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Michael D. Allen

Researcher at University of California, Los Angeles

Publications -  8
Citations -  880

Michael D. Allen is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: Chlamydomonas & Chlamydomonas reinhardtii. The author has an hindex of 7, co-authored 8 publications receiving 795 citations.

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Between a rock and a hard place: trace element nutrition in Chlamydomonas.

TL;DR: The Chlamydomonas model is ideal for future investigation of nutritional manganese deficiency and selenoenzyme function and is also suited for studies of trace nutrient interactions, nutrition-dependent metabolic changes, the relationship between photo-oxidative stress and metal homeostasis.
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Arabidopsis CHL27, located in both envelope and thylakoid membranes, is required for the synthesis of protochlorophyllide.

TL;DR: Fractionation of Arabidopsis chloroplast membranes shows that Crd1/CHL27 is equally distributed on a membrane-weight basis in the thylakoid and inner-envelope membranes.
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Manganese Deficiency in Chlamydomonas Results in Loss of Photosystem II and MnSOD Function, Sensitivity to Peroxides, and Secondary Phosphorus and Iron Deficiency

TL;DR: In this paper, the expression of MSD3 through MSD5, encoding various isoforms of the MnSODs, is upregulated severalfold in Mn-deficient cells, but neither expression nor activity of the plastid Fe-containing superoxide dismutase is changed, which contrasts with the dramatically increased MSD 3 expression and plastide Mn SOD activity in Fe-deficiency cells.
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FEA1, FEA2, and FRE1, encoding two homologous secreted proteins and a candidate ferrireductase, are expressed coordinately with FOX1 and FTR1 in iron-deficient Chlamydomonas reinhardtii.

TL;DR: The version 3.0 draft genome is surveyed to identify a ferrireductase, FRE1, and two ZIP family proteins, IRT1 and IRT2, as candidate ferrous transporters based on their increased expression in iron-deficient versus iron-replete cells.
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Fe Sparing and Fe Recycling Contribute to Increased Superoxide Dismutase Capacity in Iron-Starved Chlamydomonas reinhardtii

TL;DR: Two pathways increase the capacity of the Chlamydomonas chloroplast to detoxify superoxide during Fe limitation stress, and a novel plastid-localized MnSOD is expressed in response to Fe limitation, suggesting the operation of salvage mechanisms for intracellular recycling and reallocation.