A gene-for-gene relationship in the Triticum-ustilago system, and some remarks on host-pathogen combinations in general

1963 ◽  
Vol 69 (1) ◽  
pp. 104-109 ◽  
Author(s):  
A. J. P. Oort
1980 ◽  
Vol 58 (22) ◽  
pp. 2360-2366 ◽  
Author(s):  
Erik L. Stromberg ◽  
Malcolm E. Corden

Vessels in stems of 'Jefferson' (race 1 resistant and race 2 susceptible) and 'Bonny Best' (race 1 and 2 susceptible) tomato cultivars inoculated with Fusarium oxysporum f.sp. lycopersici race 1 or 2 were examined by scanning electron microscopy. Four days after inoculation of Jefferson with conidia of race 1, the inoculum conidia and resultant hyphae generally were collapsed, whereas in the susceptible host–pathogen combinations the inoculum conidia and hyphae appeared normal. Neither the plants of the resistant nor the susceptible host-pathogen combinations had perforation plates or tyloses within vessel elements capable of trapping conidia or effectively blocking hyphal growth. The perforation plates of all vessel elements are reduced to slightly lipped rims and thus provide unrestricted apertures for hyphal growth and conidial movement in the transpiration stream. In the susceptible host–pathogen combinations, mycelial growth often filled the vessels, but no sporulation was noted. Frequent lateral spread of the pathogen occurred between adjacent vessels through the bordered pit-pairs. Infrequent occurrence of tyloses and a lack of occlusions by tyloses in the resistant host–pathogen combination suggest that vascular wilt resistance within the stem is not due primarily to physical containment of the pathogen in the vessels. Collapsed conidia and hyphae in the resistant host–pathogen combination suggests that fungitoxic materials in the vessels suppress the pathogen and contribute to resistance.


1992 ◽  
Vol 22 (7) ◽  
pp. 1036-1043 ◽  
Author(s):  
Warren L. Nance ◽  
Gerald A. Tuskan ◽  
C. Dana Nelson ◽  
Robert L. Doudrick

Applications of molecular markers for genetic analysis of host–pathogen systems are presented within the framework of the gene-for-gene model. The literature on complementary genetic interactions in host–pathogen systems is briefly reviewed. Flor's gene-for-gene hypothesis is summarized, and the design, execution, and genetic interpretation of experiments to test this hypothesis are described in detail. Various molecular techniques that have been used to complement the traditional gene-for-gene approach are also briefly reviewed. Three alternative approaches to developing molecular markers using the gene-for-gene framework are presented to illustrate the potential for applying molecular markers in forest tree–pathogen systems. Two of these alternative approaches allow partial confirmation of a hypothesized gene-for-gene genetic model without the usual requirement for advanced pedigrees. Such alternative approaches could greatly accelerate the development of marker-aided selection for disease resistance in forest tree–pathogen systems.


1976 ◽  
Vol 82 (2) ◽  
pp. 369-374 ◽  
Author(s):  
M. S. WOLFE ◽  
J. A. BARRETT ◽  
R. C. SHATTOCK ◽  
D. S. SHAW ◽  
R. WHITBREAD

2013 ◽  
Vol 197 (4) ◽  
pp. 1262-1275 ◽  
Author(s):  
Isabelle Vogt ◽  
Thomas Wöhner ◽  
Klaus Richter ◽  
Henryk Flachowsky ◽  
George W. Sundin ◽  
...  

2021 ◽  
Vol 9 (3) ◽  
Author(s):  
Dan Wang ◽  
Dan-Dan Zhang ◽  
Toshiyuki Usami ◽  
Lei Liu ◽  
Lin Yang ◽  
...  

Deciphering the gene-for-gene relationships during host-pathogen interactions is the basis of modern plant resistance breeding. In the Verticillium dahliae -tomato pathosystem, two races (races 1 and 2) and their corresponding avirulence ( Avr ) genes have been identified, but strains that lacked these two Avr genes exist in nature.


1965 ◽  
Vol 16 (2) ◽  
pp. 131 ◽  
Author(s):  
PT Jenkins ◽  
C Reinganum

An infection of immature peach and apricot fruits by Sclerotinia fructicola (Wint.) Rehm. is described. Since infection results in macroscopically visible lesions it is proposed that this type of infection be known as "quiescent" rather than latent. Symptoms have been induced in immature apricots by inoculation with conidia of the fungus and, after a period of quiescence, progressive rots developed from such infections as the fruit ripened. The fungus was re-isolated from surface-sterilized material bearing quiescent infections. Cultural evidence, together with field observations, indicate that a quiescent infection occurs naturally in the orchard, particularly in a season of moderate to severe blossom infection. Fruit losses during a dry harvest period are ascribed in the main to the activation of quiescent infections during fruit ripening. The histology of the lesion is described. The response of the host to infection is variable, but always includes a more or less extensive collapse and necrosis of the epidermis and of one or more layers of the hypodermis. Periderm formation may be associated with the necrogenic reaction. The results of a spray trial demonstrate that some measure of control of quiescent infection can be achieved by applying eradicant sprays during blossoming, and thus provide circumstantial evidence that a proportion of such infections can be established during this period. The quiescent infection is compared with other host-pathogen combinations in which infection is followed by a period of latency or quiescence, and suggestions are put forward as to the factors governing quiescence. The concept of "latent contamination" is re-evaluated in the light of the evidence presented in the present paper. It is argued that conidia alighting on the fruit surface during the growing period are more likely to give rise to a quiescent infection than to survive to produce an infection of the ripe fruit.


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