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'Phosphate Deficiency' in keywords Facet   section ZfN Section C  [X]
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1994 (1)
1989 (1)
1Author    U. H. Eber, J. Viil, S. Neimanis, T. Mimura, K.-J DietzRequires cookie*
 Title    Photoinhibitory Damage to Chloroplasts under Phosphate Deficiency and Alleviation of Deficiency and Damage by Photorespiratory Reactions  
 Abstract    D edicated to P rofessor A chim Trebst on the occasion o f his 60th birthday Effects of Pi deficiency on photosynthesis ot isolated spinach chloroplasts were examined. The following observations were made: (1) Chloroplasts isolated in Pi-free media evolved oxygen in the light in the absence of added Pi until acid-extractable P, in the chloroplasts had decreased to 1 to 2.5 m M . This Pj was unavailable for photophosphorylation as shown by the inability of the chloroplasts to respond by oxygen evolution to the addition of PGA. In the state of Prdeficiency, stromal ATP to A DP ratios were in the light close to or below ratios observed in the dark. In the presence of 2 mM PGA, addition of 20 (j.m Pi was insufficient to increase ATP to ADP ratios, but sufficient for appreciable oxygen evolution. (2) More Pi was available for oxygen evolution of phosphate-deficient chloroplasts at low levels of C 0 2 than at high levels. This was due mainly to the suppression of oxygenation of RuBP by high C 0 2 levels which prevented formation of phosphoglycolate and the subsequent release of Pi into the chloroplast stroma. (3) More oxygen was produced by phosphate-deficient chloroplasts at a low light intensity than at a high light intensity. This was due to increased availability of endogenous Pi under low light and to photoinhibition of the chloroplasts by high light. The main product of photosynthesis of phosphate-deficient chloroplasts in the presence of a high bicarbonate concentration was starch, and the main soluble product was PGA. (4) After phosphate-deficient chloroplasts had ceased to evolve oxygen in the light, they be­ came photosensitive. Part of the loss of the capacity for oxygen evolution is attributed to leakage of PGA, but the main reason for loss of function is photoinactivation of electron transport. Both photosystems of the electron transport chain were damaged by light. (5) Protection against photoinactivation was provided by coupled electron transport. Photo­ inactivation of phosphate-deficient chloroplasts was less extensive in the presence of low C 0 2 concentrations which permitted oxygenation of RuBP than at high CO: concentrations. Electron transport to C 0 2 and other physiological electron acceptors and to the herbicide methylviologen was also protective. However, electron transport to oxygen in the Mehler reaction failed to provide appreciable protection against high light intensities, because oxygen reduction is slow and reactive oxygen species produced in the light contribute to photoinactivation. 
  Reference    Z. Naturforsch. 44c, 524 (1989); received February 3 1989 
  Published    1989 
  Keywords    Photosynthesis, Photoinhibition, Photorespiration, Electron Transport, Phosphate Deficiency, Phosphate Homeostasis 
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 TEI-XML for    default:Reihe_C/44/ZNC-1989-44c-0524.pdf 
 Identifier    ZNC-1989-44c-0524 
 Volume    44 
2Author    E. B. Racht, A. TrebstRequires cookie*
 Title    Hypothesis on the Control of D 1 Protein Turnover by Nuclear Coded Proteins in Chlamydomonas reinhardtii  
 Abstract    A hypothesis is presented on the events in the degradation of the D 1 protein of photosys­ tem II in the light. It proposes the existence of a nuclear encoded cleavage system that is turning over and which is m odulated by its phosphorylation state. A new experimental ap­ proach is presented in which the D 1 protein degradation under photoinhibitory light is tested in Chlam ydom onas reinhardtii grown under phosphate deficiency and pretreated with cyclo-heximide. Under these conditions the degradation of the D 1 protein is delayed whereas in C hlam y­ dom onas reinhardtii grown in full medium the D 1 protein is rapidly disappearing in high light upon addition o f chloramphenicol (CAP) or lincomycin for inhibiting the resynthesis of the D 1 protein . Cycloheximide (C H I) has little effect on photoinhibition in such control cells. In cells grown, however, for 20 h in phosphate deficiency -such that there is not yet loss of photosynthesis capacity -pretreatment with cycloheximide or canavanine in low light the degradation of the D 1 protein even in 6 h high light is prevented to an appreciable extent. Further addition of CAP or lincomycin has only a small effect. [14C]leucine incorporation was used to show that there is no resynthesis and that the presence of the D 1 protein is due to a delay of degradation. The results are interpreted to show that excess high light which converts the D 1 protein into a potentially, degradable m ode is not sufficient for degradation of the D 1 protein. A cleavage system is needed as well. It is postulated that under phosphate deficiency and pre­ treatment with CHI or canavanine a nuclear coded cleavage system for the D 1 protein is depleted, i.e. the cleavage system for the rapidly turning over D 1 is also turning over. It is shown that under phosphate deficiency an alkaline phosphatase activity in the chloro­ plast and the thylakoid membrane o f Chlam ydom onas reinhardtii is increased. It is proposed that the ratio of kinase/phosphatase converts an active, stable phosphorylated cleavage system into a labile unphosphorylated and turning over state. 
  Reference    Z. Naturforsch. 49c, 439 (1994); received January 31/May 13 1994 
  Published    1994 
  Keywords    Chlamydomonas, D 1 Protein, Photoinhibition, Photosystem II, Phosphate Deficiency 
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 TEI-XML for    default:Reihe_C/49/ZNC-1994-49c-0439.pdf 
 Identifier    ZNC-1994-49c-0439 
 Volume    49