Evidence map›Paper›PMID 30861003›Full record

ArticlePloS one2019

Why does the zebrafish cloche mutant develop lens cataract?

Mason Posner, Matthew S McDonald, Kelly L Murray, Andor J Kiss

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
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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

4 authors at 2 institutions in 1 country.

Mason PosnerDepartment of Biology, Ashland University, Ashland, Ohio, United States of America.ORCID 0000-0003-2817-3395
Matthew S McDonaldDepartment of Biology, Ashland University, Ashland, Ohio, United States of America.
Kelly L MurrayDepartment of Biology, Ashland University, Ashland, Ohio, United States of America.ORCID 0000-0002-4748-997X
Andor J KissCenter for Bioinformatics & Functional Genomics, Miami University, Oxford, Ohio, United States of America.
Ashland University · USMiami University · US

Funding

Using zebrafish as a model system for investigating lens development, aging and cataract.R15EY013535 · NEI · ASHLAND UNIVERSITY · PI POSNER, MASON · 2001 to 2024
$1.3M
NEI NIH HHS R15 EY013535
6 · The paper itself

Abstract

The zebrafish has become a valuable model for examining ocular lens development, physiology and disease. The zebrafish cloche mutant, first described for its loss of hematopoiesis, also shows reduced eye and lens size, interruption in lens cell differentiation and a cataract likely caused by abnormal protein aggregation. To facilitate the use of the cloche mutant for studies on cataract development and prevention we characterized variation in the lens phenotype, quantified changes in gene expression by qRT-PCR and RNA-Seq and compared the ability of two promoters to drive expression of introduced proteins into the cloche lens. We found that the severity of cloche embryo lens cataract varied, while the decrease in lens diameter and retention of nuclei in differentiating lens fiber cells was constant. We found very low expression of both αB-crystallin genes (cryaba and cryabb) at 4 days post fertilization (dpf) by both qRT-PCR and RNA-Seq in cloche, cloche sibling and wildtype embryos and no significant difference in αA-crystallin (cryaa) expression. RNA-Seq analysis of 4 dpf embryos identified transcripts from 25,281 genes, with 1,329 showing statistically significantly different expression between cloche and wildtype samples. Downregulation of eight lens β- and γM-crystallin genes and 22 retinal related genes may reflect a general reduction in eye development and growth. Six stress response genes were upregulated. We did not find misregulation of any known components of lens development gene regulatory networks. These results suggest that the cloche lens cataract is not caused by loss of αA-crystallin or changes to lens gene regulatory networks. Instead, we propose that the cataract results from general physiological stress related to loss of hematopoiesis. Our finding that the zebrafish αA-crystallin promoter drove strong GFP expression in the cloche lens demonstrates its use as a tool for examining the effects of introduced proteins on lens crystallin aggregation and cataract prevention.

Indexed as

alpha-Crystallin A Chainalpha-Crystallin B ChainAnimalsBasic Helix-Loop-Helix ProteinsCataractCrystallinsDisease Models, AnimalHematopoiesisLens, CrystallineMutationPhenotypeZebrafishZebrafish Proteinsalpha-Crystallin A Chainalpha-Crystallin B ChainBasic Helix-Loop-Helix ProteinsCrystallinsnpas4l protein, zebrafishZebrafish Proteins

Identifiers

PMID30861003
PMCPMC6413905
OpenAlexW2910200025

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.