642 I'LAXT c;rowth and plant communities 



rate of N. ghiiinosa at these temperatures is similar to that of cabbage, 

 except that growth does not fall off at 28°. At this temperature, growth 

 is greater than that at 24°. Thus the effect of temperature on virus syn- 

 thesis in inoculated leaves closely parallels the temperature eflFects on 

 host growth. One might suspect that some metabolite accompanying 

 virus synthesis in inoculated leaves was inhibitory to virus movement 

 or to virus synthesis in systemically-infected leaves. Systemically- 

 infected leaves of N. glutinosa growing at 28° and containing low 

 concentrations of virus (as determined by samples of excised discs) 

 support marked increases of virus synthesis when reinoculated. This 

 would seem to rule out the production of a toxic metabolite inhibiting 

 synthesis. Obviously the relation of temperature to virus concentration 

 in systemically-infected leaves of N. glutinosa must be afiFected by virus 

 movement. The effect of high temperature on virus accumulation in 

 plants of N. glutinosa would seem to be one of restricted invasion of 

 cells rather than restricted synthesis. 



A second type of temperature reaction is represented by tobacco- 

 mosaic virus and has been studied in detail by Bancroft and Pound 

 ( 1956 ) . With this host-virus combination, no single temperature con- 

 sistently promotes maximal virus concentrations over a given period. In 

 inoculated leaves harvested four days after inoculation, and in systemi- 

 cally-infected leaves harvested seven days after inoculation, the virus 

 concentration increases with increase in temperature, showing that 

 initially the rate of virus synthesis is a direct function of temperature. 

 Host growth also increases with increase in temperature to an optimum 

 of about 24°. At 28° growth is slightly less than at 24°. Thus the initial 

 effects of temperature on virus synthesis closely parallel the tempera- 

 ture effects of growth. 



Subsequent assays from systemically-infected tissue show an or- 

 derly shift of virus concentrations among the different temperatures. 

 The maximum virus concentration obtained depends not only upon 

 temperature but also upon the time of sampling. At each temperature, 

 virus concentration reaches a maximiun and then drops in relation to 

 host growth. When cumulative virus concentrations are plotted against 

 cumulative growth curves, it is evident that temperature determines 

 directly, or indirectly through host growth, the rate and magnitude of 

 virus accumulation in plants as well as the rate and magnitude of con- 

 centration decline after the maximum is reached ( Bancroft and Pound, 

 1956). After the maximum virus concentration is reached, a correlation 

 between the amount of host growth and \irus concentration exists: as 

 host growth increases, virus concentration decreases. The virus ap- 

 parently does not continue to multiply as rapidly as it does initially in 

 relation to host growth, and when assays are made on a host weight 

 basis the host acts as a diluent, resulting in an observed drop in virus 



