Plant Physiol. Journal of Pharmacology and Experimental Therapeutics
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Plant Physiology 71:303-306 (1983)
© 1983 American Society of Plant Biologists

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Articles

Metabolism of Magnesium Protoporphyrin Monomethyl Ester in Chlamydomonas reinhardtii1

Mark S. Crawford2 and Wei-Yeh Wang3

Department of Botany and Genetics Ph.D. Program, University of Iowa, Iowa City, Iowa 52242

The y-1 mutant of Chlamydomonas reinhardtii is defective in the conversion of protochlorophyllide (Pchlide) to chlorophyllide in the dark. Aerobic {delta}-aminolevulinic acid (ALA) feeding of y-1 cells causes protoporphyrin monomethyl ester (PME) to accumulate in addition to increased levels of Pchlide. y-1 cell homogenates are not capable of methylating protoporphyrin (PROTO) to form PME but can methylate magnesium protoporphyrin (MgP) to form magnesium protoporphyrin monomethyl ester (MgPME). Anaerobic ALA feeding of y-1 causes concomitant accumulation of PME and MgPME. y-1 cells treated with {alpha},{alpha}'-dipyridyl (DP) accumulate MgPME but not PROTO or PME. A mutant strain (bme) of Chlamydomonas has been isolated which has very little chlorophyll and accumulates PME. bme Cell homogenates can methylate MgP but not PROTO. We propose that: (a) in Chlamydomonas, PME is the initial breakdown product of MgPME; (b) both the breakdown of MgPME to PME and the conversion of MgPME to Pchlide require O2; (c) the breakdown of MgPME to PME appears to require Fe; and (d) the PME accumulated in the bme mutant is the result of an increased breakdown of MgPME.

2 M.C. was supported by a traineeship from National Institutes of Health Training Grant GM 07091-07.

3 To whom reprint requests should be addressed.

1 Supported partially by National Science Foundation Grants PCM 78 23365 and PCM 79 23059.






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Copyright © 1983 by the American Society of Plant Biologists