Cell-type-specific glutamine synthetase inhibition reveals the intercellular nitrogen economy in Anabaena sp. PCC 7120.
- 1Department of Life Sciences, Imperial College London, South Kensington Campus, London SW7 2AZ, United Kingdom.
- 2Department of Biology, University of Padova, Via Ugo Bassi 58/B, Padova 35131, Italy.
- 3Instituto de Bioquímica Vegetal y Fotosíntesis, CSIC and University of Seville, Avda. Américo Vespucio 49, 41092 Seville, Spain.
Abstract
Nitrogen homeostasis in heterocyst-forming filamentous diazotrophic cyanobacteria depends on the coordination between two cell types: heterocysts, which fix atmospheric N2, and vegetative cells, which carry out oxygenic photosynthesis. Yet the cell-type-specific contribution of glutamine synthetase (GS), the central enzyme of nitrogen assimilation, to this coordination remains poorly understood. We used cell-type-specific overexpression of IF7A, the GS posttranslational inhibitor, in both wild-type Anabaena sp. PCC 7120 and Δamt genetic backgrounds, the latter lacking the high-affinity ammonium transporters (Amt) responsible for NH4+ uptake, to dissect the contribution of each cell type to the nitrogen economy of the filament. Whole-filament GS inhibition caused photosynthetic impairment, disruption of the NtcA-PII-PipX signaling axis, and growth arrest, establishing GS in vegetative cells as rate-limiting for filament growth. Heterocyst-targeted GS inhibition triggered accumulation of the nitrogen storage polymer cyanophycin, revealing that heterocyst GS governs the routing of fixed nitrogen either toward distribution or storage. Both phenotypes were amplified in the Δamt background. Using pharmacological inhibition of GS with ammonium excretion measurements, we demonstrate that Amt transporters recover nitrogen lost by passive NH3 diffusion under diazotrophic conditions and that their absence renders the internal nitrogen economy chronically more vulnerable to GS inhibition. In natural nitrogen-limited environments, where diazotrophic cyanobacteria cannot compensate for passive nitrogen loss through external uptake, this recycling function is critical for nitrogen fixation efficiency. Overall, our findings redefine the architecture of intercellular nitrogen homeostasis in filamentous diazotrophic cyanobacteria, establishing GS and Amt transporters as interdependent determinants of intercellular nitrogen retention, distribution, and storage.
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BibTeX
@article{malatinszky2026celltypespecific,
title = {{Cell-type-specific glutamine synthetase inhibition reveals the intercellular nitrogen economy in Anabaena sp. PCC 7120.}},
author = {David Malatinszky and Mattia Storti and Enrique Flores and Patrik Jones and Giorgio Perin},
journal = {Plant physiology},
year = {2026},
month = oct,
doi = {10.1093/plphys/kiag745},
url = {https://europepmc.org/article/MED/42837622},
note = {CC BY},
}
RIS
TY - JOUR
TI - Cell-type-specific glutamine synthetase inhibition reveals the intercellular nitrogen economy in Anabaena sp. PCC 7120.
AU - David Malatinszky
AU - Mattia Storti
AU - Enrique Flores
AU - Patrik Jones
AU - Giorgio Perin
PY - 2026
DA - 2026/10/01
JO - Plant physiology
DO - 10.1093/plphys/kiag745
UR - https://europepmc.org/article/MED/42837622
AB - Nitrogen homeostasis in heterocyst-forming filamentous diazotrophic cyanobacteria depends on the coordination between two cell types: heterocysts, which fix atmospheric N2, and vegetative cells, which carry out oxygenic photosynthesis. Yet the cell-type-specific contribution of glutamine synthetase (GS), the central enzyme of nitrogen assimilation, to this coordination remains poorly understood. We used cell-type-specific overexpression of IF7A, the GS posttranslational inhibitor, in both wild-type Anabaena sp. PCC 7120 and Δamt genetic backgrounds, the latter lacking the high-affinity ammonium transporters (Amt) responsible for NH4+ uptake, to dissect the contribution of each cell type to the nitrogen economy of the filament. Whole-filament GS inhibition caused photosynthetic impairment, disruption of the NtcA-PII-PipX signaling axis, and growth arrest, establishing GS in vegetative cells as rate-limiting for filament growth. Heterocyst-targeted GS inhibition triggered accumulation of the nitrogen storage polymer cyanophycin, revealing that heterocyst GS governs the routing of fixed nitrogen either toward distribution or storage. Both phenotypes were amplified in the Δamt background. Using pharmacological inhibition of GS with ammonium excretion measurements, we demonstrate that Amt transporters recover nitrogen lost by passive NH3 diffusion under diazotrophic conditions and that their absence renders the internal nitrogen economy chronically more vulnerable to GS inhibition. In natural nitrogen-limited environments, where diazotrophic cyanobacteria cannot compensate for passive nitrogen loss through external uptake, this recycling function is critical for nitrogen fixation efficiency. Overall, our findings redefine the architecture of intercellular nitrogen homeostasis in filamentous diazotrophic cyanobacteria, establishing GS and Amt transporters as interdependent determinants of intercellular nitrogen retention, distribution, and storage.
SN - 0032-0889
SN - 1532-2548
ER -