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Root nodule endosymbioses between diazotrophic rhizobia and legumes provide the largest input of combined N to the biosphere, thus representing an alternative to harmful chemical fertilizers for sustainable crop production. Rhizobia have evolved intricate strategies to coordinate N assimilation for their own benefit with N fixation to sustain plant growth. The rhizobial N status is transduced by the NtrBC two-component system, the seemingly ubiquitous form of N signal transduction in Proteobacteria. Here, we show that the regulatory sRNA NfeR1 (nodule formation efficiency RNA) of the alfalfa symbiont is transcribed from a complex promoter repressed by NtrC in a N-dependent manner and feedback silences by complementary base-pairing. These findings unveil a more prominent role of NtrC as a transcriptional repressor than hitherto anticipated and a novel RNA-based mechanism for NtrBC regulation. The NtrBC-NfeR1 double-negative feedback loop accurately rewires symbiotic N metabolism and is likely conserved in α-rhizobia.
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http://dx.doi.org/10.1128/mbio.02003-23 | DOI Listing |
bioRxiv
August 2025
Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA.
The cell-to-cell communication process called quorum sensing enables bacteria to synchronize collective behaviors. Quorum sensing relies on the production, release, and detection of signaling molecules called autoinducers. In , the VqmA transcription factor, following binding of the DPO autoinducer, activates expression of the gene encoding the VqmR small regulatory RNA.
View Article and Find Full Text PDFMol Cell
September 2025
Division of Molecular and Cell Biology, Chester Beatty Laboratories, the Institute of Cancer Research, London SW3 6JB, UK; Cell Cycle, Biotechnology Center (BIOTEC), TU Dresden, 01307 Dresden, Germany. Electronic address:
Reactive oxygen species (ROS) influence cell proliferation and fate decisions by oxidizing cysteine residues (S-sulfenylation) of proteins, but specific targets and underlying regulatory mechanisms remain poorly defined. Here, we employ redox proteomics to identify cell-cycle-coordinated S-sulfenylation events and investigate their functional role in proliferation control. Although ROS levels rise during cell cycle progression, the overall oxidation of the proteome remains constant, with dynamic S-sulfenylation restricted to a subset of cysteines.
View Article and Find Full Text PDFDevelopment
August 2025
Friedrich Miescher Institute for Biomedical Research, Basel 4056, Switzerland.
In Hydra, a simple cnidarian model, epithelio-muscular cells shape and maintain body architecture through continuous renewal. Undifferentiated cells from the mid-body region migrate passively toward the extremities, replacing shed cells and acquiring region-specific identities. This ongoing turnover, together with Hydra's stable axial organization, provides a powerful model to study how cell type specification is integrated with body patterning.
View Article and Find Full Text PDFSci Signal
May 2025
Lyda Hill Department of Bioinformatics, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
The extension of lamellipodia, which are thin, fanlike projections at the cell periphery, requires the assembly of branched actin networks under the control of the small GTPase Rac1. In melanoma, a hyperactive P29S Rac1 mutant is associated with resistance to inhibitors that target the kinases BRAF and MAPK and with more aggressive disease because it sequesters and inactivates the tumor suppressor merlin (encoded by ) inside abnormally large lamellipodia. Here, we investigated how these merlin-inactivating lamellipodia are maintained using quantitative, live cell imaging of cell morphology and signaling dynamics.
View Article and Find Full Text PDFPLoS Comput Biol
April 2025
School of Biological and Health Systems Engineering, Arizona State University, Tempe, Arizona, United States of America.
Although the impact of resource competition on the deterministic behavior of synthetic gene circuits has been studied, its effects on gene expression noise remain obscure. In this work, we systematically analyze the role of resource competition in noise propagation within a genetic inhibition cascade circuit. We found that resource competition amplifies gene expression noise by introducing unexpected bistability and stochastic switching between the two stable states.
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