VIEW ARTICLE

Cytology and Histology

Effects of Light Intensity, Photoperiod, and Temperature on Symptom Expression and Host and Virus Ultrastructure in Saponaria vaccaria Infected with Carnation Etched Ring Virus. S. S. Hearon, Research plant pathologist, Agricultural Research, Science and Education Administration, U.S. Department of Agriculture, Beltsville, MD 20705; R. H. Lawson, Research plant pathologist, Agricultural Research, Science and Education Administration, U.S. Department of Agriculture, Beltsville, MD 20705. Phytopathology 71:645-652. Accepted for publication 21 November 1980. This article is in the public domain and not copyrightable. It may be freely reprinted with customary crediting of the source. The American Phytopathological Society, 1981. DOI: 10.1094/Phyto-71-645.

The expression of symptoms caused by carnation etched ring virus (CERV) on Saponaria vaccaria was compared at different temperatures (21, 27, and 32 C), light levels (7,532, 16, 140, and 22,596 lux [700, 1,500, and 2,100 ft-c] of cool-white fluorescent light with or without 1,076 lux [100 ft-c] of incandescent light), and photoperiods (8, 12, 14, and 16 hr/day). The temperature-induced differences in symptom expression also were related to temperature-induced differences in host cell and virus inclusion ultrastructure. Optimal conditions for rapid cytoplasmic inclusion formation, virus accumulation, and synchronous development of red local lesions were 27 C and 22,596 lux (2, 100 ft-c) of fluorescent illumination for 14–16 hr/day. High temperature, low light levels, short photoperiods, and photoinduction of flowering decreased the red local lesion response in S. vaccaria. The appearance of symptoms and the rise in infectivity in inoculated plants were slower at 21 C than at 27 C. This was correlated with a slow rate of virus inclusion formation and virion accumulation at 21 C. At 32 C, chlorotic (not red) local lesions developed and a reversible, temperature-induced inhibition of cytoplasmic inclusion formation was found. However, nuclear virions and intranuclear membranes accumulated at 32 C and nuclear pores commonly contained virons. The formation of complex networks of interconnected chambers and expanded and extended plasmodesmata within the cell wall was temperature dependent and occurred extensively at 21 but not at 32 C. When epidermal strips were treated with fluorescein isothiocyanate-conjugated antiserum to normal virus inclusions, the abnormal inclusions formed at 32 C fluoresced.