Nodule cysteine-rich peptides maintain a working balance during nitrogen-fixing symbiosis

• Published in: Nature plants Vol. 3; no. 5; p. 17048
• Main Authors: Pan, Huairong, Wang, Dong
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 04.05.2017; Nature Publishing Group
• Subjects: 38/39; 631/449/1659; 631/449/2676/2678; Antiinfectives and antibacterials; Antimicrobial peptides; Bacteria; Biomedical and Life Sciences; Cysteine; Legumes; Life Sciences; Microorganisms; Mutualism; Nitrogen; Nitrogen fixation; Nitrogenation; Nodules; Peptidase; Peptidases; Peptides; Plant Sciences; review-article; Symbiosis; Toxicity
• DOI: 10.1038/nplants.2017.48
• ISSN: 2055-0278

The nitrogen-fixing symbiosis between legumes and rhizobia is highly relevant to human society and global ecology. One recent breakthrough in understanding the molecular interplay between the plant and the prokaryotic partner is that, at least in certain legumes, the host deploys a number of antimicrobial peptides, called nodule cysteine-rich (NCR) peptides, to control the outcome of this symbiosis. Under this plant dominance, the bacteria are subject to the sub-lethal toxicity of these antimicrobial peptides, resulting in limited reproductive potential. However, recent genetic studies have added unexpected twists to this mechanism: certain NCR peptides are essential for the bacteria to adapt to the intracellular environment needed for a successful symbiosis, and the absence of these peptides can break down the mutualism. Meanwhile, some rhizobial strains have evolved a peptidase to specifically degrade these antimicrobial peptides, allowing the bacteria to escape host control. These findings challenge the preconceptions about ‘antimicrobial’ peptides, supporting the notion that their role in biotic interactions extends beyond toxicity to the microbial partners. The role of nodule cysteine-rich (NCR) peptides during the nitrogen-fixing symbiosis is complex. They are more than just antimicrobial compounds used by the host to control bacterial growth, as previously thought.