Castor bean, a non-edible monotypic species known for its unique hydroxy fatty acid, is susceptible to a range of pathogens. Wilt caused by Fusarium oxysporum f. sp. ricini is the most complex and destructive disease. Chemical control of wilt has proven ineffective due to the systemic nature of the disease and the seed and soil borne nature of the pathogen. Physical, chemical, biological, and integrated management methods have shown only limited success in controlling wilt. Host plant resistance, however, stands out as the most promising strategy, offering a viable pathway for the genetic improvement of castor beans for wilt resistance. Screening techniques are well established, and several resistant donors have already been identified. While significant progress has been made in understanding the inheritance of wilt resistance, a complete understanding of its genetic mechanisms still requires further research. Single Nucleotide Polymorphism (SNP) markers and genomic regions linked to wilt resistance have been successfully identified. Reniform nematode (Rotylenchulus reniformis) has been identified as a predisposing factor for wilt, and genomic regions linked to nematode resistance have also been identified. However, Marker-assisted selection has not yet been utilized to develop wilt-resistant castor varieties. Further research is required to explore the pathogen diversity, host-pathogen interactions, and mechanisms underlying wilt resistance including the metabolites responsible for preventing the emergence of new pathogenic races and ensuring long-term protection against wilt.
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