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. 1983 Feb;71(2):303–306. doi: 10.1104/pp.71.2.303

Metabolism of Magnesium Protoporphyrin Monomethyl Ester in Chlamydomonas reinhardtii1

Mark S Crawford 1,2, Wei-Yeh Wang 1,3
PMCID: PMC1066029  PMID: 16662822

Abstract

The y-1 mutant of Chlamydomonas reinhardtii is defective in the conversion of protochlorophyllide (Pchlide) to chlorophyllide in the dark. Aerobic δ-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 α,α′-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.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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