Cultures of the cyanobacterium, Anacystis nidulans, were grown in iron deficient medium and examined for fluorescence emission at room temperature. Iron deficiency induced several alterations in fluorescence emission kinetics which were reversed when iron was restored. When excited by 450 nm light (absorbed by chlorophyll), iron stressed cells showed an enhanced maximum fluorescence yield (Fm), due in large part to an increase in original fluorescence (Fo) and a depressed variable fluorescence. Both Fm and Fo declined during the early stages of recovery from iron deficiency. Inhibitors of chlorophyll biosynthesis (such as levulinic acid and gabaculine) had little influence on these early stages of recovery suggesting that newly synthesized chlorophyll is not responsible for the decline in Fm. In contrast, when excited by 550 or 600 nm light (absorbed by phycocyanin), iron deficient cells showed no increase in Fm. A fast rise fluorescence transient was observed which was absent in both normal or fully recovered cells. This transient was attenuated by preillumination (600 nm light), and recovered in darkness with a half time of 2–4 minutes. These results suggest that the reoxidation of acceptors on the oxidizing side of PS II is considerably slower in iron deficient cells.
No takes yet. Share an insight, caveat, or question.
James A. Guikema (1985) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: