ArticlePlant physiology1999
Characterization of two photosynthetic mutants of maize
Article in Plant physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed, 9 citations in OpenAlex.
- Gene loci in maize influencing susceptibility to chilling dependent photoinhibition of photosynthesis.Photosynthesis research · 2005Article
- Biochemical and molecular characterization of photosystem I deficiency in the NCS6 mitochondrial mutant of maize.Plant molecular biology · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We describe here the biochemical characteristics of the hcf44 and hcf47 (high chlorophyll fluorescence) mutants of maize (Zea mays L.). Both mutants were sensitive to high light intensities, exhibiting reduced growth and fluorescence intensity. Electron transport through the mutants' photosystem (PS) I and PSII reaction centers was reduced and NADP(+) photoreduction was absent. Western analysis revealed that the hcf44 mutant was missing some or all of the PsaC, PsaD, and PsaE polypeptides of the PSI reaction center, and reverse transcriptase-polymerase chain reaction demonstrated that this loss was the result of a posttranscriptional event. The hcf47 mutant had reduced levels of many PSI and PSII polypeptides. These data indicate a possible defect in the synthesis or assembly of the PsaC subunit in the hcf44 mutant, whereas the hcf47 mutant may have a more general defect in the biogenesis of photosynthetic membranes. Our results demonstrate the coordinated assembly of the peripheral proteins into the PSI complexes of higher plants and demonstrate the in vivo requirement of PsaC, PsaD, and PsaE subunits for the function of PSI in higher plants.
Identifiers
What OpenQuestion holds
Registered trials
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.