A photorespiratory mutant of Chlamydomonas reinhardtii

A mutant strain of Chlamydomonas reinhardtii, designated 18-7F, has been isolated and characterized. 18-7F requires a high CO2 concentration for photoautrophic growth in spite of the apparent induction of a functional CO2 concentrating mechanism in air-adapted cells. In 2% O2 the photosynthetic char...

Full description

Saved in:
Bibliographic Details
Published inPlant physiology (Bethesda) Vol. 93; no. 1; pp. 231 - 237
Main Authors Suzuki, K. (University of Tsukuba, Ibaraki, Japan), Marek, L.F, Spalding, M.H
Format Journal Article
LanguageEnglish
Published Rockville, MD American Society of Plant Physiologists 01.05.1990
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:A mutant strain of Chlamydomonas reinhardtii, designated 18-7F, has been isolated and characterized. 18-7F requires a high CO2 concentration for photoautrophic growth in spite of the apparent induction of a functional CO2 concentrating mechanism in air-adapted cells. In 2% O2 the photosynthetic characteristics of 18-7F and wild type are similar. In 21% O2, photosynthetic O2 evolution is severely inhibited in the mutant by preillumination in limiting CO2, although the apparent photosynthetic affinity for inorganic carbon is similar in preilluminated cells and in cells incubated in the dark prior to O2 evolution measurements. Net CO2 uptake is also inhibited when the cells are exposed to air (21% O2, 0.035% CO2, balance N2) for longer than a few minutes. [14C]Phosphoglycolate accumulates within 5 minutes of photosynthetic 14CO2 fixation in cells of 18-7F. Phosphoglycolate does not accumulate in wild type. Phosphoglycolate phosphatase activity in extracts from air-adapted cells of 18-7F is 10 to 20% of that in wild-type Chlamydomonas. The activity of phosphoglycolate phosphatase in heterozygous diploids is intermediate between that of homozygous mutant and wild-type diploids. It was concluded that the high-CO2 requiring phenotype in 18-7F results from a phosphoglycolate phosphatase deficiency. Genetic analyses indicated that this deficiency results from a single-gene, nuclear mutation. We have named the locus pgp-1
Bibliography:F60
F30
9040058
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0032-0889
1532-2548
DOI:10.1104/pp.93.1.231