Ethylene-Induced Chlorosis in the Pathogenesis of Bipolaris sorokiniana Leaf Spot of Poa pratensis

Abstract

Subjecting inoculated leaves of intact plants to a controlled atmospheric-environmental system with an atmospheric pressure of 233 millibars and 02 and CO2 parti pressures adjAsted to approximately that of normal ambient pressure during infection and disease development prevented most midvein chlorosis and complete chlorosis, but did not prevent necrotic lesion or chlorotic halo development. Under the hypobaric conditions, chlorophyll loss during disease development was reduced to 22% compared with controls at 96 hours. The observations suggest that ethylene may function late in pathogenesis of this host-pathogen interaction and is responsible for much of the chlorophyll loss after its maximum production at 48 hours.

Vegetative growth and sporulation of Bipolaris sorokiniana on infected leaves of Poa pratensis exposed to postemergence herbicides

“…The increase in disease severity on attached leaves in response to the herbicides is unknown; however, 2,4-D decreases total soluble sugars in P. pratensis (Madsen and Hodges 1983a), and the decrease has been correlated with larger lesions (Robinson and Hodges 1977). The increase in production of ethylene in response to chlorophenoxy herbicides (Penner and Ashton 1966) and in response to infection by B. sorokiniana (Hodges 1990;Hodges and Coleman 1984) also contributes to increased disease severity. Factors that enhance disease severity probably also enhance the rate of decline of infected leaf tissue; this action may permit more aggressive hyphal growth and sporulation.…”

“…sorokirziarzn leaf spot development after infection (Hodges 1978(Hodges , 1980Hodges and Coleman 1984;Nilsen et al 1979), and they can stimulate or inhibit in vitro growth and development of the pathogen (Hodges 1977). Irz virro effects of herbicides o n B. sorokinilma, however, provide little knowledge of how the pathogen grows and reproduces on infected leaves after detachment from plants exposed to the herbicides prior to or during infection.…”

Chlorosis of Sequentially Older Leaves of Poa pratensis Induced by Biologically Active Products of Bipolaris sorokiniana

“…Ethylene is the primary substance responsible for chlorosis of P. pratemis leaves infected by B. .forokiniatia (Hodges and Coleman, 1984;Hodges, 1990;Campbell, 1993, 1994) and subjecting infected plants to hypobaric conditions or to substances that block the biosynthesis or mode of action of ethylene will substantially decrease the loss of chlorophyll from the leaves without preventing infection and lesion development (Hodges and Coleman, 1984;Hodges, 1990;Campbell, 1993, 1994). These procedures decrease general leaf-chlorosis and chlorosis that occurs along the midvein of the leaf between lesions, but they do not prevent development of chlorotic halos surrounding the lesions.…”

“…Much of the leaf chlorosis that occurs in response to infection by B. sorokiniana is related to an increase in endogenous ethylene of infected leaves (Hodges, 1990;Hodges and Coleman, 1984). Chlorophyll loss from the increase in ethylene ranges from 22 to 63% by 96 h after infection.…”

“…Chlorophyll loss from the increase in ethylene ranges from 22 to 63% by 96 h after infection. When the mode of action and/or biosynthesis of ethylene is blocked during pathogenesis there is a substantial decrease in the loss of chlorophyll by infected leaves (Nilsen and Hodges, 1983;Hodges and Coleman, 1984;Hodges, 1990;Campbell, 1993, 1994). There remains, however, a 7-15% loss of chlorophyll that is not prevented by the control of the ethylene.…”