO - 10.1002/advs.76978
UR - https://doi.org/10.1002/advs.76978
AB - Alkaline environments disrupt ammonia excretion and challenge nitrogen metabolism in aquatic invertebrates, but the underlying cellular mechanisms remain unclear. To elucidate the adaptive mechanisms of crustaceans in highly alkaline environments, the responses of Macrobrachium hainanense to acute carbonate alkalinity stress are characterized using single‐cell RNA sequencing. High alkalinity inhibits normal ammonia excretion, leading to ammonia accumulation in the hemolymph, gill injury, mitochondrial dysfunction, and elevated oxidative stress. Marked heterogeneous remodeling occurs across distinct cell populations; pillar cells, nephrocytes, and semi‐granulocytes play primary roles in nitrogen metabolic regulation, acid‐base homeostasis, and immune defense, respectively. Further analyses identify glutamate dehydrogenase (GDH) as a key regulator of alkalinity adaptation. Inhibition of GDH significantly reduces alkaline tolerance, exacerbating tissue damage and metabolic disturbances while impairing ATP maintenance and inducing mitochondrial dysfunction under alkaline stress. Furthermore, GDH suppression inhibits urea metabolism while enhancing purine catabolism, indicating an adaptive shift in nitrogen metabolic strategy. This study provides a single‐cell resolution of crustacean alkalinity adaptation and identifies GDH‐mediated metabolic remodeling as a determinant of the environmental stress response. These findings offer theoretical insights into the regulatory mechanisms underlying stress adaptation in invertebrates.
SN - 2198-3844
ER -