Chloroplast biogenesis: biosynthesis of protochlorophyll(ide) via acidic and fully esterified biosynthetic branches in higher plants

McCarthy, Susan A.; Mattheis, James R.; Rebeiz, Constantin A.

doi:10.1021/bi00531a007

Cited by 13 publications

(1 citation statement)

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“…These HPLC peaks contained only nonesterified Pchlide; therefore, there may have been a greater reduction in an acidic/esterified Pchlide pool than is reflected in the reductions shown here. However, the study by McCarthy et al (25) of AFM on Pchlide and proto IX may be related to uneven distribution of AFM throughout the intact cotyledons. In the illuminated efflux and pigment synthesis experiments, it appeared that tissue in the center of the cotyledons was less affected by AFM than that at the periphery so that synthesis of Pchlide may have been less inhibited in cells in the center, while outer cells were more greatly affected and so accumulated high levels of proto IX.…”

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Accumulation of Photodynamic Tetrapyrroles Induced by Acifluorfen-Methyl

Witkowski

Halling²

1988

Plant Physiol.

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Treatment with acifluorfen-methyl (AFM), methyl 542-chloro-4-Itrifluoromethyll phenoxy)-2-nitrobenzoate, inhibited protochlorophyllide synthesis in dark-held, 5-amino levulinic acid-fed, excised cotyledons of cucumber (Cucumis sativus L.). Protochlorophyllide and protoporphyrin IX levels in AFM-treated cotyledons were inversely related and dependent on AFM concentration; as the herbicide dose increased, protoporphyrin IX levels also increased with a concomitant loss of protochlorophyllide. Significant protoporphyrin IX accumulation was induced by concentrations of AFM from the linear region of the membrane disruption dose response curve. The patterm of precursor accumulation seen in HPLC chromatograms from extracts of AFM-treated tissue indicate that Mg insertion into the tetrapyrrole ring is inhibited, suggesting interference with Mg-chelatase. An inhibitor of 5-amino levulinic acid synthesis, gabaculine (3-amino-2,3-dihydrobenzoic acid), completely blocked the membrane disruption activity of AFM in illuminated cotyledons. Protoporphyrin IX accumulating in AFM-treated tissues may serve as the primary photosensitizer for initiating lipid peroxidation.As a consequence of the rapid induction of lipid peroxidation, illumination ofplant tissues treated with p-nitro DPEI herbicides results in the disruption ofa wide range ofbiological constituents and functions (18,26). This broadly destructive activity by the DPE herbicides has made it difficult to monitor specific interactions between these compounds and light-dependent in vivo physiological processes. These effects lead to one of the most readily visible manifestations of the treatment of whole plants with DPE herbicides: the bleaching of the foliar tissue as a consequence of pigment photooxidation.In an earlier study (15) greening was induced in AFM-treated cucumber cotyledons without triggering a loss in plasmalemma membrane integrity under a regime oflow intensity, intermittent illumination. Yet, even under these conditions, we observed significant reductions in the levels of Chl accumulated in AFMtreated tissue. These results suggested the possibility that, in addition to the pigment bleaching in DPE-treated plant tissue which occurs under continuous illumination, AFM might also directly inhibit pigment biosynthesis in a manner not related to photooxidation.We have since found further evidence that the DPE herbicides directly inhibit Chl synthesis prior to the formation of Pchl(ide).' Abbreviations: DPE, diphenyl ether; AFM, acifluorfen-methyl; ALA, 6-amino levulinic acid; Pchl(ide), a mixture of Pchlide and Pchlide ester; proto IX, protoporphyrin IX; Mg-proto IX, Mg-protoporphyrin IX; Mgproto IX Me, Mg-protoporphyrin IX monomethyl ester; LA, levulinic acid: LSD (0.05), least significant difference at the 5% probability level.

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confidence: 94%