ArticleG3 (Bethesda, Md.)2013
Genetic interactions of Arabidopsis thaliana damaged DNA binding protein 1B (DDB1B) with DDB1A, DET1, and COP1.
Article in G3 (Bethesda, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- How Do Plants Cope with DNA Damage? A Concise Review on the DDR Pathway in Plants.International journal of molecular sciences · 2023Review
- Mutations inFrontiers in plant science · 2022Article
- Conservation of centromeric histone 3 interaction partners in plants.Journal of experimental botany · 2020Article
- Protecting DNA from errors and damage: an overview of DNA repair mechanisms in plants compared to mammals.Cellular and molecular life sciences : CMLS · 2017Review
- Arabidopsis DDB1-CUL4 E3 ligase complexes in det1 salt/osmotic stress resistant germination.Plant signaling & behavior · 2016Article
- DNA damage and repair in plants - from models to crops.Frontiers in plant science · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Damaged DNA Binding protein 1 (DDB1)-CULLIN4 E3 ubiquitin ligase complexes have been implicated in diverse biological processes in a range of organisms. Arabidopsis thaliana encodes two homologs of DDB1, DDB1A, and DDB1B. In this study we use a viable partial loss of function allele of DDB1B, ddb1b-2, to examine genetic interactions with DDB1A, DET1 and COP1. Although the ddb1b-2 ddb1a double mutant is lethal, ddb1a ddb1b-2/+ and ddb1b-2 ddb1a/+ heterozygotes exhibit few developmental phenotypes but do exhibit decreased tolerance of ultraviolet light. In addition, germination in ddb1a and ddb1a ddb1b-2/+ was found to be sensitive to salt and mannitol, and both DDB1 single mutants as well as the heterozygotes exhibited heat sensitivity. DE-ETIOLATED1 (DET1) and CONSTITUTIVE PHOTOMORPHOGENIC1 (COP1) are negative regulators of light development which interact with DDB1-CUL4 complexes. Although ddb1a strongly enhances det1 phenotypes in both dark- and light-grown seedlings, ddb1b-2 weakly enhanced the det1 short hypocotyl phenotype in the dark, as well as enhancing anthocyanin levels and suppressing the det1 low chlorophyll phenotype in light-grown seedlings. In adults, ddb1a suppresses det1 early flowering and enhances the det1 dwarf phenotype. A similar trend was observed in ddb1b-2 det1 double mutants, although the effects were smaller in magnitude. In cop1 mutants, ddb1b-2 enhanced the cop1-4 short hypocotyl phenotype in dark and light, enhanced anthocyanin levels in cop1-1 in the light, but had no effect in adults. Thus the requirement for DDB1B varies in the course of development, from COP1-specific effects in hypocotyls to DET1-specific in adults.
Indexed as
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.