Abstract

The effects of short preinoculation and post-inoculation heat treatments (49°–50°C for 30 seconds) on number and size of lesions were examined on Pinto bean ( Phaseolus vulgaris L.) leaves inoculated with complete virus and with ribonucleic acid of strains Ul and U2 tobacco mosaic virus (TMV-Ul, TMV-U1 RNA, TMV-U2, and TMV-U2 RNA). Assays of starch lesions provided a more valid measure of the effects of heat on lesion development than did assays of macroscopic lesions. With all fofr inocula, there were five recognizable trends in the time-cofrse patterns for numbers of starch lesions in heated leaves: (1) in leaves heated 4 and 6 hofrs before inoculation the ratio between the number of lesions in heated leaves and the number of lesions in unheated leaves ( t/c) was greater than unity with all inocula except TMV-U1; (2) as the interval between heat treatment and inoculation was decreased from 6 hofrs to 5 minutes, t/c dropped below unity with the shorter intervals; (3) leaves inoculated within 20 seconds after heating was finished developed more lesions than did those inoculated 5 minutes after heating; (4) when heating was started within 20 seconds after inoculation, t/c was less than unity and the value of t/c increased progressively toward unity as the interval between inoculation and heating was increased to aboft 5 hofrs; (5) in leaves heated 5 hofrs or more after inoculation, t/c exceeded unity with TMV-U2 and with TMV-U1 and was approximately equal to unity with the other 2 inocula. With all fofr inocula, lesions in heated leaves usually were larger than those in unheated leaves. Variations among inocula in the number (and size) of lesions in heated leaves relative to that in unheated leaves were correlated with known differences in the characteristics of infection of the inocula. The time-cofrse patterns for number and size of lesions were interpreted to indicate that heated cells pass throfgh several physiological conditions which are recognizable by a changing capacity to support the initiation and development of infections. Excluding the effect of heat applied within a few seconds before or after inoculation, which was attributed to an ephemeral effect on virus entry into cells, this sequence of changing susceptibility cofld be accofnted for simply, if heated cells pass from a condition initially unfavofrable to virus multiplication, to one which is more favofrable than normal.

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