An unusual organization of the genes encoding cytochrome b 559 in Chlamydomonas reinhardtii: psbE and psbF genes are separately transcribed from different regions of the plastid chromosome

1995 ◽  
Vol 246 (5) ◽  
pp. 600-604 ◽  
Author(s):  
Tsafrir S. Mor ◽  
Itzhak Ohad ◽  
Joseph Hirschberg ◽  
Himadri B. Pakrasi
2002 ◽  
Vol 14 (11) ◽  
pp. 2659-2679 ◽  
Author(s):  
Jude E. Maul ◽  
Jason W. Lilly ◽  
Liying Cui ◽  
Claude W. dePamphilis ◽  
Webb Miller ◽  
...  

2021 ◽  
Author(s):  
Waeil Al Youssef ◽  
Regina Feil ◽  
Maureen Saint-Sorny ◽  
Xenie Johnson ◽  
John E. Lunn ◽  
...  

Singlet oxygen (1O2) induces retrograde signalling in chloroplasts. Using a novel mutant screen, we identified a mutation in the TREHALOSE-6-PHOSPHATE PHOSPHATASE 1 (T6PP1) gene that results in accumulation of trehalose 6-phosphate, a reprogramming of cell metabolism, and impairment of 1O2-induced retrograde signalling in Chlamydomonas reinhardtii. From transcriptomic analysis and metabolite profiling, we conclude that accumulation or deficiency of certain metabolites directly affect 1O2-signalling. 1O2-inducible GLUTATHIONE PEROXIDASE 5 (GPX5) gene expression is suppressed by increased content of fumarate, an intermediate in the tricarboxylic acid cycle (TCA cycle) in mitochondria and dicarboxylate metabolism in the cytosol, while it is promoted by another TCA cycle intermediate, aconitate. Furthermore, genes encoding known essential components of chloroplast-to-nucleus 1O2-signalling show decreased transcript levels in a t6pp1 mutant, which can be rescued by exogenous application of aconitate. We demonstrate that chloroplast retrograde signalling involving 1O2 depends on mitochondrial and cytosolic processes and that the metabolic status of the cell determines the response to 1O2.


2014 ◽  
Vol 13 (5) ◽  
pp. 591-613 ◽  
Author(s):  
Ursula Goodenough ◽  
Ian Blaby ◽  
David Casero ◽  
Sean D. Gallaher ◽  
Carrie Goodson ◽  
...  

ABSTRACT When the sta6 (starch-null) strain of the green microalga Chlamydomonas reinhardtii is nitrogen starved in acetate and then “boosted” after 2 days with additional acetate, the cells become “obese” after 8 days, with triacylglyceride (TAG)-filled lipid bodies filling their cytoplasm and chloroplasts. To assess the transcriptional correlates of this response, the sta6 strain and the starch-forming cw15 strain were subjected to RNA-Seq analysis during the 2 days prior and 2 days after the boost, and the data were compared with published reports using other strains and growth conditions. During the 2 h after the boost, ∼425 genes are upregulated ≥2-fold and ∼875 genes are downregulated ≥2-fold in each strain. Expression of a small subset of “sensitive” genes, encoding enzymes involved in the glyoxylate and Calvin-Benson cycles, gluconeogenesis, and the pentose phosphate pathway, is responsive to culture conditions and genetic background as well as to boosting. Four genes—encoding a diacylglycerol acyltransferase ( DGTT2 ), a glycerol-3-P dehydrogenase ( GPD3 ), and two candidate lipases (Cre03.g155250 and Cre17.g735600)—are selectively upregulated in the sta6 strain. Although the bulk rate of acetate depletion from the medium is not boost enhanced, three candidate acetate permease-encoding genes in the GPR1/FUN34/YaaH superfamily are boost upregulated, and 13 of the “sensitive” genes are strongly responsive to the cell's acetate status. A cohort of 64 autophagy-related genes is downregulated by the boost. Our results indicate that the boost serves both to avert an autophagy program and to prolong the operation of key pathways that shuttle carbon from acetate into storage lipid, the combined outcome being enhanced TAG accumulation, notably in the sta6 strain.


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