|LIN, SEN - Washington State University|
|NIU, YI - Washington State University|
|MEDINA, CESAR AUGUSTO - Washington State University|
Submitted to: Plant Biotechnology Journal
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/8/2022
Publication Date: 1/21/2022
Citation: Lin, S., Niu, Y., Medina, C., Yu, L. 2022. Two linked resistance genes function divergently in defence against Verticillium wilt in alfalfa. Plant Biotechnology Journal. 20(4):619-621. https://doi.org/10.1111/pbi.13779.
Interpretive Summary: Autotetraploid alfalfa (Medicago sativa L.) is an important forage crop grown worldwide. Growth of alfalfa is greatly influenced by a soil-born fungus disease, Verticillium wilt (VW) which causes severe yield loss every year. This study identified two linked resistance genes that are involved in alfalfa resistance to Verticillium alfalfae. Highly resistant and susceptible alfalfa lines were used in this study to analyze a pair of linked resistance genes that have very similar DNA sequences. This work revealed that this pair of resistance genes have different functions and play opposite roles in disease resistance. The results are useful for developing new alfalfa varieties that have improved resistance to Verticillium wilt and also for better understanding how plants respond to pathogen attack.
Technical Abstract: Verticillium wilt (VW) is a soil-born fungus disease and causes severe yield loss in alfalfa. However, the genetic controlling to VW resistance in alfalfa is still not clear. Here we report two linked resistance (R) genes, MsVR38 and MsVR39 involved in VW resistance in alfalfa. We found that MsVR39 plays a positive role in VW resistance, whereas negative regulation was found in MsVR38. The sequence analysis of MsVR38 showed one nucleotide missing in the resistant plant but not the susceptible line, indicating the normal expression of MsVR38 affected the activation of resistance gene MsVR39. Investigation of Medicago truncatula knockout mutants MtVR130 and MtVR140, which correspond to MsVR38 and MsVR39 respectively, demonstrated that the knockout of MtVR130 conferred greater resistance to VW than was observed in the wildtype. Bioassay of stem infection from M. truncatula mutants and wildtype also demonstrated that Mtvr130 is more resistant to V. alfalfae than Mtvr140 and the wildtype. A possible mechanism is that when a pair of highly identical TIR-NBS-LRR genes are both normally expressed, they are more likely to form heterodimers, which inhibits the expression of the resistance gene MsVR39, resulting in susceptibility to VW disease.