Metabolism of Magnesium Protoporphyrin Monomethyl Ester in Chlamydomonas reinhardtii

Abstract

The y-1 mutnat of C. 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 was isolated which had very little chlorophyll and accumulated PME. bme Cell homogenates can methylate MgP but not PROTO. Apparently, in Chlamydomonas, PME is the initial breakdown product of MgPME; both the breakdown of MgPME to PME and the conversion of MgPME to Pchlide require O2; the breakdown of MgPME to PME appears to require Fe; and the PME accumulated in the bme mutant is the result of an increased breakdown of MgPME.