|ELDAKAK, MOUSTAFA - Alexandria University Of Egypt|
|DAS, AAYUDH - University Of Vermont|
|ZHUANG, YONGBIN - University Of Colorado|
|GLOVER, KARL - South Dakota State University|
|YEN, YANG - South Dakota State University|
Submitted to: Pathogens
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/18/2018
Publication Date: 6/22/2018
Citation: Eldakak, M., Das, A., Zhuang, Y., Glover, K.D., Rohila, J.S., Yen, Y. 2018. A quantitative proteomic view of the function of Qfhb1, a major QTL for Fusarium head blight resistance in wheat. Pathogens, 7, 58.
Interpretive Summary: Fusarium Head Blight (FHB) is a fungal disease that does serious crop damage to many cereal crops in both semitropical and temperate regions of the world. Among several FHB resistance QTLs, Qfhb1 is the major QTL (syn. Qfhs.ndsu.3BS, Fhb1), located on wheat chromosome 3BS; and is responsible for up to 60% of the variation for FHB resistance in wheat under various genetic backgrounds and environments. Till date very little is known about mechanisms and roles of this QTL in FHB resistance. During this investigation we examined differentially accumulated proteins (DAPs) in two wheat NILs 260-1-1-2 (the fhb1+NIL) and 260-1-1-4 (the fhb1-NIL) at very early stages of plant-pathogen interactions. At 50% anthesis stage, point inoculations were done and samples of the inoculated spikelets were collected at 24 h after inoculation. After protein extraction, 2D-DIGE assays were performed and 80 high-ranking DAPs were selected to be identified by mass spectrometry. The proteomic data suggests that the absence of Qfhb1 makes the fhb1-NIL vulnerable to F. graminearum attack by constitutively impairing the: production of functional proteins; detection and reduction of oxidative stresses, repair of cell membranes, and enhancing starch synthesis from sucrose. The study suggests that initiation of FHB symptoms development could result from the hypersensitive response of wheat plant to the invading F. graminearum, and that Qfhb1 largely functions to either reduce the suicide response of plant cells or influence the plant cells to not respond to the infection. The data suggest that wheat might be using more than one functional gene in the Qfhb1 to counter the observed susceptible activities of FHB pathogenesis because several diverse pathways were found to be involved. Alternatively, a master regulator for all of these diverse pathways may exist in this QTL, but none was recognized among the DAPs identified by mass spectrometry in this study.
Technical Abstract: Fusarium head blight (FHB; caused by Fusarium graminearum) is a detrimental disease of wheat (Triticum aestivum L.) and barley (Hordeum vulgare L.). Although Qfhb1 (syn. Qfhs.ndsu.3BS, Fhb1) is likely the most widely utilized quantitative trait locus for FHB resistance, little is known about its resistance mechanism(s). We elucidated FHB resistance mechanisms by investigating proteomic signatures presented by Qfhb1 via 2D-DIGE and mass spectrometry after 24 hours of F. graminearum infection in a pair of contrasting wheat near isogenic lines (NIL), having or not having Qfhb1. We studied 80 high-ranking differentially accumulated protein (DAP) spots, and found that 50 were specific to the fhb1-NIL, seven were specific to the fhb1+NIL, and 14 were shared by both, with the rest being not significant to either NIL. This remarkable difference between the NILs indicates that F. graminearum infection impacted the fhb1-NIL with much greater intensity than it impacted the fhb1+NIL. The proteomic data suggests that absence of Qfhb1 makes the fhb1-NIL vulnerable to F. graminearum attack by constitutively impairing production of functional proteins, and detection and reduction of oxidative stresses, repair of cell membrane, and sucrose homeostasis by enhancing starch synthesis from sucrose. In the absence of Qfhb1, F. graminearum infection severely damaged photosynthetic machinery; altered the metabolism of carbohydrates, nitrogen and phenylpropanoids; disrupted the balance of proton gradients across relevant membranes; disturbed homeostasis of many important signaling molecules such as sucrose, ROS, NO, SA, ET, ABA and GSH; induced the mobility of cellular repairing; and reduced translational activities. These changes in the fhb1-NIL lead to strong defense responses centered on the hypersensitive response (HSR), resulting in suicide attempts of the infected cells and, thus, initiation of FHB development. Therefore, this study suggests that Qfhb1 largely functions to either alleviate HSR or manipulate the host cells to not respond to Fusarium infection.