ArticleGenetics2013
Heritable loss of replication control of a minichromosome derived from the B chromosome of maize.
Article in Genetics, 2013. 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
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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, 12 citations in OpenAlex.
- Cytomolecular characterization and origin of de novo formed maize B chromosome variants.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2016Article
- Stable mitotic inheritance of rice minichromosomes in cell suspension cultures.Plant cell reports · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During an accumulation regime of a small telomere-truncated B chromosome, a derivative with large variations in size and multiple punctate centromere loci exhibiting amplified copy numbers was discovered. Multiple centromere satellite loci or transgene signals were documented in amplified chromosomes, suggesting over-replication. Immunolocalization studies revealed multiple foci of biochemical markers characteristic of active centromeres such as CENP-C and phosphorylation of histones H3S10 and H2AThr133. The amplified chromosomes exhibit an absence of chromosome disjunction in meiosis I and an infrequent chromosome disjunction in meiosis II. Despite their unusual structure and behavior these chromosomes were observed in the lineage for seven generations during the course of this study. While severely truncated relative to a normal B chromosome, the progenitor minichromosome is estimated to be at least several megabases in size. Given that the centromere and transgene signals at opposite ends of the chromosome generally match in copy number, the replication control is apparently lost over several megabases.
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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.