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Background <p>The occurrence of fusarium wilt (FW) and sterility mosaic disease (SMD) in conducive conditions cause significant yield losses in pigeonpea. FW hampers the yield of pigeonpea world-wide due to sudden wilting of plants. SMD gives significant challenges to the pigeonpea cultivation in India and its neighbouring countries with the potential to result in a complete crop failure. Identification of resistant genotypes and genetic markers associated with FW and SMD resistance may aid in developing pigeonpea varieties with enhanced resistance. The present study employed 176-genotype diversity panel to identify candidate genomic regions associated with FW and SMD resistance in pigeonpea. A total of 869,447 filtered SNP markers were used for genome wide association studies (GWAS) analysis.</p> Results <p>GWAS analysis identified associated genomic regions for FW on chromosome CcLG05, CcLG10, and CcLG11 and for SMD on CcLG09. Four resistant sources, namely, ICP20096, ICP20097, ICPL87119 and ICP13304 were identified for both FW and SMD resistance. Total 12 markers from chromosome CcLG11 for FW and 4 markers from chromosome CcLG09 for SMD were validated using the KASP genotyping approach. This study has also identified resistant haplotypes for FW on chromosome CcLG10 and CcLG11 and for SMD on chromosome CcLG09. Moreover, this study has identified four InDels for FW on chromosome CcLG5 in <i>two component response regulator </i> (<i>Cc_11098</i>) gene and four InDels (2 for each gene) for SMD on chromosome CcLG09 in genes, namely, <i>LRR and NB-ARC domain disease resistance protein</i> (<i>Cc_21069</i>) and <i>flavonoid 3’</i>,<i> 5’-hydroxylase</i> (<i>Cc_21070</i>).</p> Conclusion <p>The validated markers and donor lines in this study offer valuable tools and resources for the genetic improvement of pigeonpea cultivars with enhanced FW and SMD resistance. Moreover, using the material and outcome from this study and our previous study, a gene stacking strategy suggested to improve FW and SMD resistance in pigeonpea.</p>

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Mapping Fusarium wilt and sterility mosaic disease resistance-associated genomic regions and haplotype variants in pigeonpea

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月24日

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  • Sagar Krushnaji Rangari,
  • Suma Krishnappa,
  • Mamta Sharma,
  • Vinay K. Sharma,
  • Hirenallur Chandappa Lohithaswa,
  • Namita Dube,
  • Sunil S. Gangurde,
  • Vinay Sharma,
  • Ragavendran Abbai,
  • Naresh Bomma,
  • Shruthi Belliappa,
  • Karma L. Bhutia,
  • Mahendar Thudi,
  • Prakash I. Gangashetty,
  • Manish K. Pandey

摘要

Background

The occurrence of fusarium wilt (FW) and sterility mosaic disease (SMD) in conducive conditions cause significant yield losses in pigeonpea. FW hampers the yield of pigeonpea world-wide due to sudden wilting of plants. SMD gives significant challenges to the pigeonpea cultivation in India and its neighbouring countries with the potential to result in a complete crop failure. Identification of resistant genotypes and genetic markers associated with FW and SMD resistance may aid in developing pigeonpea varieties with enhanced resistance. The present study employed 176-genotype diversity panel to identify candidate genomic regions associated with FW and SMD resistance in pigeonpea. A total of 869,447 filtered SNP markers were used for genome wide association studies (GWAS) analysis.

Results

GWAS analysis identified associated genomic regions for FW on chromosome CcLG05, CcLG10, and CcLG11 and for SMD on CcLG09. Four resistant sources, namely, ICP20096, ICP20097, ICPL87119 and ICP13304 were identified for both FW and SMD resistance. Total 12 markers from chromosome CcLG11 for FW and 4 markers from chromosome CcLG09 for SMD were validated using the KASP genotyping approach. This study has also identified resistant haplotypes for FW on chromosome CcLG10 and CcLG11 and for SMD on chromosome CcLG09. Moreover, this study has identified four InDels for FW on chromosome CcLG5 in two component response regulator (Cc_11098) gene and four InDels (2 for each gene) for SMD on chromosome CcLG09 in genes, namely, LRR and NB-ARC domain disease resistance protein (Cc_21069) and flavonoid 3’, 5’-hydroxylase (Cc_21070).

Conclusion

The validated markers and donor lines in this study offer valuable tools and resources for the genetic improvement of pigeonpea cultivars with enhanced FW and SMD resistance. Moreover, using the material and outcome from this study and our previous study, a gene stacking strategy suggested to improve FW and SMD resistance in pigeonpea.