Cochliobolus victoriae. [Descriptions of Fungi and Bacteria].

A description is provided for Cochliobolus victoriae. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Oats (Avena) and other Gramineae (57, 2062, 4012). DISEASE: Victoria blight of oats. GEOGRAPHICAL DISTRIBUTION: Australia, Brazil, Canada, Netherlands, Switzerland, UK (Scotland) and USA (CMI Map 267, ed. 2, 1968). Records not yet mapped: India, Irish Republic, Malaysia, Zambia and Zimbabwe. TRANSMISSION: Presumably air dispersed (no detailed studies apparently reported); the fungus also occurs on seed.

Pathological changes in ultrastructure: false plasmolysis

Shrinkage of plant protoplasts in hypotonic solutions or even in distilled water has been long known as an erratic response to injury. Although the mechanism for it is not known, this phenomenon, termed "induced", "stimulative", or "false" plasmolysis, has been considered to be comparable to spore formation in algae and fungi or to vacuolar contraction in protozoa. Studies of the mechanism of false plasmolysis have been precluded by the inability to induce the phenomenon consistently in large numbers of cells. Victorin treatment of root cap cells from Victoria-blight susceptible oats was found to result consistently in false plasmolysis. Ultrastructure studies of such cells showed that synthesis of new membranes was not involved in victorin-induced false plasmolysis. Discontinuities in the plasmalemma and tonoplast rule out active movement of water as a causative factor for protoplast shrinkage. The mechanism responsible for false plasmolysis appears to be an increased permeability of membranes to water, followed by disruption of the vacuole and a reduction of plasmalemma area by a process similar to pinocytosis.

ASSOCIATED INHERITANCE OF REACTION TO RACES OF CROWN RUST, PUCCINIA CORONATA AVENAE ERIKSS., AND TO VICTORIA BLIGHT, HELMINTHOSPORIUM VICTORIAE M. AND M., IN OATS

The oat variety Victoria has been shown by various investigators to be resistant to most races of crown rust but susceptible to a disease known as Victoria blight. This disease was observed for the first time in the United States in 1944 and in Canada in 1947. Susceptibility to this disease has been considered, by several workers, to be linked with the Victoria type of resistance to crown rust. The present investigations indicate that Victoria has more than one major gene for resistance to crown rust. These findings are based on data from a study of advanced generation selections of Victoria parentage and from inheritance studies involving varieties with the Victoria resistance to crown rust, such as Garry and R.L. 1987. Lines were obtained from Garry and from F3 populations of different crosses with the following three types of disease reactions: (1) lines susceptible to Victoria blight and resistant to all crown rust races studied, namely, races 1, 2, 3, 4, 5, 6, 24, 34, 34A. 38, 45, and 57; (2) lines resistant to Victoria blight and susceptible to crown rust races 4, 5, 34A, and 57, but resistant to the other races; (3) lines resistant to Victoria blight and susceptible to all races. Inheritance studies of three crosses, Garry × Exeter, Garry × Roxton, and Roxton × R.L. 1987, indicate that susceptibility to Victoria blight is dominant and governed by a single major gene; that resistance to races 4, 5, 34A, and 57 of crown rust is dominant and governed by a single major gene, but linked with susceptibility to Victoria blight; and that resistance to race 45, as well as races 1, 2, 3, 6. 24, 34, and 38, which appear to be similar to race 45 in inheritance, is conditioned by three dominant genes, one of which is associated, with susceptibility to Victoria blight.