ARS | Publication request: WHAT IS KNOWN ABOUT INFECTION PATHWAYS IN FUSARIUM HEAD BLIGHT

Submitted to: National Fusarium Head Blight Forum Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: December 8, 2001
Publication Date: N/A

Technical Abstract: The epidermis of the exposed outer surfaces of the florets of wheat and barley consists of very thick-walled cells. These armored cells apparently are not penetrated directly from outer surfaces by Fusarium graminearum. The palea and lemma that enclose the floret each have several rows of stomates that can be entered by hyphae of F. graminearum. Another possible avenue of entry is the mouth at the apex of the floret. Exposed adaxial surfaces of the awn, palea and lemma near the floret mouth can be colonized by F. graminearum mycelia. The mycelia can also colonize interior surfaces of the palea and lemma. Another potential pathway of entry is the crevice between the palea and lemma, especially near the floret base. Within tissues, F. graminearum can grow between cells instead of entering them, establishing a biotrophic relationship with host tissues. How and where the intercellular fungus penetrates cells for subsequent growth within cells is not known. Once established within the floret, the fungus colonizes and follows vascular tissues in the floret stalk through the rachilla or rachis into other florets. The molecular and physiological responses of heads to invasion by head blight Fusaria are largely uninvestigated, whether in resistant or susceptible plants. Fungus-produced trichothecene toxins such as deoxynivalenol contribute to virulence of F. graminearum. There is much to be learned about pathogenesis in fusarium head blight at both the molecular and cellular levels.