Evidence map›Paper›PMID 15604707›Full record

ArticlePlant molecular biology2004

Expression of a yeast acetyl CoA hydrolase in the mitochondrion of tobacco plants inhibits growth and restricts photosynthesis.

Lilia Bender-Machado, Michael Bäuerlein, Fernando Carrari, Nicolas Schauer, Anna Lytovchenko, Yves Gibon, Amelie A Kelly, Marcello Loureiro, Bernd Müller-Röber, Lothar Willmitzer and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Plant molecular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 31% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. On the free energy that drove primordial anabolism.International journal of molecular sciences · 2009
    Review
  8. Article
  9. Article
  10. Article
  11. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 2 countries.

Lilia Bender-MachadoMax-Planck-Institut für Molekulare Pflanzenphysiologie, Am Mühlenberg 1, 14476 Golm, Germany.
Michael Bäuerlein
Fernando Carrari
Nicolas Schauer
Anna Lytovchenko
Yves Gibon
Amelie A Kelly
Marcello Loureiro
Bernd Müller-Röber
Lothar Willmitzer
Alisdair R Fernie
Max Planck Institute of Molecular Plant Physiology · DEUniversidade Federal de Viçosa · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acetyl Coenzyme A (acetyl CoA) is required in the mitochondria to fuel the operation of the Krebs cycle and within the cytosolic, peroxisomal and plastidial compartments wherein it acts as the immediate precursor for a wide range of anabolic functions. Since this metabolite is impermeable to membranes it follows that discrete pathways both for its synthesis and for its utilization must be present in each of these organelles and that the size of the various compartmented pools are independently regulated. To determine the specific role of acetyl CoA in the mitochondria we exploited a transgenic approach to introduce a yeast acetyl CoA hydrolase (EC 3.1.2.1.) into this compartment in tobacco plants. Despite the facts that the introduced enzyme was correctly targeted and that there were marked reductions in the levels of citrate and malate and an increase in the acetate content of the transformants, the transgenic plants surprisingly exhibited increased acetyl CoA levels. The lines were further characterised by a severe growth retardation, abnormal leaf colouration and a dramatic reduction in photosynthetic activity correlated with a marked reduction in the levels of transcripts of photosynthesis and in the content of photosynthetic pigments. The altered rate of photosynthesis in the transgenics was also reflected by a modified carbon partitioning in leaves of these lines, however, further studies revealed that this was most likely caused by a decreased source to sink transport of carbohydrate. In summary these results suggest that the content of acetyl CoA is under tight control and that alterations in the level of this central metabolite have severe metabolic and developmental consequences in tobacco.

Indexed as

Gene Expression Regulation, EnzymologicAcetate-CoA LigaseAcetyl-CoA HydrolaseBiological TransportCarbohydrate MetabolismGene Expression Regulation, PlantGlutamic AcidGlutamineGlyceric AcidsGlycineIntramolecular TransferasesMitochondriaNicotianaPhenotypePhotosynthesisPlant Leaves3-phosphoglycerateAcetate-CoA LigaseAcetyl-CoA Hydrolaseglutamate-1-semialdehyde 2,1-aminomutaseGlutamic AcidGlutamineGlyceric AcidsGlycineIntramolecular TransferasesPyruvate Dehydrogenase ComplexRibulose-Bisphosphate CarboxylaseRNA, PlantSaccharomyces cerevisiae ProteinsStarchSucroseUridine Diphosphate Glucose

Identifiers

PMID15604707
OpenAlexW259511049

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.