Genetics & Molecular Biology28 January 2026

Rhodococcus erythropolis: Genomic Plasticity Drives Herbicide Resistance

Source PublicationApplied and Environmental Microbiology

Primary AuthorsKosztik, Baka, Táncsics et al.

Visualisation for: Rhodococcus erythropolis: Genomic Plasticity Drives Herbicide Resistance
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Strain NI86/21 of Rhodococcus erythropolis utilises a massive, mosaic genome to degrade agricultural herbicides, specifically thiocarbamates and atrazine. This capacity stems from horizontally acquired genetic islands that remain metabolically silent until activated by environmental toxins, offering a blueprint for bioremediation strategies.

Genomic Plasticity in Rhodococcus erythropolis

Agricultural soils face persistent contamination pressure. Bacteria must adapt rapidly or perish. Rhodococcus erythropolis NI86/21, isolated from the rhizosphere of Hungarian maize, presents a distinct survival strategy. It possesses an exceptionally large genome of 8.046 Mb. A significant portion exists outside the main chromosome, comprising 1.22 Mb of extrachromosomal elements. This includes three circular and two fragmented linear plasmids. This genetic bulk is not debris. It represents a sophisticated survival arsenal.

Comparative analysis identified five horizontally acquired genomic islands (HGTi). These total 0.64 Mb. They display a mosaic-like architecture derived from plasmids, phages, and chromosomal segments of other Nocardiaceae. However, maintaining foreign DNA is expensive. The organism must balance acquisition with efficiency. The study measured how the bacterium manages this trade-off.

Mechanism: Silencing and Inducible Defence

Liquid chromatography-tandem mass spectrometry (LC-MS/MS) mapped the protein expression landscape. Results indicated a strategic suppression. Only 53 per cent of genes within horizontally acquired islands expressed proteins, compared to 73 per cent of core chromosomal genes. This indicates a default 'silencing' mode. The bacterium suppresses foreign code to conserve energy.

The exception is critical. HGTi_V encodes a cytochrome P450 monooxygenase (CYP116). Under normal conditions, it remains quiet. Upon exposure to herbicides, this system activates. It specifically targets thiocarbamates and atrazine for degradation. Recombination events occur frequently between chromosomal and mobile elements. This creates a fluid structure. The genome acts as an evolutionary sandbox, testing new configurations without destabilising core functions.

Global Convergence and Bioremediation Impact

Geography does not limit this genetic strategy. The researchers identified an identical CYP450 locus in Rhodococcus sp. TE1, a strain isolated from treated soil in Canada. Two distinct strains, separated by an ocean, acquired the exact same catabolic module. This demonstrates independent, convergent evolution driven by similar selective pressures. A high GC-content Rhodococcus likely served as the donor for both.

For bioremediation, this implies that specific functional genes are highly mobile. Rhodococcus erythropolis effectively assembles a toolkit for chemical degradation from the surrounding microbial community. The findings suggest that native soil populations possess a rapid, plastic response system to agrochemicals. This adaptability complicates genome assembly but ensures survival in toxic environments.

Cite this Article (Harvard Style)

Kosztik et al. (2026). 'Genomic and proteomic analyses of the maize root isolate <i>Rhodococcus erythropolis</i> NI86/21 reveal extensive genome plasticity and parallel evolution of herbicide degradation.'. Applied and Environmental Microbiology. Available at: https://doi.org/10.1128/aem.02407-25

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BioremediationAtrazine and thiocarbamate biodegradation mechanismsRhodococcus erythropolisHow does Rhodococcus erythropolis degrade herbicides?