Macrophomina Phaseolina Pathogenicity and Management in Agricultural Crops

Macrophomina phaseolina is a necrotrophic fungal pathogen of global importance, causing charcoal rot, stem blight and root rot in more than 500 plant species. It survives in soil as long-lived microsclerotia that germinate under high temperature and drought stress, penetrate host tissues using an array of cell-wall-degrading enzymes and toxins, and colonise vascular elements to induce wilting and yield loss. The infection cycle often begins with a brief biotrophic phase, during which the pathogen evades or suppresses initial defences, before switching to necrotrophy and extensive tissue maceration. Management strategies combine cultural practices—such as crop rotation, soil solarisation and irrigation management—to reduce microsclerotia density, with chemical fungicides where permitted. Biological control using antagonistic bacteria or fungi has shown promise but requires refinement under field conditions. Breeding for host resistance remains the most sustainable long-term solution: recent advances in genomic selection, marker-assisted stacking of resistance loci and identification of quantitative trait loci have accelerated development of tolerant cultivars in soybean, strawberry and other crops. Integrating agronomic measures, predictive breeding and an improved understanding of host–pathogen interactions under climate change is essential to safeguard yields in diverse agroecosystems.

Research from Nature Portfolio

Large-scale field evaluation of diverse soybean genotypes under hot-spot conditions identified several lines with negligible disease incidence and low Area Under Disease Progress Curve values over multiple seasons. Multi-trait analyses pinpointed ideotypes combining high yield with charcoal rot resistance, and unique alleles on two linkage groups were associated with superior performance. These findings offer practical targets for marker-assisted breeding in tropical environments. A foundational study in sesame elucidated the biotrophy-to-necrotrophy switch: microscopy and transcriptional profiling revealed that resistant hosts delay transition to necrotrophy, mount timely antioxidant and secondary metabolite responses, and activate jasmonate-ethylene signalling. This work underlines the dynamic nature of host defence and the need to tailor resistance traits to distinct infection phases.

Macrophomina Phaseolina Pathogenicity and Management in Agricultural Crops publication trend

The graph below shows the total number of articles in macrophomina phaseolina pathogenicity and management in agricultural crops across all publications each year (not limited to Nature Index journals).

Technical terms

Necrotroph: A pathogen that kills host cells and feeds on the dead tissue.

Microsclerotia: Small, melanised survival structures formed by the fungus in soil and plant debris.

Biotrophy-to-necrotrophy switch (BNS): The transition from a living-cell feeding phase to tissue-killing necrotrophy during infection.

Area Under Disease Progress Curve (AUDPC): A quantitative measure of disease intensity over time.

Transgressive segregation: The appearance of progeny with traits beyond the parental range, often due to novel allele combinations.

Quantitative trait locus (QTL): A genomic region associated with variation in a quantitative phenotypic trait such as disease resistance.

References

1. Transgressive segregation, hopeful monsters, and phenotypic selection drove rapid genetic gains and breakthroughs in predictive breeding for quantitative resistance to Macrophomina in strawberry. Horticulture Research (2024).
2. Identification and genetic diversity analysis of high-yielding charcoal rot resistant soybean genotypes. Scientific Reports (2023).
3. Biotrophy-necrotrophy switch in pathogen evoke differential response in resistant and susceptible sesame involving multiple signaling pathways at different phases. Scientific Reports (2017).
4. Tools to kill: Genome of one of the most destructive plant pathogenic fungi Macrophomina phaseolina. BMC Genomics (2012).