Dissecting resistance mechanisms to cereal yellow dwarf virus in wheat
Resistance to Cereal yellow dwarf virus (CYDV) was introgressed into wheat from a wild relative, Thinopyrum intermedium. It was speculated that the resistance inhibited the replication of CYDV. However, until recently, experiments designed to address this hypothesis had never been carried out. My Ph.D. dissertation focuses on dissecting the mechanisms of this resistance. At the site of infection, CYDV subgenomic RNA was detected. This finding negated the above hypothesis and demonstrated that CYDV could replicate within the resistant host. However, CYDV could not spread systemically. This lack of systemic infection was not a consequence of an exclusion of CYDV from phloem. Cellular localization studies showed the presence of CYDV in companion cells, sieve elements, and phloem parenchyma of inoculated leaves. Nonetheless, it appeared that CYDV could not initiate systemic movement from these infected cells. Immunolocalization studies show that callose was not responsible for inhibiting the spread. Although CYDV is phloem limited, it was also detected in epidermis, mesophyll and bundle sheath cells of the inoculated leaves. The infection of these non-phloem cells may be the result of direct inoculations by aphid vectors. By comparing the percentage of infected non-phloem cells between susceptible and resistant wheat cultivars, it was evident that the resistance interfered with phloem feeding of aphids. This result was concomitant with a higher DIMBOA concentration in the uninoculated seedlings of resistant P29 compared to the susceptible wheat line Abe. This hydroxamic acid has been associated with feeding deterrence in aphids. The resistance to CYDV was primarily dosage-dependent. If the 1-leaf stage seedlings were heavily inoculated, the resistance could be overcome and resulted in a systemic infection. As these plants matured, the resistance was restored and inhibited the spread of CYDV. The above studies demonstrated that Th. intermedium-derived resistance in the wheat germplasm P29 interferes with several steps in the establishment of CYDV infection.
Anderson, Purdue University.
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