Evidence map›Paper›PMID 12631716›Full record

ArticleMolecular biology of the cell2003

Global transcription analysis of Krebs tricarboxylic acid cycle mutants reveals an alternating pattern of gene expression and effects on hypoxic and oxidative genes.

Mark T McCammon, Charles B Epstein, Beata Przybyla-Zawislak, Lee McAlister-Henn, Ronald A Butow

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
–field-weighted citation impact
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

37 citing papers in PubMed.

  1. Article
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  8. Mitochondrial retrograde signaling regulates neuronal function.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  9. Article
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  12. Article
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  15. Article
  16. Alternative splicing regulates targeting of malate dehydrogenase in Yarrowia lipolytica.DNA research : an international journal for rapid publication of reports on genes and genomes · 2012
    Article
  17. Review
  18. Article
  19. Article
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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

5 authors.

Mark T McCammonDepartment of Biochemistry, University of Texas Health Science Center at San Antonio, 78229-3900, USA. mccammon@uthscsa.edu
Charles B Epstein
Beata Przybyla-Zawislak
Lee McAlister-Henn
Ronald A Butow

Funding

MOLECULAR GENETICS OF ISOCITRATE DEHYDROGENASESR01GM051265 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI MCALISTER-HENN, LEE · 1994 to 2011
$3.3M
REGULATION OF MITOCHONDRIAL BIOGENESIS IN YEASTR37GM022525 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI BUTOW, RONALD A · 1998 to 2007
$3.1M
CYTOSOLIC SOURCES OF NADPH AS ANTIOXIDANTSR01AG017477 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI MCALISTER-HENN, LEE · 2000 to 2009
$2.1M
MAPPING NETWORKS OF GENE INTERACTIONS IN YEASTR01CA077811 · NCI · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI BUTOW, RONALD A · 1997 to 1999
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REGULATION OF MITOCHONDRIAL BIOGENESIS IN YEASTR01GM022525 · NIGMS · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI BUTOW, RONALD A · 1985 to 1997
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NCI NIH HHS CA-77811NIA NIH HHS AG-17477NIA NIH HHS R01 AG017477NIGMS NIH HHS GM-22525NIGMS NIH HHS GM-51265NIGMS NIH HHS R01 GM051265NIGMS NIH HHS R37 GM022525
6 · The paper itself

Abstract

To understand the many roles of the Krebs tricarboxylic acid (TCA) cycle in cell function, we used DNA microarrays to examine gene expression in response to TCA cycle dysfunction. mRNA was analyzed from yeast strains harboring defects in each of 15 genes that encode subunits of the eight TCA cycle enzymes. The expression of >400 genes changed at least threefold in response to TCA cycle dysfunction. Many genes displayed a common response to TCA cycle dysfunction indicative of a shift away from oxidative metabolism. Another set of genes displayed a pairwise, alternating pattern of expression in response to contiguous TCA cycle enzyme defects: expression was elevated in aconitase and isocitrate dehydrogenase mutants, diminished in alpha-ketoglutarate dehydrogenase and succinyl-CoA ligase mutants, elevated again in succinate dehydrogenase and fumarase mutants, and diminished again in malate dehydrogenase and citrate synthase mutants. This pattern correlated with previously defined TCA cycle growth-enhancing mutations and suggested a novel metabolic signaling pathway monitoring TCA cycle function. Expression of hypoxic/anaerobic genes was elevated in alpha-ketoglutarate dehydrogenase mutants, whereas expression of oxidative genes was diminished, consistent with a heme signaling defect caused by inadequate levels of the heme precursor, succinyl-CoA. These studies have revealed extensive responses to changes in TCA cycle function and have uncovered new and unexpected metabolic networks that are wired into the TCA cycle.

Indexed as

Gene Expression ProfilingGene Expression Regulation, FungalTranscription, GeneticAconitate HydrataseCitric Acid CycleKetoglutarate Dehydrogenase ComplexMutationOligonucleotide Array Sequence AnalysisOxidation-ReductionOxygenSaccharomyces cerevisiaeAconitate HydrataseKetoglutarate Dehydrogenase ComplexOxygen

Identifiers

PMID12631716
PMCPMC151572

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.