Physiological observations of extranuclear temperature-sensitive lethality in Nicotiana tabacum L

Summary Ultrastructural observations of extranuclear temperature-sensitive induced lethality in a mutant of Nicotiana tabacum L. have shown that chloroplasts in this mutant gradually degenerate in plants grown at reduced temperatures, while mitochondria remain intact (Nessler and Wernsman, 1979). To further elucidate the organellar site of temperature sensitivity in this same tobacco mutant, leaf chlorophyll content, rates of oxygen exchange and ribulose 1,5 bisphosphate carboxylase (RuBPCase) activities were examined in temperature sensitive and control genotypes at varying time intervals during 35 days exposure to lethal temperatures (13°C day/8°C night). Rates of photosynthetic oxygen evolution by leaf disks rapidly declined in mutant plants after one week at low temperatures and remained significantly lower than rates in controls. Total chlorophylls in both mutant and control plants gradually decreased with the increased time at reduced temperatures. This decrease in chlorophyll content of temperature sensitive plants was not sufficiently rapid to account for the sharp drop observed in photosynthetic rates and probably resulted from the disruption of chloroplast membranes. Mitochondrial function in mutant plants was apparently unaffected by prolonged exposure to lethal temperatures as evidenced by the almost constant rates of respiratory oxygen uptake seen throughout the experiment. RuBPCase activities on a leaf area basis were similar in mutant and control plants over the last four sampling dates (days 14–35); thus this enzyme does not appear to be the site of the temperature-sensitive lesion. The loss of chlorophylls, rapid decline in photosynthetic oxygen evolution and continued respiratory oxygen uptake reported here for mutant plants grown at lethal temperatures supports the concept that the chloroplast is the site of extranuclear temperature-sensitivity in this tobacco genotype.