Evidence map›Paper›PMID 16319818›Full record

ArticleMolecular vision2005

Genomic organization of zebrafish cone-rod homeobox gene and exclusion as a candidate gene for retinal degeneration in niezerka and mikre oko.

Deborah C Otteson, Motokazu Tsujikawa, Tushara Gunatilaka, Jarema Malicki, Donald J Zack

Open access · greenAbstract read
In one paragraph

Article in Molecular vision, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.1field-weighted citation impact, top 52% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Toward a better understanding of human eye disease insights from the zebrafish, Danio rerio.Progress in molecular biology and translational science · 2011
    Review
  3. 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

5 authors at 1 institution in 1 country.

Deborah C OttesonGuerrieri Center for Genetic Engineering and Ophthalmology, Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA. dotteson@optometry.uh.edu
Motokazu Tsujikawa
Tushara Gunatilaka
Jarema Malicki
Donald J Zack
Johns Hopkins Medicine · US

Funding

REGULATION OF RHODOPSIN GENE EXPRESSIONR01EY009769 · NEI · JOHNS HOPKINS UNIVERSITY · PI ZACK, DONALD J. · 1992 to 2014
$8.1M
Visual Science Training ProgramT32EY007143 · NEI · JOHNS HOPKINS UNIVERSITY · PI Laura Ensign, JEREMY NATHANS · 1995 to 2026
$6.2M
ZEBRAFISH NEURONAL PATTERNING LOCI OME &NOKR01EY011882 · NEI · MASSACHUSETTS EYE AND EAR INFIRMARY · PI MALICKI, JAREMA · 1998 to 2001
$527k
Regulation of Rhodopsin Expression: The Role of RKLFF32EY013499 · NEI · JOHNS HOPKINS UNIVERSITY · PI OTTESON, DEBORAH C · 2001 to 2002
$79k
NEI NIH HHS EY09769NEI NIH HHS EY11882NEI NIH HHS F32 EY013499NEI NIH HHS F32EY13499NEI NIH HHS R01 EY009769NEI NIH HHS R01 EY011882NEI NIH HHS T32 EY007143
6 · The paper itself

Abstract

purposeTo determine the genomic organization of the zebrafish crx gene and to evaluate if mutations in crx are responsible for the retinal degeneration phenotype in the zebrafish (Danio rerio) mutants niezerka (nie(m743)) and mikre oko (mok(m632)).

methodsOverlapping fragments were PCR amplified from genomic DNA isolated from homozygous mutant embryos and wild-type siblings (sibs). Amplicons were sequenced and sequence data assembled into contigs. Genomic organization was determined by alignment of contigs with published cDNA sequences and zebrafish genomic sequence from Sanger and Ensembl databases. Linkage analysis used DNA from mapping panels of single homozygous mutant animals with mixed genetic backgrounds.

resultsThe analysis indicated that the zebrafish crx gene consisted of three exons and 2 introns, and spans 3.8 kb of genomic DNA. The splice junctions were all located within the coding region. Highly repetitive sequences present in non-coding regions of crx and extended tetra-nucleotide repeats in intronic regions were associated with sequence variation between different strains. Homozygous mok(m632) or nie(m743) mutants and their respective wild-type sibs, showed identical patterns of heterozygosity and sequence variations within each line. No mutation in crx were identified in homozygous mok(m632) or nie(m743). Consistent with the absence of identified mutations, linkage analysis excluded linkage of the mutant phenotypes to crx.

conclusionsDespite the presence of sequence variations in their respective genetic backgrounds, within each line the sequence of crx was identical. Consistent with the absence of mutations, further analysis excluded linkage of the mutant phenotypes to crx. Analysis is in progress to map these loci and identify the genes responsible for the retinal degeneration phenotype in these mutant lines.

Indexed as

Animals, Genetically ModifiedAnimalsBase SequenceCrosses, GeneticDNA Mutational AnalysisExonsFemaleGenetic LinkageGenotypeHomeodomain ProteinsIntronsMaleMolecular Sequence DataMutationPhenotypePolymerase Chain Reactioncone rod homeobox proteinHomeodomain ProteinsTrans-Activators

Identifiers

PMID16319818
PMCPMC2879142
OpenAlexW228795221

What OpenQuestion holds

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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.